Amoebic dysentery-What is amoebic dysentery?
Amoebic dysentery (amebicdysentery), also known as intestinal amebiasis (intestinalamebiasis), by pathogenic Entamoeba histolytica protozoa invade the colon wall caused by gastrointestinal diseases mainly dysentery symptoms. Lesions in the colon, ileocecal easy to relapse becomes chronic. The protozoa also by the intestinal wall by the blood flow - lymphatic or direct migration to the liver, lung, brain and other organs become intestinal amoebiasis, especially amoebic liver abscess is most prevalent.
Edit SummaryAmoebic dysentery - Basic OverviewFor the body only pathogenic amoeba, amoebic dysentery dysentery amoeba (dissolved histolytica, Amoebahistolytica) in human tissues and faeces large trophozoites the small trophozoites and cysts of three forms. Trophozoites in vitro resistance to weak, easy death. Cysts strong resistance to the outside world.(A) the size of 20 ~ 40μm the trophozoites large trophozoites rely pseudopodia certain direction, found in the feces or intestinal tissue of patients with acute swallowed tissues and erythrocytes, it is also known as tissue-type trophozoites. Small trophozoites 6 ~ 20μm size, pseudopodia, to host intestinal fluid, bacteria, fungi as food, do not eat red blood cells, also known as the intestine-type trophozoites. When host declining health, the secretion of soluble tissue enzymes, combined with their own movement and invade the intestinal submucosa becomes large trophozoites; into cysts pre intestine conditions change a negative effect on their activities, and then turn into cysts. The trophozoites dissemination.
(B) cysts are more common in the feces of latent infection and chronic patients, rounded, 5 ~ 20μm size, mature cysts have four nuclear Entamoeba histolytica infection type, infectious. Cysts in the stool on the outside resistant survive for at least 2 weeks, 5 weeks of water, the refrigerator 2 months, more resistant to chemical disinfectants, can tolerate 0.2% potassium permanganate for several days, the ordinary drinking disinfecting chlorine concentration of its no role in the killing, but the heat (50 ℃) and dry and very sensitive.
Entamoeba histolytica culture bacteria was symbiosis. A symbiotic culture has been successful, provided the conditions for the the pure antigen preparation and in-depth research Entamoeba histolytica.
Amoebic dysentery - EpidemiologyAmoebic dysentery and chronic patients, convalescent patients and cyst carriers is the main source of infection of the disease. Gastrointestinal spread through contaminated water, vegetables, fruits and food can also be spread indirectly through contaminated hands, supplies flies, cockroaches and other oral. Ordinary population susceptible to infection immunity (ie, does not produce protective antibodies), it is easy to re-infection. Of the disease throughout the world, prevalent in tropical and subtropical regions. China is more common in the north. The incidence rate in rural areas than in urban; men than in women, adults more often than children, most of them are sporadic, even outbreaks due to water pollution and other factors.Pathogenesis and pathological changes: amoeba cysts into the digestive tract, the lower section of the small intestine is trypsin and other digestive juices to digest, parasite excystation escape, and repeatedly divide to form the majority of small trophozoites, a stranger in the land of the ileocecal colon parts of the health of the host medium and small trophozoites with feces down below to sigmoid becomes cysts excreted, not pathogenic. Under suitable conditions, such as gastrointestinal function of the body is reduced; certain bacterial episome-like factor, enhanced virulence nourishing; trophozoites release of lysosomal enzymes, hyaluronidase, proteolytic enzymes and rely on its pseudopodia mechanical activity, invade the intestinal mucosa, destroying tissue formation of small abscesses and latent form (beaker-like) ulcers, deep muscle, causing extensive tissue damage trophozoites with necrotic material and blood from the intestinal tract, showing symptoms of dysentery.
Chronic changes in the mucosal epithelial hyperplasia, ulcers formed at the bottom of the granulation tissue around the ulcer, see the fibrous tissue hyperplasia, the formation of intestinal amebiasis. Trophozoites may also enter the intestinal wall vein into the liver through the portal vein or lymphatic cause the intrahepatic vein thrombosis and its surrounding inflammation, liver parenchymal necrosis, forming intrahepatic abscess right lobe. And can emboli forms of inflow of the lung, brain, such as the formation of migratory abscess. The the intestinal trophozoites also directly spread and surrounding tissue formation rectovaginal fistula, or a variety of lesions of the skin and mucosal ulcers. Individual cases can cause intestinal bleeding, intestinal perforation with peritonitis, appendiceal inflammation.
Visible under a microscope necrosis its primary lesions, lymphocytes, and a small amount of neutrophil infiltration. Serious bacterial infection was acute diffuse inflammatory changes, more inflammatory cell infiltration and edema, necrosis change. The lesion site visible multiple amoebic trophozoites, mostly gathered at the edges of the ulcer.
Amoebic dysentery - pathology classificationCommon type: onset and more slowly. Often abdominal pain, diarrhea. Diarrhea several times a day to more than ten times. The tenesmus varying degrees. The defecate medium, often pus or mucus typical stool was jam-like, corrupt stench. Can also be expressed as a simple diarrhea. Right lower quadrant tenderness. The course of a few days or a few weeks to relieve itself, if not treated, easy to relapse.
Fulminant: rare. Rapid onset, high fever, chills, diarrhea Day festivals worldwide, will be before a severe abdominal cramps, tenesmus obvious. The stool mucus bloody or blood samples, Stink. And vomiting, dehydration, rapid collapse. The physical examination see significant abdominal distension, diffuse abdominal tenderness, hepatomegaly. Not timely rescue, the concurrent intestinal bleeding, intestinal perforation, can cause death.
Chronic: symptoms persist or recurrent. Often abdominal pain, bloating, alternating diarrhea and constipation. Due to long-term bowel dysfunction in patients with weight loss, anemia, malnutrition or symptoms of neurasthenia. Colon wall thickening even palpable block of material, and tenderness.
Amoebic dysentery - Clinical performanceAmoebic dysentery average incubation period of 1 to 2 weeks (4 days to a few months), there are different types of clinical manifestations.(A) asymptomatic (cysts carriers) This type of clinical often not symptoms, the amoeba cysts found multiple Feces.
(B) The general type of onset and more slowly, systemic poisoning mild symptoms, often without fever, mild abdominal pain, diarrhea, a day will be about 10 times more than in moderate amount, blood and mucus, blood and necrotic tissue was jam mixed kind, with the stench of corruption, containing the dysentery amoeba trophozoites with a large number of red blood cells piles, one of its features. Low lesion with tenesmus sense. Abdominal tenderness in the right side of the main. Above symptoms and relieve itself. Can also be due to inadequate treatment of relapse.
(C) strong light seen in physical symptoms are mild, daily schedules thin paste or dilute water will be within 3 to 5 times, or diarrhea alternating with constipation appears, no diarrhea, only a sense of abdominal discomfort or pain, stool occasionally mucus or a small amount of blood to be investigated and the disease cysts and trophozoites. Without complications, the prognosis is good.
(D) fulminant rare, severe infection of the pathogen, or concurrent intestinal bacterial infections, and physical weakness, was fulminant. Abrupt onset of obvious symptoms of poisoning, chills, high fever, delirium, toxic intestinal paralysis. Severe abdominal pain and tenesmus, frequent diarrhea, dozens of times a day, or even incontinence, fecal, bloody, wash the flesh water or dilute watery, resembling acute dysentery, but fecal Stink, amebic trophozoites containing a large number of activities for its unique. Abdominal tenderness evident. To peripheral circulatory disorders often due to dehydration, or accompanied by a disturbance of consciousness, and even intestinal bleeding, intestinal perforation, peritonitis and other complications, the prognosis is poor.
(E) chronic type often due to improper treatment of the acute phase alternating diarrhea and constipation occur, so that the clinical symptoms of recurrent, persistent or February unhealed. Often cold, tired, eating carelessly and attack. Patients often feel lower abdominal pain, the long of fatigue, anemia and malnutrition. Right lower quadrant and thickening of the colon, mild tenderness; liver enlargement accompanied by tenderness. Feces mixed with pus and blood, trophozoites, sometimes with cysts.
(F) other type amebiasis visible urinary tract, reproductive system, skin infections, etc., but rare. Also the onset of complications, easily misdiagnosed.
Amoebic dysentery - etiology and pathogenesisEntamoeba histolytica life history, including trophozoites and cysts Phase. The basic process of the life history: cysts → trophozoites → cysts. Trophozoites have large, the small trophozoites stars, small trophozoites (luminal) of a diameter of about 10 ~~ 20μm, there is a single vesicular nucleus; large trophozoites (tissue-type) having a diameter of 20-40μm, cytosolic ectoplasm transparent, endoplasmic thick, which can contain glycogen, phagocytosis of red blood cells and tissue debris. Trophozoites of amoeba pathogenic stage, but non-infectious. Cysts seen of chronic amoebic ill or cysts carriers forming stool, a diameter of 5-20μm, Mature cysts 4 nuclear. The cyst is the infectious stage of the parasite.
Intestinal amoebiasis Entamoeba histolytica invasion of the colon wall diseases caused by oral infection, the main symptoms of diarrhea, abdominal pain, and it is also known as amoebic dysentery. 4 nuclear cysts with fecal contaminated water or food into the digestive tract, and can withstand stomach acid digestion, passed the upper section of the stomach and small intestine, excystation alkaline digestive juice to the lower segment of the small intestine develop into 4 small nourish body. The small trophozoites second division under suitable conditions proliferation, and down to the colon with feces. When the body's defenses are weakened bowel dysfunction, small trophozoites into the intestinal mucosa, phagocytosis of red blood cells and tissue cells into trophozoites, and a large number of proliferation, destruction of intestinal tissue, and the formation of ulcers.
Entamoeba histolytica pathogenic mechanism is not yet fully understood. Trophozoite surface film adhesion protein play an important part in the process of parasite invasion of host intestinal wall. As its a glycoprotein called adhesins or lectins, receptor like binding occurs with the mammalian target cells glycocalyx of galactose or acetyl galactosamine (Gal / GalNAc), so that nourish The body is adhered to the target cell. The trophozoite also secrete a into holes peptide and a variety of proteolytic enzymes. The former can be embedded in the target cell membrane and the target cell membrane permeability changes, dissolution occurs so that the cell host tissue; the latter can be dissolved. These factors are conducive to Entamoeba histolytica trophozoites invade host organization, the portal of entry is the opening of the midgut gland. From all aspects of the host pathogenic factors may include changes in innate susceptible hormones (such as adrenaline), the intestine environment (pH, redox potential, intestinal flora, etc.), malnutrition, primary and successors onset immunodeficiency and comorbidity. [1]
Amoebic dysentery - concurrent symptomsAmoebic dysentery complications points enteral, parenteral two categories:(A) of the intestinal mucosa ulceration depth of myometrial invasion and vascular complications when, can cause varying degrees of intestinal bleeding and intestinal perforation, the acute perforation may occur diffuse peritonitis or abdominal abscess. Chronic perforation is more common than acute perforation. Abdominal X-ray examination see subdiaphragmatic free gas can be diagnosed. Can also cause appendicitis. Amoeba tumors (colon granuloma), but not chronic inflammatory reactions, and the formation of granulomas, colon wall, can cause intussusception or obstruction. Biopsy help diagnosis.
(B) parenteral complications are the most common liver abscess, abscess perforation can be extended to nearby tissues and organs. By the trail directly involving the brain, lung, testicular, prostate, ovarian and other.
Amebic liver abscess (Amoebicliverabscess) can occur in the whole process of the disease, or the disease after a few weeks to several years. More to the long-term irregular fever onset, body temperature up to 39 ℃, common remittent fever, often accompanied by the right upper quadrant or right lower chest pain, liver enlargement of significant main clinical manifestations of tenderness. Abscess mostly single, mostly in the right lobe of the liver, because with the right lobe of the 4/5 of the entire liver volume, and intestinal lesions in the ileocecal department most of the blood circulation through the superior mesenteric vein inflow of the right lobe of the liver. Significant local symptoms and signs of liver abscess in the left lobe, in a relatively short time, but the diagnosis more difficult. Abscess superficial can have localized tenderness or with a sense of volatility, see this time line transhepatic liver-colored, fishy smell of pus containing dissolved necrosis of liver cells, red blood cells, fat, Charcot-Leyden crystals, trophozoites not more common, can be found in the abscess cavity wall, but did not find cysts. If the bacterial infection, abscess, yellow-green or yellow-white pus.
Chronic cases of fever and more obvious, weight loss, anemia, malnutrition, edema. Peripheral blood: WBC count increased the early period, the latter can be reduced to normal. The stool examination protozoa positive rate is not high. C duodenal drainage tube bile visible trophozoites.
Liver function tests are mostly normal transaminase, serum cholinesterase decreased slightly elevated alkaline phosphatase. X-ray examination showed the right diaphragm elevation, activity limitation, The local uplift diagnostic significance. Left lobe abscess, barium meal examination showed the pressure on the lesser curvature of the stomach and gastric body to the left phenomenon. B-type ultrasonic isotope liver scan, CT scan, magnetic resonance imaging and other tests to help diagnose.
Amoebic lung abscess and more swollen abscess secondary to its main symptoms of bacterial lung abscess, bronchiectasis similar. , And coughed up a lot of brown pus concurrent bronchopulmonary fistula. Can be complicated by pleurisy with pleural effusion, as was brown in the diagnosis. Amebic pericarditis is rare and may be left lobe amoebic liver abscess penetration pericardial Erzhi. Symptoms similar to bacterial pericarditis, is the most dangerous complications of the disease.
Amoebic dysentery intestinal complications and extraintestinal complications.
(1) intestinal complications
The ① intestinal bleeding: intestinal wall ulcer involving the blood vessels, can cause intestinal bleeding. How much blood loss ranged bleeding patients often appear pale, pulse breakdown and drop in blood pressure, hemorrhagic shock performance.② intestinal perforation: more common in fulminant. Perforation site cecum, appendix, and ascending colon is more common. Acute perforated diffuse peritonitis can cause serious illness. Chronic perforation caused by the surrounding tissue adhesion, the formation of a local abscess.③ appendicitis: of amebic appendicitis symptoms similar to ordinary appendicitis, easy to abscess formation, if chronic diarrhea or amoebic dysentery history, found in the feces of the amoeba trophozoites or cysts, contribute to the differential diagnosis of the two.The ④ nondysenteric colonic lesions: caused by proliferative lesions, including ameboma, intestinal of amebic granuloma and fibrous stenosis. The inflammatory pseudotumor ameboma the large intestine, abdominal pain and bowel habits change the most part with intermittent dysentery, can induce intussusception and intestinal obstruction, the main signs: the right iliac palpable removable, smooth goose egg-shaped or bowels like blocks, X-line to see occupying lesions have a good effect against amoebic treatment.
(2) parenteral complications: amoeba trophozoites from the intestinal blood lymphatic spread to distant organs and cause a variety of parenteral complications, such as the liver, lungs, pleura, pericardium, brain, peritoneum and genitourinary Road to form abscesses or ulcers, which is the most common liver abscess.
Amoebic dysentery - Differential DiagnosisThe diagnosis of amoebic dysentery (a)1, the clinical manifestations of slow onset, mild symptoms, diarrhea, fewer and dark red Secheng sauce-like droppings of the disease should be considered.
2 detection of Entamoeba histolytica, fecal examination under a microscope for diagnosis important basis. The bloody mucus loose stools Yi find trophozoites, cysts fecal matter part is easy to find.
3, sigmoidoscopy varying sizes scattered in the shape of the latent ulcer edge slightly elevated, blush, ulcers mostly normal mucosa. Scraped from the ulcer specimens microscopic examination found the pathogen more opportunities.
X-ray barium enema intestinal stenosis, ameboma a certain value.
The serological examination available amoebic pure antigen detection of specific antibodies, formation of antibodies vivo invasive lesions square cyst carriers antibody test was negative. Commonly indirect hemagglutination, ELISA, indirect fluorescent antibody, counter immuno electrophoresis, agar diffusion precipitation test.
(B) Differential Diagnosis
This disease and bacillary dysentery. Japan schistosomiasis, Gram giardiasis, intestinal tuberculosis, nonspecific ulcerative colitis differentiated. Amebic liver abscess subphrenic abscess, cholelithiasis identification of primary liver cancer, liver bursitis.
Amoebic dysentery - treatment methodGeneral treatment of amoebic dysentery (a)
Acute phase should rest in bed, gut isolation until the symptoms disappear, stool for three consecutive times finding out trophozoites and cysts, better nutrition, infusion or transfusion when necessary. With acute and chronic dysentery.
(B) the pathogen treatment
Metronidazole (Flagyl) Adult 0.4 ~ 0.6g, 3 times a day, and even served 5 to 7 days, children 15mg/kg, 3 times a day, once every 3 to 5 days. Not oral administration the available intravenous injection of 0.5%, can change oral oral. Medication during Jijiu, pregnant women and lactating women Jifu. Chronic cases, can be used to retain the enema. Attention to the side effects of the drug: nausea, dizziness, palpitations, leukopenia, and other.
2, the tinidazole (metronidazole sulfonyl imidazole) adult daily 2.0g daily for children 50mg/kg every morning serving Dayton, the 3rd one course of treatment. Thiazole can also use the piperazine denitrification 0.18,3 / d, children 10mg / (kg · d), treatment 7 ~~ 10d, when necessary, and even served 1 to 2 courses.
3, dehydroepiandrosterone emetine (dehydroepiandrosterone ipecac base): Adults 60 ~ 80mg, pediatric lmg / kg, twice a day, intramuscular injection, once every 5 to 10 days. More toxic hydrochloric emetine small, less serious side effects.
4 emetine (hydrochloric acid emetine): the adult 60mg, pediatric lmg / kg, twice a day, intramuscular injection on the 6th. To the onset of myocardial damage and toxic myositis, treatment should be bed rest, often observe blood pressure, pulse, electrocardiogram, prior to each injection to listen to heart sounds, blood pressure, and are subject to change, you should consider the reduction or withdrawal. Pregnant women and heart, kidney patients hanged. Large trophozoites have a direct role in the killing, and quickly to control the symptoms of acute dysentery and extraintestinal complications, but the small intestinal lumen trophozoites and cysts invalid.
5 dichloro San: 0.5g, 3 times a day, and even served on the 10th.
In the application of these drugs a course, you are required to use one of the following drugs continue treatment. Metronidazole can be used alone.
① sulfonamide iodine quinoline: 0.5 g / d, used in conjunction 10d.② Iodoquinol: 0.6g, 3 / d, and even served 20d.③ paromomycin: 0.5g / d, 10d for a treatment course. Fulminant optional By Miding 3d, a course of metronidazole, while adding norfloxacin or tobramycin or ceftriaxone latamoxef to combat secondary bacterial infection.
Chinese medicine treatment: alone or in combination with other anti-amoebic drugs.
① Differential Treatment: the same bacillary dysentery.
(2) selection of effective herbs such as Pulsatilla, javanica, garlic, etc. in the light of local conditions.
7, with cysts treatment: can I dichloro scattered 0.5g 3 / d, a total of 10d; or metronidazole 0.4g / d for 5 days.
8, contact medical observation necessary clothing metronidazole a course of treatment. Stool changes, should be promptly smear or culture dysentery amoeba.
(C) the treatment of amoebic liver abscess
1, metronidazole 0.4g, 3 times a day, the inflammation of the course of 2 to 3 weeks, a abscess period of 4 weeks, abscess smaller puncture pus.
2, phosphate chloroquine 0.5g, 3 times a day, after 2 0.25g daily three times, once every three weeks. The medication is not effective seven days can change his drug.
3, liver puncture pus while medication can puncture the abscess, the abscess is greater pus into the Tugen base 30 to 60mg. The pus should be culture sensitive antibiotics should be added, if secondary bacterial infection.
Amoebic dysentery - herbal unilateralAmoebic dysentery Chinese herbal treatment of amoebic dysentery javanica, Pulsatilla and garlic.(1) Brucea javanica: evergreen shrub or small tree of Simaroubaceae Brucea javanica mature seeds, mainly produced in Guangxi, Guangdong and other provinces. Autumn fruit ripening harvest, dried, shelled Ren the dry longan meat and encapsulated swallow, or pressure to oil, made of pills or tablets clothing. Taste the bitter cold of the character, in the final of the large intestine, the liver. Detoxify, anti-malaria cut malaria, the effect of corrosion wart. Oral available to treat Noxious Heat dysentery, cold product Jiu Li and dysentery, topical can cure corns wart. According to previous treatment experience cold product Jiu Li, Modern clinical for the treatment of amoebic dysentery, to take oral enema and methods. Oral, each adult 10 to 20, children 2 years old, swallow capsules, 3 times daily for 7 to 10 days for a course of treatment, and 20 Brucea javanica pestle, adding 1% sodium bicarbonate solution 200ml, soak 2 hours as a retention enema daily, has a good effect on the acute and chronic amoebic dysentery. Its mechanism of action is of Brucea javanica its active ingredients the amoeba have to kill and inhibition. The goods on the gastrointestinal tract, liver and kidney damage are not appropriate to use Jiufu. Gastrointestinal bleeding and liver kidney patients, should be hanged or caution.
(2) Pulsatilla: Ranunculaceae perennial herb Pulsatilla root. Distributed in Northeast China, Inner Mongolia, and North. Spring before flowering or late fall when the leaves yellow before harvest to retain the root head white fluff, remove the leaves and residual stems and fibrous roots, wash dirt, dried, raw with. The medicinal taste the bitter cold, owned by the large intestine through, there are detoxification, cooling blood Zhilishen efficacy, clinical commonly used to treat hot Noxious dysentery, Qin skin compatibility Jiantang wash available Yin Yang, trichomonas vaginitis. FDA treatment of bacillary dysentery and amoebic dysentery, and have good results. Such as the treatment of amoebic dysentery, Single Pulsatilla 15 ~ 30g, decoction, 3 service points, seven days for a course of treatment; seriously ill by another FDA 30 ~ 60g, Jianshui retention enema daily, quite good effect. The main mechanism of Pulsatilla treatment of amoebic dysentery: Pulsatilla decoction and saponins contained obvious anti-amoeba role.
(3) Garlic: Liliaceae perennial herb of fresh garlic stems. All over the country set out to training. May leaf blight excavation, dry medicine. The potency Weixin temperature, spleen, stomach, lung meridian. The scattered carbuncle swelling, detoxification insecticidal efficacy, clinical commonly used to treat a carbuncle swollen sore ringworm sores pruritus, cough tuberculosis Dayton, dysentery, diarrhea, hookworm and enterobiasis of. Garlic on acute and chronic amoebic dysentery are effective in the prevention and control of dual-purpose. The single fresh garlic, or 10 ~ 15g garlic mash, sugar water, blunt. Garlic syrup, or oral administration of 10% per serving 5 ~ 20ml, 3 times day. Or garlic extract 100ml of 10% retention enema once a day, once every 6 days.
Amoebic dysentery - formation characteristicsAmoebic dysentery, bacillary dysentery in the early stages of disease usually presents with diarrhea without blood and pus, later typical pus and blood will be the cause of this phenomenon is caused by the intestinal pathological changes of bacillary dysentery patients.Shigella through the mouth into the digestive tract, in the stomach by gastric acid that kill. People lowered immunity, Shigella stomach into the small intestine, the large population of some dead bacteria release endotoxin, stimulate the intestinal wall so that the increased permeability. Toxins being absorbed into the bloodstream, which may eventually be discharged from the colon mucosa, irritable colon and cause mucosal damage, on this basis, Shigella, and intestinal bacteria in the mucosal surface and submucosal breeding further disruptive, causing inflammation reaction.
Early onset of secretion of Shigella endotoxin and inflammation stimulate the intestinal wall nerve endings, causing intestinal cramps, bowel movements increased intestinal wall to absorb moisture and lower bowel wall vascular serous exudate, and suffered from diarrhea; Thereafter, intestinal diffuse congestion and edema, massive neutrophil infiltration, accompanied by a lot of mucus and fibrin exudate, and finally to the formation of ulcers, bleeding, mucous pus before.
Amoebic dysentery stool characteristics with intestinal lesions into different, some form of liquid, some were semi-mobile, and even shaped stool, which can be no blood or mucus attached. Dysentery attack, the amoeba in intramural breeding, causing tissue necrosis, or invasion deeper, more bleeding, necrotic tissue mixed with blood with stool, constitutes a amoebic dysentery unique jam color, kind of frozen fish, the stench of fecal matter more bloody stool.
Amoebic dysentery - prevention and control points1 pay attention to food hygiene, personal hygiene and civilized way of life, do not drink unboiled water, do not eat unclean fruits and raw vegetables, and develop hors d'health habits food wash their hands before and after production.2. Strengthen manure management, health management of livestock pens, according to local conditions good manure treatment, improved sanitation.Protection of public water to prevent fecal contamination. Drinking water should be boiled.Strengthen the health management of the canteen. Operation of food production and staff should have health supervision measures.5. Vigorously fight flies, cockroaches, fly-proof cover or other measures to avoid contamination of the food is.6. Patients should be treated quickly, outbreaks have been reported in infectious disease management approach, disinfection, isolation processing. Should be made to check on family members or contacts.The number of cases in an area, to quickly for laboratory tests to confirm the diagnosis and for epidemiological investigation and take appropriate measures.
Amoebic dysentery - Safety Tips1. Of the disease throughout the world, prevalent in tropical and subtropical regions. China's more common in the north. The incidence rate in rural areas than in urban; men than in women, adults more often than children, most of them are sporadic, summer and autumn higher incidence of water pollution and other factors, even the outbreak.
2. Chronic amoebic dysentery usually caused by the acute phase of improper treatment or patients with poor physical symptoms recurring more than 2 months delayed healing, exacerbation of clinical symptoms similar to patients with acute and chronic illness anemia, weight loss, nutrition bad and hepatomegaly.
3. Modern medicine of the disease of chronic disease and asymptomatic parasite is the main source of infection of the disease, its discharge feces amoeba cysts by hands, food, drinking water, flies and cockroaches pathway by Mouth digestive tract into the body.
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Tuesday, November 6, 2012
Gastrorrhagia-Stomach Bleeding
Gastrorrhagia-What is stomach bleeding?
Cause stomach bleeding for many reasons, not necessarily are gastric ulcer caused stomach bleeding and other diseases can also cause stomach bleeding, stomach ulcers are a digestive disease, more common in clinical, and stomach bleeding gastric ulcer. concurrent symptoms, from 20% to 30% of patients with ulcers have stomach bleeding, so if the patient's friends appeared stomach bleeding Do not worry, be sure to go to regular hospital for examination, find out the reasons for the cause of treatment. Often associated with stomach bleeding disease
More than 40% of stomach bleeding stomach bleeding from the stomach, duodenal ulcer caused the overworked, irregular diet, mood disorders, stress and other gastrointestinal history of crowd morbidity; followed by stomach bleeding caused by acute hemorrhagic gastritis both causes stomach bleeding mostly after formal treatment can be an effective treatment. Addition of stomach bleeding caused by cirrhosis of the liver, cirrhosis patients tend to develop into esophageal varices, and then eat coarse food, emotional over-stimulation, esophageal and gastric veins burst occurs bleeding. The stomach bleeding up to 10% mortality was not to underestimate gastrorrhagia. If hematemesis or melena, we must consider the possible gastric and duodenal ulcer bleeding. Some people only melena main complaint, some patients showed a sudden syncope, and even shock, after a series of checks sent to hospital emergency stomach, duodenal ulcer bleeding.
Stomach bleeding - CausesCause of cause stomach bleeding a lot, but the most common bleeding caused by rupture of the stomach, duodenal ulcer and esophageal varices.
Gastrorrhagia1, stomach, duodenum diseases: gastric ulcer, duodenal ulcer, acute gastric erosion, stress ulcer, chronic gastritis, gastric cancer, gastric polyps, gastric leiomyosarcoma, gastric leiomyoma mucosal prolapse post-operative anastomotic ulcer, intussusception, gastric granulomatous lesions, duodenal diverticulum.
2, esophageal disease: esophageal varices, esophageal responsibilities door-Weiss syndrome, hiatal hernia, esophagitis, esophageal ulcers, esophageal cancer, esophageal benign esophageal diverticulum.
Vascular lesions: aortic aneurysm, splenic artery aneurysms, small aneurysms parietal, hemangioma, the gastric submucosal arteriovenous malformation, hereditary hemorrhagic telangiectasia.
4, hepatobiliary and pancreatic disease: cirrhosis with portal hypertension, liver cancer with portal hypertension, portal vein thrombosis, portal vein obstruction syndrome, biliary tract bleeding, ampullary cancer, pancreatic duodenum, acute pancreatitis.
5, systemic disease and other: epidemic hemorrhagic fever, leptospirosis, pulmonary heart disease, emphysema co-infection, blood coagulation disorders, leukemia, purpura, hemophilia, disseminated intravascular coagulation, lymphoma , uremia, amyloidosis, sarcoidosis.
Cause stomach bleeding for many reasons, not necessarily are gastric ulcer caused stomach bleeding and other diseases can also cause stomach bleeding, stomach ulcers are a digestive disease, more common in clinical, and stomach bleeding gastric ulcer. concurrent symptoms, from 20% to 30% of patients with ulcers have stomach bleeding, so if the patient's friends appeared stomach bleeding Do not worry, be sure to go to regular hospital for examination, find out the reasons for the cause of treatment. Often associated with stomach bleeding disease
More than 40% of stomach bleeding stomach bleeding from the stomach, duodenal ulcer caused the overworked, irregular diet, mood disorders, stress and other gastrointestinal history of crowd morbidity; followed by stomach bleeding caused by acute hemorrhagic gastritis both causes stomach bleeding mostly after formal treatment can be an effective treatment. Addition of stomach bleeding caused by cirrhosis of the liver, cirrhosis patients tend to develop into esophageal varices, and then eat coarse food, emotional over-stimulation, esophageal and gastric veins burst occurs bleeding. The stomach bleeding up to 10% mortality was not to underestimate gastrorrhagia. If hematemesis or melena, we must consider the possible gastric and duodenal ulcer bleeding. Some people only melena main complaint, some patients showed a sudden syncope, and even shock, after a series of checks sent to hospital emergency stomach, duodenal ulcer bleeding.
Stomach bleeding - CausesCause of cause stomach bleeding a lot, but the most common bleeding caused by rupture of the stomach, duodenal ulcer and esophageal varices.
Gastrorrhagia1, stomach, duodenum diseases: gastric ulcer, duodenal ulcer, acute gastric erosion, stress ulcer, chronic gastritis, gastric cancer, gastric polyps, gastric leiomyosarcoma, gastric leiomyoma mucosal prolapse post-operative anastomotic ulcer, intussusception, gastric granulomatous lesions, duodenal diverticulum.
2, esophageal disease: esophageal varices, esophageal responsibilities door-Weiss syndrome, hiatal hernia, esophagitis, esophageal ulcers, esophageal cancer, esophageal benign esophageal diverticulum.
Vascular lesions: aortic aneurysm, splenic artery aneurysms, small aneurysms parietal, hemangioma, the gastric submucosal arteriovenous malformation, hereditary hemorrhagic telangiectasia.
4, hepatobiliary and pancreatic disease: cirrhosis with portal hypertension, liver cancer with portal hypertension, portal vein thrombosis, portal vein obstruction syndrome, biliary tract bleeding, ampullary cancer, pancreatic duodenum, acute pancreatitis.
5, systemic disease and other: epidemic hemorrhagic fever, leptospirosis, pulmonary heart disease, emphysema co-infection, blood coagulation disorders, leukemia, purpura, hemophilia, disseminated intravascular coagulation, lymphoma , uremia, amyloidosis, sarcoidosis.
Respiratory Muscle Fatigue
Respiratory muscle fatigue-What is the respiratory muscle fatigue?
Respiratory muscle fatigue or respiratory muscle dysfunction is very common in chronic lung disease and ICU hospitalized patients. For a long time, respiratory muscle fatigue or failure is not taken seriously. Timely detection and treatment of respiratory muscle fatigue can correct abnormal respiratory mechanics, and reduce the work of breathing, improve oxygenation, to shorten the duration of mechanical ventilation. Therefore, evaluation of respiratory muscle function in critically ill patients in recent years has become an important part of the intensive care.
Edit Summary- Overview of respiratory muscle fatigueBreathing exercise breathing exercise is a prerequisite to change thoracic volume depend on the activities of the respiratory muscles, causing lung contraction provide the driving force for the realization of pulmonary ventilation.Respiratory muscles of the human body is the belch muscle and intercostal muscles (including aid room, outside the muscle), there are the muscles of the abdomen and the neck accessory muscles of breathing only difficulty breathing when involved in assisted breathing.
Respiratory muscles and other muscles of the body, all belong to the skeletal muscle. Respiratory muscle are different from most skeletal muscle, it is the only life depends on skeletal muscle contraction regularly throughout the life course, and never-ending. Therefore, the respiratory muscles is an important part of the respiratory pump, is the completion of the power of the external respiratory function. In order to guarantee enough power breathing, respiratory muscle strength and endurance must maintain a certain strength. Due to illness and other reasons, the respiratory muscles to long-term overload, can not produce and maintain muscle strength, namely atony called respiratory muscle fatigue. Effective alveolar ventilation due to respiratory muscle weakness, reduce, and eventually can lead to respiratory failure.
Generally believed that chronic obstructive pulmonary disease patients (including chronic bronchitis, emphysema, asthma), the air over the resistance continues to increase, and the long period of hypoxemia, carbon dioxide retention and systemic malnutrition state, prone to respiratory muscle fatigue. Followed by neuromuscular diseases, such as bilateral diaphragm paralysis, myasthenia gravis, Guillain-Barre syndrome, some poisoning, and cardiogenic shock, septic shock, toxic shock can cause respiratory muscle weakness, fatigue, Finally, leading to respiratory failure.
Respiratory muscle fatigue - academic explainRespiratory muscle fatigue treatment instrument 1 definition of respiratory muscle fatigue according to the definition set by the 1988 U.S. Heart, Lung, and Blood Institute (NHLBI), respiratory muscle fatigue refers to the force of contraction of the respiratory muscles bear the load and (or) contraction speed reduced, and this reduction can rest and recover.2, the so-called respiratory muscle fatigue muscle activity under load and cause it to produce a reduced ability of the strength and speed of the decline in this ability can rest and recovery. Discuss endometriosis endometrial growth function The parts of the tissue outside the uterine cavity covering mucosa.
3, respiratory muscle fatigue is caused by a variety of respiratory muscle contraction and relaxation activities can not produce the need to maintain a certain amount of alveolar ventilation pleural pressure, the muscle itself can be manifested as muscle strength, and (or) systolic and diastolic velocity decreased, and The decline in this ability after a rest can be restored.
, Respiratory muscle fatigue respiratory muscle contraction can not produce the gas required to maintain adequate alveolar pressure, thereby affecting gas exchange, respiratory muscle fatigue is the development of a variety of clinical conditions hypercapnia respiratory failure final common pathway.
, Respiratory muscle fatigue is not against the burden of respiratory muscle strength and endurance respiratory muscle contraction that can not produce the driving pressure required to maintain adequate alveolar ventilation which is the main reason ventilator dependent. The factors leading to respiratory muscle fatigue: the endogenous end expiratory positive pressure (PEEP).
Respiratory muscle fatigue, respiratory muscle fatigue is the respiratory muscle activity under load and cause it to generate force and (or) the speed of a reduced ability to decline in this ability can rest and recovery. Respiratory muscle fatigue (pump failure) is breathing failure an important part of the disease process.
7, the so-called respiratory muscle fatigue is the case of the continued contraction of the respiratory muscles, can no longer maintain the required or intended muscle occlusion side: right nine cases, 17 cases left. The occlusive reasons: cerebral thrombosis nine cases of cerebral infarction 17 atrial fibrillation patients (9 cases).
Respiratory muscle fatigue - etiologyThe majority of patients with respiratory muscle fatigue in patients with respiratory muscle fatigue is caused by the disease itself, has been found to sepsis (sepsis), multiple organ failure, mechanical ventilation hypercapnia (acidosis), and a variety of drugs can cause abnormal neuromuscular function and become the important disease pathophysiology process.In short, the respiratory muscle fatigue and weakness, health search is very common in the critically ill COPD and other chronic diseases in addition to the effects of the disease itself, a variety of drugs, such as glucocorticoids muscle relaxants aminoglycoside antibiotics can induce or aggravate respiratory muscle fatigue, breathing specificity, and accuracy of the machine improper application can also be caused by diaphragmatic dysfunction various checks respiratory muscle fatigue are poor and difficult routine clinical applications attention to clinical examination to detect the presence of respiratory muscle fatigue.
Respiratory muscle fatigue - pathogenesisTreatment of respiratory muscle fatigue instrument respiratory muscles, including the diaphragm intercostal muscles, the abdominal muscles can be divided into inspiratory muscles (diaphragm, intercostal muscle, sternocleidomastoid sternocleidomastoid and scalene according to the functional classification of respiratory muscle) and expiratory muscle (intercostal muscle abdominal muscle) according to the nature of the muscle fibers can be divided into red muscle fibers (also known as slow contraction fatigue resistant fibers or fiber type Ⅰ) and white muscle fibers (also known as fast contraction fibers or II class fiber ). The Class Ⅱ fibers can be divided into resistance to fatigue fast contraction fibers (Ⅱ A fibers) and fast contraction fast fatigue fiber (II)The main function of the respiratory muscles is complete breathing exercise followed by participation in the cough expectoration vomiting. 2/3 of the diaphragm about the most important role shoulder throughout the respiratory function of 3% to 90% of the tidal volume of diaphragmatic contraction. When the auxiliary respiratory muscles involved in the contraction increased minute ventilation or presence of diaphragmatic fatigue. In quiet breathing expiratory muscle does not participate in the contraction in respiratory function increases intercostal muscle and abdominal expiratory muscle contraction, squeezing the diaphragm to the chest cavity, the diaphragm muscle fiber is the best bit early long tension.
1.COPD patients with skeletal muscle dysfunction (including respiratory muscles) in patients with COPD decreased exercise tolerance has a direct relationship. COPD patients with skeletal muscle structure changes showed a decline in muscle weight, changes in the structure of the muscle fibers (I class fiber reducing the proportion of the increase in the proportion of class II fibers, fiber atrophy of class Ⅰ and Ⅱ A I class and II class fiber diameter decreases) reduce the number of capillaries in skeletal muscle per unit area of the tree (oxidase activity decreased) function to change the performance of muscle strength reduced the partial oxygen uptake and oxygen transport significantly limited maximal exercise decreased endurance and metabolic changes. The main reason for the above structural and functional changes the: ① long-term hypoxemia, hypercapnia infection and chronic malnutrition; ② accompanied by electrolyte disorders (hypokalemia, hypophosphatemia, low magnesium) heart failure muscle disuse atrophy; ③ glucocorticoid-induced acute and chronic myopathy. Due to lung hyperinflation in COPD patients with severe airway obstruction, so that the mechanical characteristics of the respiratory system were to change significantly, significantly negative contraction of the diaphragm in the beginning of a long position shrink the efficiency significantly reduce health search combined with the various factors can easily lead to diaphragmatic fatigue and failure.
Characteristics of sepsis in patients with sepsis (Sepsis) system blood flow is normal or increased tissue oxygen uptake capacity decreased local perfusion reduction and tissue hypoxemia. Respiratory muscle, sepsis and shock the total perfusion increased Zhui but barriers to local microvascular perfusion and increased work of breathing can still cause respiratory muscle hypoxia and respiratory muscle dysfunction.
Mechanical ventilation on respiratory muscle mechanical ventilation for respiratory muscle function has two sides alternative or auxiliary respiratory muscles acting on the one hand fatigue of respiratory muscles to rest on the other hand lead to respiratory muscle disuse atrophy, respiratory muscle strength decreased and endurance produces ventilator dependent. Skeletal muscle atrophy major changes include:
(1) muscle weight was significantly reduced.
(2) the decline in protein synthesis.
(3) muscle fiber mesh diameter reduction.
(4) reduces the number of anti-fatigue fiber slow contraction.
Respiratory muscle fatigue (5) decreased mitochondrial glucose oxidation and decomposition. Although the respiratory muscles have unique characteristics different from ordinary skeletal muscle network, but can be found in the long-term controlling mechanical ventilation reduce the activity of the diaphragmatic EMG, transdiaphragmatic pressure decreased respiratory muscle endurance, reduce. Brochard et al healthy baboons for 11 days the controlling ventilation discovered a 25% reduction in Pdi Stamina reduced by 36% mechanical ventilation health search whether another major determinants of respiratory muscle atrophy muscle fiber length muscle fibers length of long-term fixed Zhui under its normal length, it is very easy to produce fatigue can avoid the occurrence of muscle atrophy; rather more than the length of its base.4, over a period of time in mechanically ventilated patients, respiratory muscle function in the process of weaning, respiratory muscle function is to determine whether weaning one of the key factors. Most difficult weaning patients in the clinical respiratory muscle fatigue Cohen et al found 12 cases of patients with difficult weaning study 7 patients EMG spectrum changed and prompts diaphragmatic fatigue, six cases of the six patients had abnormal abdominal breathing breathing Frequency faster, some patients with frequent cause of failure and respiratory muscle fatigue diaphragmatic fatigue weaning accelerate faster and PaCO2 increased suggesting that these patients breathing frequency and PaCO2 increased EMG spectral changes in breathing frequency.
5 the polyneuropathy sepsis in critically ill patients, multiple organ failure (MOF) can occur in patients with polyneuropathy main sensory - motor nerve damage, called critical illness polyneuropathy in ICU about more than 70% of patients with varying degrees of neuropathy. Bolton electrophysiological studies of 43 patients with sepsis and MOF patients, 30 patients have abnormal axonal degeneration associated with sensory and motor potential, 15 patients with clinical manifestations weakness weaning failure, critical illness multiple neural reflex diminished or disappeared The main clinical manifestations of lesions extremities weakness with atrophy, weakening or disappearance of sensory dysfunction deep reflection cranial nerve function is normal Zhui critical illness polyneuropathy self-limiting, and can be fully restored after a period of time, but the EMG there is a surviving abnormal Zhui now think this secondary neuromuscular disease is caused by the difficulty of weaning and prolong the ICU stay an important factor in 62% of patients with weaning difficulties relating.
Critical illness polyneuropathy mechanism is not yet clear, nutritional disorders poisoning, metabolic abnormalities, and vascular factors might be involved in the occurrence of neuropathy has also been suggested that the hypoxic edema caused by ischemia in the nerve and blood - nerve barrier damage nerve damage the main reason for the diagnosis of critical illness polyneuropathy mainly by electrophysiological studies, peripheral nerve axon injury is the main electrophysiological changes typical performance for seven days after the onset of resting EMG fibrillation potential incubation period of change and positive sharp wave neural potential map manifests itself in the segment of the proximal and distal nerve impulse conduction velocity normal reduce mixed muscle action potential amplitude. Typical change of primary demyelination of nerve conduction velocity decreased significantly extend the distal latency of compound muscle action potential scattering, block and F-wave potential of increased little in critical illness polyneuropathy patients appear.
6. Drugs on respiratory muscle function
Respiratory muscle fatigue (1) corticosteroids: high-dose or long-term use of glucocorticoids can cause a variety of side effects, including myopathy. Animal experiments confirmed that health search corticosteroids can significantly reduce the force of contraction of the diaphragm hormone induced myopathy pathological basis may reduce the fast contraction fibers (I type) protein synthesis, increased catabolism lead to the type of muscle fiber atrophy. Currently, corticosteroids induced myopathy the exact mechanism is not yet clear, but fast contraction fibers atrophy inevitably lead to muscle contraction capacity decreased when accompanied by application of muscle relaxants or patients are prone to increased work of breathing, diaphragmatic fatigue tissue blood perfusion can be further deterioration of the function of the respiratory muscles. Studies have reported that the incidence of corticosteroid-induced acute severe asthma myopathy up to 10%(2) neuromuscular blocker: application of mechanical ventilation, neuromuscular blocking agents (NBA) the health search of purpose is to help the smooth implementation of mechanical ventilation, improve the coordination of human - machine to reduce oxygen consumption in patients with intracranial hypertension avoid intracranial pressure fluctuations in the late 1970s, a British survey showed that 90% health search ICU patients routine application of muscle relaxants. For nearly 20 years, due to the emergence of powerful sedatives, the ventilator performance improvement and in-depth understanding of the pharmacological properties of NBA, especially NBA can cause muscle relaxation delay and myopathy there is a decreasing trend in the application of muscle relaxants NBA direct toxic effect on the muscle is not yet clear but it can enhance muscle function already exists an abnormal increase in the role of muscle toxicity of drugs or drug metabolites, the muscle relaxant effect continued to extend and can cause acute myopathy. At the same time, the application of certain drugs to prolong and enhance the role of the NBA.
Respiratory muscle fatigue - symptomsClinical manifestations: respiratory rate, breathing out of sync (such as periodic abdominal pressure and chest pressure breathing alternately, confusion, and not parallel abdominal pressure breathing abdominal bimodal breathing exercise) and paradoxical abdominal respiration.
Complications: concurrent diaphragmatic fatigue.
Respiratory muscle fatigue - CheckLaboratory tests
Respiratory muscle fatigue drug, maximum inspiratory pressure (MIP) with the greatest effort in the residual gas bit (RV) or functional residual air-bit (FRC) http://www.huoguan.com blocked airway suction can maximum inspiratory mouth pressure. The MIP measured clinical significance is: inspiratory muscle function in neuromuscular disease evaluation and diagnosis of the disease and the severity of the judgment parameters when MIP <normal expected value of 30%, and prone to respiratory failure; (2) evaluation of pulmonary disease (COPD) patients with respiratory muscle function in the thoracic deformity and drug intoxication; (3) used to predict weaning is generally believed that the MIP <-30cmH20 the likelihood of successful weaning. But with MIP predict weaning false negative rate is very high, mainly due to patients is not well with the measurements.Maximal expiratory pressure (MEP) in total lung capacity (TLC) airway blocked with maximum efforts to breath can generate maximum oral expiratory pressure they reflect all indicators of respiratory muscle strength is not entirely representative of the diaphragm function. Near the mouth end of the endotracheal tube with a pressure sensor value as the measurement value determination of MIP and MEP measurements repeated several times, take good reproducibility of mechanically ventilated patients when When obvious Zhui the airflow obstruction, the measurement of these indicators be affected, each measurement variability increases Moreover, the results also influenced by the patient's subjective efforts the normal MIP is no unified standard laboratory reports a very different health search, and certainly there are differences between Asians and Westerners kinds.
Transdiaphragmatic pressure (Pdi) Pdi is the diaphragmatic contraction of the diaphragm chest, ventral pressure difference on behalf of the diaphragmatic contractility largest transdiaphragmatic pressure (Pdimax) of means in functional residual air-bit (or residual gas bits), airway blocking state the utmost to inhale the Zhui Pdi max Pdimax, reflects pressure when the diaphragm for maximum contraction is not a reliable indicator of diaphragmatic fatigue evaluation of respiratory muscle strength Zhui Pdi the Pdimax lower when Pdi maintained at 40% level of http://www.huoguan.com of Pdimax suggesting diaphragmatic fatigue. Determination of transdiaphragmatic pressure more complex subject esophageal balloon and intragastric balloon pressure of the esophagus and gastric pressure were measured the inspiratory phase difference between the two shall Pdi
3, the diaphragm tension - time index (TTdi) of the indicators reflect good indicator of respiratory muscle endurance in terms of evaluation of respiratory muscle endurance is more important than strength muscle endurance depends on the energy supplied to the muscle fiber composition and the size of the work is done. Acting the size depends on the power of muscle contraction and sustained Zhui time. Diaphragmatic strength of individual differences, in order to reduce individual differences, diaphragmatic contraction the Pdi average of Pdimax ratio is used to reflect the strength of contraction, the Zhui the ratio of inspiratory time (Ti) and total respiratory cycle time (Ttot) reflect the product of the duration of both diaphragmatic contractility is TTdi. Formula: TTdi = Pdi / Pdimax, x Ti / Ttot. When TTdi value <0.15 in the case of the presence of inspiratory resistance load prone fatigue, while when TTdi value> 0.15 diaphragmatic fatigue time will be significantly shortened. It should be noted that the Determination of TTdi is completed in the case of artificial resistance, there may be a wide gap between how to determine respiratory muscle fatigue in various disease states, domain values need to be further explored with spontaneous breathing.
Other laboratory examinations
Respiratory muscle fatigue drugs. Diaphragmatic EMG EMG can be used for the detection of diaphragmatic intercostal muscle and physiological activity of the abdominal muscles during mechanical ventilation in critically ill patients is difficult to conventional for electromyography physiological examination carried out, and check interfering factors. repeatability and accuracy of the results are poor thin needle through the skin to the diaphragmatic percutaneous electrode than percutaneous electrode obtained data are accurate and reliable. EMG different Zhui frequency spectrum mainly between 20 ~ 250Hz, the spectral distribution of the change Zhui increase fatigue early in the process performance of the first diaphragm muscle Zhui reduce fatigue EMG spectrum of low-frequency component (L), high-frequency reduce health search component (H), H / L than the decline in the underlying value of 20% means that the spectrum significantly change the high frequency components from the accumulation of the metabolic toxic substances in the muscle caused a short recovery period (a few minutes) and the low-frequency components by muscle structural changes caused by the recovery takes more than 24h dynamic observation of EMG can be early detection of the presence of respiratory muscle fatigue. Clinically, such as the low-frequency components in the process of withdrawal of mechanical ventilation increase prompted at least 24 ~ 48h to the fatigue of respiratory muscle contractile function was restored.Phrenic nerve electrical stimulation of phrenic nerve stimulation of the diaphragmatic contraction is mainly dominated by the phrenic nerve with Pdi observed after stimulation of the phrenic nerve of the body surface or needle electrodes or the EMG diaphragmatic function may reflect the advantages of the method is to objectively evaluate diaphragmatic Zhui contractile properties and mechanical characteristics of the chest wall without self-effort or breathing affect shortcomings is to stimulate local pain, electrodes accurate positioning difficult, especially in patients with irritability postural change will affect the accuracy of the measurement. COPD and obese patients if there is the sternocleidomastoid muscle hypertrophy is difficult to accurately stimulate the phrenic nerve diaphragmatic stimulation been the restrictions mainly used for patients with stable disease research in the application of critically ill patients. Recently, someone using electromagnetic stimulation of the phrenic nerve to study the function of the diaphragm, found that magnetic stimulation and direct stimulation of the phrenic nerve, can be effective in stimulating the diaphragm contraction to overcome the shortcomings of direct stimulation of, for critically ill patients the diaphragmatic function studies have achieved good results.
Respiratory muscle fatigue - Differential Diagnosis1, according to a history of the respiratory underlying disease history.
2, the clinical manifestations of respiratory rate, respiratory synchronization.
Blood creatine increased phospholipid kinase, can be diagnosed under 3.
Extend the treatment of respiratory muscle fatigue instrument muscle relaxant effect more common in long-term application of a large number of patients with muscle relaxants or application of drugs affecting neuromuscular function at the same time, about 5% incidence in the ICU, extend the length of ICU stay. NBA induced acute myopathy incidence than the muscle relaxant effect extended the most low incidence seen in acute asthma exacerbation and large doses of hormones and NBA. In a prospective clinical study, Leatherman 25 cases accepted of Vecuronium and the cortex hormone treatment of asthma patients to observe found 19 cases of patients with increased creatine phosphokinase (CPK) 19 patients had clinical signs of myopathy, its severity related with the duration of mechanical ventilation. The major clinical manifestations of NBA-related myopathy the long sustained muscle weakness, muscle relaxants is disabled critical illness induced neuropathy and hormone-induced myopathy is difficult to identify. Some acute myopathy patients serum CPK increased, but some patients did not CPK increased with the severity of the myopathy, blood collection to check the timing of periodically dynamic review CPK helpful to determine the incidence of myopathy various etiologies The muscle weakness characteristics for clinicians Reference.Respiratory muscle fatigue - treatment and preventionDrug treatment of respiratory muscle fatigue is still very controversial experiments show that aminophylline can increase the force of contraction of the diaphragm muscle and endurance, but the accuracy of the method used to evaluate diaphragmatic function experiments concluded poor reliability. Experiments showed that the digoxin, β2 agonists, caffeine can increase diaphragmatic strength, but its exact effect needs to be further confirmed. In patients with COPD, recently been used anabolic hormones (growth hormone, testosterone, etc.) to increase muscle skeletal muscle strength to improve the quality of life of its exact effect and the price / benefit ratio needs further evaluation.
Prognosis: The prognosis of this disease and the incidence incentives disease duration, and age and physical condition.
Respiratory muscle fatigue prevention: If respiratory muscle fatigue or failure cupping network plays an important role in the incidence of respiratory failure and should be the first to correct and remove incentives that cause respiratory muscle dysfunction general principle: ensure adequate respiratory muscle energy supply , including nutritional supplements to correct electrolyte abnormalities, especially phosphorus and magnesium abnormalities, to correct hypoxemia and hypercapnia improve cardiac output. ② specific treatment for respiratory muscle fatigue, including nutritional supplements respiratory muscle function exercise such as respiratory muscle rest.1. Nutritional supplement research shows that the majority of COPD patients with nutritional and metabolic disorders mainly for patients at high metabolic state, when energy demand is greater than the energy supply of a variety of factors can affect the energy supply of patients with adverse effects such as loss of appetite and gastrointestinal nutrients eating hypoxemia consumption of high-carbohydrate, increased CO2 production beyond the ventilation capacity. Animal experiments and human studies have confirmed that malnutrition in type II muscle fiber atrophy can cause muscle weakness, vital capacity and maximum voluntary ventilation volume maximum oral suction pressure when the patient's actual body weight less than 71% of the average standard weight significantly lower than normal, nutritional supplements can increase the suction pressure and weight. Give enough heat to enhance the function of the respiratory muscles, improve the success rate of weaning course there are still some dispute the efficacy of nutritional supplementation on muscle fatigue, resulting in conclusions different reasons and the extent of malnutrition in patients with appropriate nutritional supplements in the weaning process, nutritional supplement, and time factors In addition, nutritional supplements ability to impact the prognosis of patients with COPD also need to be further confirmed.
Functional exercise on respiratory muscle function targeted exercise will not only improve the function of the respiratory muscles, can increase overall athletic ability that breathing exercises usually only applies to patients with moderate ventilatory dysfunction accompanied by shortness of breath, severe ventilatory dysfunction by should not be applied breathing exercise. Breathing exercises should follow three basic principles: load, targeted and reversible exercise should be gradual, and should not be anxious in a certain intensity of load for a particular long-term exercise main objective to increase respiratory muscle strength and endurance, and enhance the resistance to fatigue. Excessive exercise may aggravate respiratory muscle fatigue and lead to muscle damage.
Respiratory muscle training methods are mainly three kinds:
(1) resistance methods: Patients with small holes through the respirator to breathe, inhale increased load on the respiratory muscles, breath unaffected
Repeat breathing apparatus (2) over-breathing: patients through an indicative target ventilation level, autonomous rapid ventilation to maintain alveolar concentration of oxygen and carbon dioxide concentration within the physiological limits. The ventilation level should reach 70% to 90% of maximum voluntary ventilation in patients with COPD should reach the upper limit of the above range.
(3) the domain value load method: preset suction pressure, suction valve open when the patient's inspiratory pressure reaches the value of this domain, complete the suction if the suction pressure of cupping network is less than a preset pressure value can not breathe . Other methods include systemic exercise, abdominal breathing deep slow breathing, reduce lip breathing, external diaphragm pacing.
The exact effect of muscle function exercise also needs further evaluation cupping network, most studies suggest that a reasonable exercise can increase the strength and endurance of the respiratory muscles, improve exercise capacity of patients to relieve breathing difficulties, and improve the quality of life. But studies suggest that muscles after respiratory muscle function improved, but did not enhance the overall athletic ability.
Respiratory muscle fatigue after the rest of the rest of respiratory muscle fatigue of respiratory muscles can restore function. Commonly used positive pressure ventilation or partly replace the respiratory muscles to complete the ventilation of the fatigue of respiratory muscles rest. Ventilation can be selected through the nose and mouth mask non-invasive positive pressure ventilation on unconsciousness, the multiple hemodynamic instability due to the cooperation respiratory secretions should be taken in patients with endotracheal intubation establishment of artificial airway breathing in patients with chronic respiratory failure muscle dysfunction multi advocate the use of noninvasive positive pressure ventilation in patients with chronic respiratory failure in chronic neuromuscular disorders thoracic deformity has also made a good effect, but the effect of differences in COPD patients, the main problem is the non-invasive ventilation is really reduced the activities of the diaphragm so that the diaphragm really get adequate rest ventilation length of time, the size of the auxiliary ventilation pressure, the severity of the patient's underlying disease and drug use can affect the majority point of view of non-invasive ventilation efficacy judgments tend if correctly applied Noninvasive ventilation by reducing respiratory muscles acting good respiratory muscle function, could allow many patients to avoid endotracheal intubation. Of course, non-invasive ventilation to improve the condition there are other mechanisms, such as: re-tune to set the sensitivity of the respiratory center to carbon dioxide, hypoxia and CO2 retention respiratory muscle function by improving blood gas to reduce excessive rest cause respiratory muscle disuse atrophy caused respiratory machine dependent. Is difficult to determine the clinical respiratory muscle rest and be the ideal limit of the load, the general principles to get enough rest by 24 ~ 48h control ventilation or a high level of pressure support ventilation, respiratory muscle fatigue, reduce the intensity of ventilatory support in a timely manner gradually increase the load of the patient's breathing, and actively prepare for weaning.
Respiratory muscle fatigue or respiratory muscle dysfunction is very common in chronic lung disease and ICU hospitalized patients. For a long time, respiratory muscle fatigue or failure is not taken seriously. Timely detection and treatment of respiratory muscle fatigue can correct abnormal respiratory mechanics, and reduce the work of breathing, improve oxygenation, to shorten the duration of mechanical ventilation. Therefore, evaluation of respiratory muscle function in critically ill patients in recent years has become an important part of the intensive care.
Edit Summary- Overview of respiratory muscle fatigueBreathing exercise breathing exercise is a prerequisite to change thoracic volume depend on the activities of the respiratory muscles, causing lung contraction provide the driving force for the realization of pulmonary ventilation.Respiratory muscles of the human body is the belch muscle and intercostal muscles (including aid room, outside the muscle), there are the muscles of the abdomen and the neck accessory muscles of breathing only difficulty breathing when involved in assisted breathing.
Respiratory muscles and other muscles of the body, all belong to the skeletal muscle. Respiratory muscle are different from most skeletal muscle, it is the only life depends on skeletal muscle contraction regularly throughout the life course, and never-ending. Therefore, the respiratory muscles is an important part of the respiratory pump, is the completion of the power of the external respiratory function. In order to guarantee enough power breathing, respiratory muscle strength and endurance must maintain a certain strength. Due to illness and other reasons, the respiratory muscles to long-term overload, can not produce and maintain muscle strength, namely atony called respiratory muscle fatigue. Effective alveolar ventilation due to respiratory muscle weakness, reduce, and eventually can lead to respiratory failure.
Generally believed that chronic obstructive pulmonary disease patients (including chronic bronchitis, emphysema, asthma), the air over the resistance continues to increase, and the long period of hypoxemia, carbon dioxide retention and systemic malnutrition state, prone to respiratory muscle fatigue. Followed by neuromuscular diseases, such as bilateral diaphragm paralysis, myasthenia gravis, Guillain-Barre syndrome, some poisoning, and cardiogenic shock, septic shock, toxic shock can cause respiratory muscle weakness, fatigue, Finally, leading to respiratory failure.
Respiratory muscle fatigue - academic explainRespiratory muscle fatigue treatment instrument 1 definition of respiratory muscle fatigue according to the definition set by the 1988 U.S. Heart, Lung, and Blood Institute (NHLBI), respiratory muscle fatigue refers to the force of contraction of the respiratory muscles bear the load and (or) contraction speed reduced, and this reduction can rest and recover.2, the so-called respiratory muscle fatigue muscle activity under load and cause it to produce a reduced ability of the strength and speed of the decline in this ability can rest and recovery. Discuss endometriosis endometrial growth function The parts of the tissue outside the uterine cavity covering mucosa.
3, respiratory muscle fatigue is caused by a variety of respiratory muscle contraction and relaxation activities can not produce the need to maintain a certain amount of alveolar ventilation pleural pressure, the muscle itself can be manifested as muscle strength, and (or) systolic and diastolic velocity decreased, and The decline in this ability after a rest can be restored.
, Respiratory muscle fatigue respiratory muscle contraction can not produce the gas required to maintain adequate alveolar pressure, thereby affecting gas exchange, respiratory muscle fatigue is the development of a variety of clinical conditions hypercapnia respiratory failure final common pathway.
, Respiratory muscle fatigue is not against the burden of respiratory muscle strength and endurance respiratory muscle contraction that can not produce the driving pressure required to maintain adequate alveolar ventilation which is the main reason ventilator dependent. The factors leading to respiratory muscle fatigue: the endogenous end expiratory positive pressure (PEEP).
Respiratory muscle fatigue, respiratory muscle fatigue is the respiratory muscle activity under load and cause it to generate force and (or) the speed of a reduced ability to decline in this ability can rest and recovery. Respiratory muscle fatigue (pump failure) is breathing failure an important part of the disease process.
7, the so-called respiratory muscle fatigue is the case of the continued contraction of the respiratory muscles, can no longer maintain the required or intended muscle occlusion side: right nine cases, 17 cases left. The occlusive reasons: cerebral thrombosis nine cases of cerebral infarction 17 atrial fibrillation patients (9 cases).
Respiratory muscle fatigue - etiologyThe majority of patients with respiratory muscle fatigue in patients with respiratory muscle fatigue is caused by the disease itself, has been found to sepsis (sepsis), multiple organ failure, mechanical ventilation hypercapnia (acidosis), and a variety of drugs can cause abnormal neuromuscular function and become the important disease pathophysiology process.In short, the respiratory muscle fatigue and weakness, health search is very common in the critically ill COPD and other chronic diseases in addition to the effects of the disease itself, a variety of drugs, such as glucocorticoids muscle relaxants aminoglycoside antibiotics can induce or aggravate respiratory muscle fatigue, breathing specificity, and accuracy of the machine improper application can also be caused by diaphragmatic dysfunction various checks respiratory muscle fatigue are poor and difficult routine clinical applications attention to clinical examination to detect the presence of respiratory muscle fatigue.
Respiratory muscle fatigue - pathogenesisTreatment of respiratory muscle fatigue instrument respiratory muscles, including the diaphragm intercostal muscles, the abdominal muscles can be divided into inspiratory muscles (diaphragm, intercostal muscle, sternocleidomastoid sternocleidomastoid and scalene according to the functional classification of respiratory muscle) and expiratory muscle (intercostal muscle abdominal muscle) according to the nature of the muscle fibers can be divided into red muscle fibers (also known as slow contraction fatigue resistant fibers or fiber type Ⅰ) and white muscle fibers (also known as fast contraction fibers or II class fiber ). The Class Ⅱ fibers can be divided into resistance to fatigue fast contraction fibers (Ⅱ A fibers) and fast contraction fast fatigue fiber (II)The main function of the respiratory muscles is complete breathing exercise followed by participation in the cough expectoration vomiting. 2/3 of the diaphragm about the most important role shoulder throughout the respiratory function of 3% to 90% of the tidal volume of diaphragmatic contraction. When the auxiliary respiratory muscles involved in the contraction increased minute ventilation or presence of diaphragmatic fatigue. In quiet breathing expiratory muscle does not participate in the contraction in respiratory function increases intercostal muscle and abdominal expiratory muscle contraction, squeezing the diaphragm to the chest cavity, the diaphragm muscle fiber is the best bit early long tension.
1.COPD patients with skeletal muscle dysfunction (including respiratory muscles) in patients with COPD decreased exercise tolerance has a direct relationship. COPD patients with skeletal muscle structure changes showed a decline in muscle weight, changes in the structure of the muscle fibers (I class fiber reducing the proportion of the increase in the proportion of class II fibers, fiber atrophy of class Ⅰ and Ⅱ A I class and II class fiber diameter decreases) reduce the number of capillaries in skeletal muscle per unit area of the tree (oxidase activity decreased) function to change the performance of muscle strength reduced the partial oxygen uptake and oxygen transport significantly limited maximal exercise decreased endurance and metabolic changes. The main reason for the above structural and functional changes the: ① long-term hypoxemia, hypercapnia infection and chronic malnutrition; ② accompanied by electrolyte disorders (hypokalemia, hypophosphatemia, low magnesium) heart failure muscle disuse atrophy; ③ glucocorticoid-induced acute and chronic myopathy. Due to lung hyperinflation in COPD patients with severe airway obstruction, so that the mechanical characteristics of the respiratory system were to change significantly, significantly negative contraction of the diaphragm in the beginning of a long position shrink the efficiency significantly reduce health search combined with the various factors can easily lead to diaphragmatic fatigue and failure.
Characteristics of sepsis in patients with sepsis (Sepsis) system blood flow is normal or increased tissue oxygen uptake capacity decreased local perfusion reduction and tissue hypoxemia. Respiratory muscle, sepsis and shock the total perfusion increased Zhui but barriers to local microvascular perfusion and increased work of breathing can still cause respiratory muscle hypoxia and respiratory muscle dysfunction.
Mechanical ventilation on respiratory muscle mechanical ventilation for respiratory muscle function has two sides alternative or auxiliary respiratory muscles acting on the one hand fatigue of respiratory muscles to rest on the other hand lead to respiratory muscle disuse atrophy, respiratory muscle strength decreased and endurance produces ventilator dependent. Skeletal muscle atrophy major changes include:
(1) muscle weight was significantly reduced.
(2) the decline in protein synthesis.
(3) muscle fiber mesh diameter reduction.
(4) reduces the number of anti-fatigue fiber slow contraction.
Respiratory muscle fatigue (5) decreased mitochondrial glucose oxidation and decomposition. Although the respiratory muscles have unique characteristics different from ordinary skeletal muscle network, but can be found in the long-term controlling mechanical ventilation reduce the activity of the diaphragmatic EMG, transdiaphragmatic pressure decreased respiratory muscle endurance, reduce. Brochard et al healthy baboons for 11 days the controlling ventilation discovered a 25% reduction in Pdi Stamina reduced by 36% mechanical ventilation health search whether another major determinants of respiratory muscle atrophy muscle fiber length muscle fibers length of long-term fixed Zhui under its normal length, it is very easy to produce fatigue can avoid the occurrence of muscle atrophy; rather more than the length of its base.4, over a period of time in mechanically ventilated patients, respiratory muscle function in the process of weaning, respiratory muscle function is to determine whether weaning one of the key factors. Most difficult weaning patients in the clinical respiratory muscle fatigue Cohen et al found 12 cases of patients with difficult weaning study 7 patients EMG spectrum changed and prompts diaphragmatic fatigue, six cases of the six patients had abnormal abdominal breathing breathing Frequency faster, some patients with frequent cause of failure and respiratory muscle fatigue diaphragmatic fatigue weaning accelerate faster and PaCO2 increased suggesting that these patients breathing frequency and PaCO2 increased EMG spectral changes in breathing frequency.
5 the polyneuropathy sepsis in critically ill patients, multiple organ failure (MOF) can occur in patients with polyneuropathy main sensory - motor nerve damage, called critical illness polyneuropathy in ICU about more than 70% of patients with varying degrees of neuropathy. Bolton electrophysiological studies of 43 patients with sepsis and MOF patients, 30 patients have abnormal axonal degeneration associated with sensory and motor potential, 15 patients with clinical manifestations weakness weaning failure, critical illness multiple neural reflex diminished or disappeared The main clinical manifestations of lesions extremities weakness with atrophy, weakening or disappearance of sensory dysfunction deep reflection cranial nerve function is normal Zhui critical illness polyneuropathy self-limiting, and can be fully restored after a period of time, but the EMG there is a surviving abnormal Zhui now think this secondary neuromuscular disease is caused by the difficulty of weaning and prolong the ICU stay an important factor in 62% of patients with weaning difficulties relating.
Critical illness polyneuropathy mechanism is not yet clear, nutritional disorders poisoning, metabolic abnormalities, and vascular factors might be involved in the occurrence of neuropathy has also been suggested that the hypoxic edema caused by ischemia in the nerve and blood - nerve barrier damage nerve damage the main reason for the diagnosis of critical illness polyneuropathy mainly by electrophysiological studies, peripheral nerve axon injury is the main electrophysiological changes typical performance for seven days after the onset of resting EMG fibrillation potential incubation period of change and positive sharp wave neural potential map manifests itself in the segment of the proximal and distal nerve impulse conduction velocity normal reduce mixed muscle action potential amplitude. Typical change of primary demyelination of nerve conduction velocity decreased significantly extend the distal latency of compound muscle action potential scattering, block and F-wave potential of increased little in critical illness polyneuropathy patients appear.
6. Drugs on respiratory muscle function
Respiratory muscle fatigue (1) corticosteroids: high-dose or long-term use of glucocorticoids can cause a variety of side effects, including myopathy. Animal experiments confirmed that health search corticosteroids can significantly reduce the force of contraction of the diaphragm hormone induced myopathy pathological basis may reduce the fast contraction fibers (I type) protein synthesis, increased catabolism lead to the type of muscle fiber atrophy. Currently, corticosteroids induced myopathy the exact mechanism is not yet clear, but fast contraction fibers atrophy inevitably lead to muscle contraction capacity decreased when accompanied by application of muscle relaxants or patients are prone to increased work of breathing, diaphragmatic fatigue tissue blood perfusion can be further deterioration of the function of the respiratory muscles. Studies have reported that the incidence of corticosteroid-induced acute severe asthma myopathy up to 10%(2) neuromuscular blocker: application of mechanical ventilation, neuromuscular blocking agents (NBA) the health search of purpose is to help the smooth implementation of mechanical ventilation, improve the coordination of human - machine to reduce oxygen consumption in patients with intracranial hypertension avoid intracranial pressure fluctuations in the late 1970s, a British survey showed that 90% health search ICU patients routine application of muscle relaxants. For nearly 20 years, due to the emergence of powerful sedatives, the ventilator performance improvement and in-depth understanding of the pharmacological properties of NBA, especially NBA can cause muscle relaxation delay and myopathy there is a decreasing trend in the application of muscle relaxants NBA direct toxic effect on the muscle is not yet clear but it can enhance muscle function already exists an abnormal increase in the role of muscle toxicity of drugs or drug metabolites, the muscle relaxant effect continued to extend and can cause acute myopathy. At the same time, the application of certain drugs to prolong and enhance the role of the NBA.
Respiratory muscle fatigue - symptomsClinical manifestations: respiratory rate, breathing out of sync (such as periodic abdominal pressure and chest pressure breathing alternately, confusion, and not parallel abdominal pressure breathing abdominal bimodal breathing exercise) and paradoxical abdominal respiration.
Complications: concurrent diaphragmatic fatigue.
Respiratory muscle fatigue - CheckLaboratory tests
Respiratory muscle fatigue drug, maximum inspiratory pressure (MIP) with the greatest effort in the residual gas bit (RV) or functional residual air-bit (FRC) http://www.huoguan.com blocked airway suction can maximum inspiratory mouth pressure. The MIP measured clinical significance is: inspiratory muscle function in neuromuscular disease evaluation and diagnosis of the disease and the severity of the judgment parameters when MIP <normal expected value of 30%, and prone to respiratory failure; (2) evaluation of pulmonary disease (COPD) patients with respiratory muscle function in the thoracic deformity and drug intoxication; (3) used to predict weaning is generally believed that the MIP <-30cmH20 the likelihood of successful weaning. But with MIP predict weaning false negative rate is very high, mainly due to patients is not well with the measurements.Maximal expiratory pressure (MEP) in total lung capacity (TLC) airway blocked with maximum efforts to breath can generate maximum oral expiratory pressure they reflect all indicators of respiratory muscle strength is not entirely representative of the diaphragm function. Near the mouth end of the endotracheal tube with a pressure sensor value as the measurement value determination of MIP and MEP measurements repeated several times, take good reproducibility of mechanically ventilated patients when When obvious Zhui the airflow obstruction, the measurement of these indicators be affected, each measurement variability increases Moreover, the results also influenced by the patient's subjective efforts the normal MIP is no unified standard laboratory reports a very different health search, and certainly there are differences between Asians and Westerners kinds.
Transdiaphragmatic pressure (Pdi) Pdi is the diaphragmatic contraction of the diaphragm chest, ventral pressure difference on behalf of the diaphragmatic contractility largest transdiaphragmatic pressure (Pdimax) of means in functional residual air-bit (or residual gas bits), airway blocking state the utmost to inhale the Zhui Pdi max Pdimax, reflects pressure when the diaphragm for maximum contraction is not a reliable indicator of diaphragmatic fatigue evaluation of respiratory muscle strength Zhui Pdi the Pdimax lower when Pdi maintained at 40% level of http://www.huoguan.com of Pdimax suggesting diaphragmatic fatigue. Determination of transdiaphragmatic pressure more complex subject esophageal balloon and intragastric balloon pressure of the esophagus and gastric pressure were measured the inspiratory phase difference between the two shall Pdi
3, the diaphragm tension - time index (TTdi) of the indicators reflect good indicator of respiratory muscle endurance in terms of evaluation of respiratory muscle endurance is more important than strength muscle endurance depends on the energy supplied to the muscle fiber composition and the size of the work is done. Acting the size depends on the power of muscle contraction and sustained Zhui time. Diaphragmatic strength of individual differences, in order to reduce individual differences, diaphragmatic contraction the Pdi average of Pdimax ratio is used to reflect the strength of contraction, the Zhui the ratio of inspiratory time (Ti) and total respiratory cycle time (Ttot) reflect the product of the duration of both diaphragmatic contractility is TTdi. Formula: TTdi = Pdi / Pdimax, x Ti / Ttot. When TTdi value <0.15 in the case of the presence of inspiratory resistance load prone fatigue, while when TTdi value> 0.15 diaphragmatic fatigue time will be significantly shortened. It should be noted that the Determination of TTdi is completed in the case of artificial resistance, there may be a wide gap between how to determine respiratory muscle fatigue in various disease states, domain values need to be further explored with spontaneous breathing.
Other laboratory examinations
Respiratory muscle fatigue drugs. Diaphragmatic EMG EMG can be used for the detection of diaphragmatic intercostal muscle and physiological activity of the abdominal muscles during mechanical ventilation in critically ill patients is difficult to conventional for electromyography physiological examination carried out, and check interfering factors. repeatability and accuracy of the results are poor thin needle through the skin to the diaphragmatic percutaneous electrode than percutaneous electrode obtained data are accurate and reliable. EMG different Zhui frequency spectrum mainly between 20 ~ 250Hz, the spectral distribution of the change Zhui increase fatigue early in the process performance of the first diaphragm muscle Zhui reduce fatigue EMG spectrum of low-frequency component (L), high-frequency reduce health search component (H), H / L than the decline in the underlying value of 20% means that the spectrum significantly change the high frequency components from the accumulation of the metabolic toxic substances in the muscle caused a short recovery period (a few minutes) and the low-frequency components by muscle structural changes caused by the recovery takes more than 24h dynamic observation of EMG can be early detection of the presence of respiratory muscle fatigue. Clinically, such as the low-frequency components in the process of withdrawal of mechanical ventilation increase prompted at least 24 ~ 48h to the fatigue of respiratory muscle contractile function was restored.Phrenic nerve electrical stimulation of phrenic nerve stimulation of the diaphragmatic contraction is mainly dominated by the phrenic nerve with Pdi observed after stimulation of the phrenic nerve of the body surface or needle electrodes or the EMG diaphragmatic function may reflect the advantages of the method is to objectively evaluate diaphragmatic Zhui contractile properties and mechanical characteristics of the chest wall without self-effort or breathing affect shortcomings is to stimulate local pain, electrodes accurate positioning difficult, especially in patients with irritability postural change will affect the accuracy of the measurement. COPD and obese patients if there is the sternocleidomastoid muscle hypertrophy is difficult to accurately stimulate the phrenic nerve diaphragmatic stimulation been the restrictions mainly used for patients with stable disease research in the application of critically ill patients. Recently, someone using electromagnetic stimulation of the phrenic nerve to study the function of the diaphragm, found that magnetic stimulation and direct stimulation of the phrenic nerve, can be effective in stimulating the diaphragm contraction to overcome the shortcomings of direct stimulation of, for critically ill patients the diaphragmatic function studies have achieved good results.
Respiratory muscle fatigue - Differential Diagnosis1, according to a history of the respiratory underlying disease history.
2, the clinical manifestations of respiratory rate, respiratory synchronization.
Blood creatine increased phospholipid kinase, can be diagnosed under 3.
Extend the treatment of respiratory muscle fatigue instrument muscle relaxant effect more common in long-term application of a large number of patients with muscle relaxants or application of drugs affecting neuromuscular function at the same time, about 5% incidence in the ICU, extend the length of ICU stay. NBA induced acute myopathy incidence than the muscle relaxant effect extended the most low incidence seen in acute asthma exacerbation and large doses of hormones and NBA. In a prospective clinical study, Leatherman 25 cases accepted of Vecuronium and the cortex hormone treatment of asthma patients to observe found 19 cases of patients with increased creatine phosphokinase (CPK) 19 patients had clinical signs of myopathy, its severity related with the duration of mechanical ventilation. The major clinical manifestations of NBA-related myopathy the long sustained muscle weakness, muscle relaxants is disabled critical illness induced neuropathy and hormone-induced myopathy is difficult to identify. Some acute myopathy patients serum CPK increased, but some patients did not CPK increased with the severity of the myopathy, blood collection to check the timing of periodically dynamic review CPK helpful to determine the incidence of myopathy various etiologies The muscle weakness characteristics for clinicians Reference.Respiratory muscle fatigue - treatment and preventionDrug treatment of respiratory muscle fatigue is still very controversial experiments show that aminophylline can increase the force of contraction of the diaphragm muscle and endurance, but the accuracy of the method used to evaluate diaphragmatic function experiments concluded poor reliability. Experiments showed that the digoxin, β2 agonists, caffeine can increase diaphragmatic strength, but its exact effect needs to be further confirmed. In patients with COPD, recently been used anabolic hormones (growth hormone, testosterone, etc.) to increase muscle skeletal muscle strength to improve the quality of life of its exact effect and the price / benefit ratio needs further evaluation.
Prognosis: The prognosis of this disease and the incidence incentives disease duration, and age and physical condition.
Respiratory muscle fatigue prevention: If respiratory muscle fatigue or failure cupping network plays an important role in the incidence of respiratory failure and should be the first to correct and remove incentives that cause respiratory muscle dysfunction general principle: ensure adequate respiratory muscle energy supply , including nutritional supplements to correct electrolyte abnormalities, especially phosphorus and magnesium abnormalities, to correct hypoxemia and hypercapnia improve cardiac output. ② specific treatment for respiratory muscle fatigue, including nutritional supplements respiratory muscle function exercise such as respiratory muscle rest.1. Nutritional supplement research shows that the majority of COPD patients with nutritional and metabolic disorders mainly for patients at high metabolic state, when energy demand is greater than the energy supply of a variety of factors can affect the energy supply of patients with adverse effects such as loss of appetite and gastrointestinal nutrients eating hypoxemia consumption of high-carbohydrate, increased CO2 production beyond the ventilation capacity. Animal experiments and human studies have confirmed that malnutrition in type II muscle fiber atrophy can cause muscle weakness, vital capacity and maximum voluntary ventilation volume maximum oral suction pressure when the patient's actual body weight less than 71% of the average standard weight significantly lower than normal, nutritional supplements can increase the suction pressure and weight. Give enough heat to enhance the function of the respiratory muscles, improve the success rate of weaning course there are still some dispute the efficacy of nutritional supplementation on muscle fatigue, resulting in conclusions different reasons and the extent of malnutrition in patients with appropriate nutritional supplements in the weaning process, nutritional supplement, and time factors In addition, nutritional supplements ability to impact the prognosis of patients with COPD also need to be further confirmed.
Functional exercise on respiratory muscle function targeted exercise will not only improve the function of the respiratory muscles, can increase overall athletic ability that breathing exercises usually only applies to patients with moderate ventilatory dysfunction accompanied by shortness of breath, severe ventilatory dysfunction by should not be applied breathing exercise. Breathing exercises should follow three basic principles: load, targeted and reversible exercise should be gradual, and should not be anxious in a certain intensity of load for a particular long-term exercise main objective to increase respiratory muscle strength and endurance, and enhance the resistance to fatigue. Excessive exercise may aggravate respiratory muscle fatigue and lead to muscle damage.
Respiratory muscle training methods are mainly three kinds:
(1) resistance methods: Patients with small holes through the respirator to breathe, inhale increased load on the respiratory muscles, breath unaffected
Repeat breathing apparatus (2) over-breathing: patients through an indicative target ventilation level, autonomous rapid ventilation to maintain alveolar concentration of oxygen and carbon dioxide concentration within the physiological limits. The ventilation level should reach 70% to 90% of maximum voluntary ventilation in patients with COPD should reach the upper limit of the above range.
(3) the domain value load method: preset suction pressure, suction valve open when the patient's inspiratory pressure reaches the value of this domain, complete the suction if the suction pressure of cupping network is less than a preset pressure value can not breathe . Other methods include systemic exercise, abdominal breathing deep slow breathing, reduce lip breathing, external diaphragm pacing.
The exact effect of muscle function exercise also needs further evaluation cupping network, most studies suggest that a reasonable exercise can increase the strength and endurance of the respiratory muscles, improve exercise capacity of patients to relieve breathing difficulties, and improve the quality of life. But studies suggest that muscles after respiratory muscle function improved, but did not enhance the overall athletic ability.
Respiratory muscle fatigue after the rest of the rest of respiratory muscle fatigue of respiratory muscles can restore function. Commonly used positive pressure ventilation or partly replace the respiratory muscles to complete the ventilation of the fatigue of respiratory muscles rest. Ventilation can be selected through the nose and mouth mask non-invasive positive pressure ventilation on unconsciousness, the multiple hemodynamic instability due to the cooperation respiratory secretions should be taken in patients with endotracheal intubation establishment of artificial airway breathing in patients with chronic respiratory failure muscle dysfunction multi advocate the use of noninvasive positive pressure ventilation in patients with chronic respiratory failure in chronic neuromuscular disorders thoracic deformity has also made a good effect, but the effect of differences in COPD patients, the main problem is the non-invasive ventilation is really reduced the activities of the diaphragm so that the diaphragm really get adequate rest ventilation length of time, the size of the auxiliary ventilation pressure, the severity of the patient's underlying disease and drug use can affect the majority point of view of non-invasive ventilation efficacy judgments tend if correctly applied Noninvasive ventilation by reducing respiratory muscles acting good respiratory muscle function, could allow many patients to avoid endotracheal intubation. Of course, non-invasive ventilation to improve the condition there are other mechanisms, such as: re-tune to set the sensitivity of the respiratory center to carbon dioxide, hypoxia and CO2 retention respiratory muscle function by improving blood gas to reduce excessive rest cause respiratory muscle disuse atrophy caused respiratory machine dependent. Is difficult to determine the clinical respiratory muscle rest and be the ideal limit of the load, the general principles to get enough rest by 24 ~ 48h control ventilation or a high level of pressure support ventilation, respiratory muscle fatigue, reduce the intensity of ventilatory support in a timely manner gradually increase the load of the patient's breathing, and actively prepare for weaning.
Upper Airway Obstruction
Upper airway obstruction-What is on the airway obstruction?
Upper airway obstruction (UAO) is severely hampered by a variety of reasons due to upper airway airflow medical emergency, its clinical manifestations are not specific, confused easy with bronchial asthma and obstructive pulmonary disease, and other diseases. The disease is more common in children and rare in adults. There is no specific clinical manifestations of upper airway obstruction, manifested as irritating dry cough, shortness of breath and difficulty breathing; mainly dyspnea breathing difficulties, activities can cause breathing difficulties increased significantly, and often occur due to changes in posture array onset seizures.
Upper airway obstruction - Description
Upper airway obstruction - DescriptionAirway obstruction in the upper airway obstruction (upperairwayobstruction, UAO) is severely hampered by a variety of reasons due to upper airway airflow medical emergency, its clinical manifestations are not specific, easy with bronchial asthma and obstructive pulmonary disease and other diseases confused. Clinically, the disease is more common in children is relatively rare in adults. Upper airway obstruction caused by many reasons, which derived foreign matter other than those caused by the most common, and the rest of the more common laryngeal movement disorders, infections, tumors, trauma, and iatrogenic. Timely understanding and treatment of upper airway obstruction has extremely important clinical implications, since the majority of patients with previously healthy, can be fully recovered by the effective treatment.Upper airway obstruction - symptoms and signs
Airway obstruction in the upper airway obstruction early general without any performance, often start blocking more serious symptoms. Acute upper airway obstruction abrupt onset, severe illness, and even lead to suffocation and death, often obvious signs and symptoms. There is no specific clinical manifestations of upper airway obstruction, manifested as irritating dry cough, shortness of breath and difficulty breathing; mainly dyspnea breathing difficulties, activities can cause breathing difficulties increased significantly, and often occur due to changes in posture array onset seizures. A small number of patients with snoring at night, awakened several times and dyspnea, manifested as sleep apnea syndrome. Caused by inhalation of foreign bodies, choking history, often obvious respiratory distress, looked very painful, from time to time scratching throat. Occasionally chronic upper airway obstruction caused by pulmonary edema and recurrent pulmonary edema performance. The symptoms and signs of upper airway obstruction and the extent and nature of the obstruction. The majority of upper airway obstruction seen in clinical incomplete obstruction. The main signs of inspiratory stridor, significantly more than in the neck, the lungs can also be heard and but weak, sniff can cause wheezing significantly increased. Stridor prompted more serious obstruction, airway diameter is often less than 5 mm. The inspiratory stridor multi prompted extrathoracic upper airway obstruction, more common on the vocal cords or vocal parts; biphasic stridor prompted obstruction breath of song's intensity changes and more tips in the subglottic trachea; curved neck obstruction occurred The thorax the entrance. Children are barking cough, especially at night appear more tips as bronchitis, throat, salivation, difficulty swallowing, fever but no cough is more common in severe epiglottitis. Some patients, there may be a change in sound, location and nature of its changing characteristics and disease, such as unilateral vocal cord paralysis hoarseness; bilateral vocal cord paralysis sound normal, but the wheezing; the glottis over parts lesions often appear low voice , but no hoarseness; the oral abscess contents like sound.
Upper airway obstruction - disease etiologyClinical, upper airway obstruction, although relatively rare, but may be caused by a variety of diseases, such main reasons include: ① airway cicatricial stenosis: multi-intubation or incision treatment; ② airway wall lesions: such as inflammation of the soft tissue of the throat, pharyngeal abscess, enlarged tonsils, vocal cord paralysis, laryngeal or tracheal tumor, tracheomalacia, recurrent polychondritis go far; ③ airway cavity lesions: airway foreign body is more common, and with pedicle endotracheal polyps or tumors and inflammatory granuloma; ④ airway the external oppression: around the airway space-occupying lesions such as thyroid cancer, abscess, hematoma or gas compression; ⑤ airway secretions retention: respiratory tract bleeding or a large number of sputum failed to cough up the large number of inhalation of gastric contents. The cause common cause of upper airway obstruction in adults and children of different anatomical sites, are summarized in Table 1, for reference in clinical diagnosis. A handful of cases, the functional vocal cord abnormalities or psychological factors, may also cause upper airway obstruction.
Upper airway obstruction - pathophysiologicalUpper airway obstruction airway anatomy: the conducting airways of the respiratory system, including the nose, throat, trachea, main bronchus, lobe bronchus and segmental bronchi, bronchioles until the terminal bronchioles part. Different mechanics and other respiratory physiological functions around the small airways and central airways of the respiratory tract is generally divided into three parts: (1) the small airways, airway diameter less than 2mm; ② large airways refers to Long protruding below to 2mm diameter airway; ③ The upper airway, from the nose to carina period of the respiratory tract, including the nose, pharynx, larynx and trachea. Usually pleural entrance or sternum notch is bounded by the upper extrathoracic upper airway and intrathoracic airway is divided into two parts of the upper airway. The extrathoracic on airway mandibular inferior vena (including a region of Ludwig angina), the retropharyngeal chamber (including the produce area retropharyngeal abscess) and throat. Generalized throat to the base of the tongue, down to the trachea, can be divided into the supraglottic larynx (epiglottis, aryepiglottic fold and false vocal cords), glottis (including the the arytenoid vocal cords plane structure) and subglottic area (about 1.5 ~ 2.0cm, cricoid surrounding the airways). The total length of the trachea for l0 ~ 13cm, wherein a length of about 6 intrathoracic ~~ 9cm. The extrathoracic tracheal length of about 2 ~ 4cm, the entrance to the chest from the lower edge of the cricoid, front chest about above the suprasternal notch 1 to 3cm. Normal endotracheal coronal diameter, male the l3 ~ 25mm, 10 ~ 21mm female. Cause tracheal diameter narrowing factors are the following: (1) Saber sheath trachea; ② amyloidosis; ③ recurrent polychondritis; ④ Wegener granulomatosis; the ⑤ tracheobronchial flat osteochondral angioplasty; of ⑥ rhinoscleroma disease; ⑦ complete cricoid ; ⑧ Down syndrome. Pathophysiology of upper airway obstruction: Under normal circumstances, when breathing, respiratory muscle contraction intrathoracic pressure lower airway pressure below atmospheric pressure, the gas from the outside world into the lungs; Instead, breath, respiratory muscle relaxation chest The increased pressure within the gas excreted by the lungs. Acute upper airway obstruction can directly affect the ventilation function of the body, the oxygen of the outside world can not be inhaled into the lungs, the carbon dioxide produced by the metabolism can not be eliminated from the body, causing acute respiratory failure, such as failure to obtain timely medical treatment, every serious shortage oxygen and carbon dioxide retention leads to death. Chest part of the upper airway at atmospheric pressure under the intrathoracic part in the pleural cavity under pressure role. The trachea both sides of the inside and outside pressure difference for the cross-wall pressure. Pleural cavity pressure greater than the outside pressure when the trachea, cross-wall positive pressure airway tend to close; pressure is greater than when the transmural pressure is negative, endotracheal the tracheal outside pressure, tracheal smooth. Upper airway obstruction affecting the patient's ventilatory function, due to the decrease in alveolar ventilation, airway obstruction can be produced in the patient's movement on Health hypoxemia, but its mostly normal dispersion function. Upper airway obstruction location, extent, nature (fixed or variable type) and expiratory or inspiratory pressure changes caused by patients with different pathophysiological changes produce inspiratory airflow limitation, expiratory airflow limitation, or both limited. Clinically, depending on the respiratory airflow obstruction of upper airway obstruction is divided into the following three kinds: variable extrathoracic airway obstruction, of variable intrathoracic upper airway obstruction and a fixed upper airway obstruction.A variable extrathoracic upper airway obstruction variable blocking the tracheal lumen of the size of the site of obstruction may be due to the tracheal changes in the internal and external pressures and changes in the upper airway obstruction. Variable extrathoracic upper airway obstruction found in patients suffering from diseases such as tracheomalacia and vocal cord paralysis. Under normal circumstances, the chest on the outer periphery of the airway pressure throughout the respiratory cycle are under atmospheric pressure, the inspiratory airway pressure decreases, causing the cross-wall pressure increases, and its direction of action grounds tube outward tube, causing chest on the gas Road tend to shrink. Variable extrathoracic upper airway obstruction in patients, sniff, the result of the Venturi effect and turbulence the obstruction distal airway pressure was significantly reduced, significantly increased transmural pressure caused by the obstruction site of airway caliber further narrow The inspiratory airflow serious disruption; contrary, when its forced expiratory endotracheal pressure increased, due to the cross-wall pressure decreases, the extent of blocking eased. Therefore, in this patient dynamic flow - volume loop tracings showed inspiratory flow limitation and showed inspiratory and expiratory flow limitation lighter does not appear platform, or even render normal graphics.Variable intrathoracic upper airway obstruction variable intrathoracic upper airway obstruction, seen in intrathoracic airway of tracheomalacia and tumor patients. Intrathoracic airway pressure around the pleural cavity pressure close to the external pressure (pleural cavity pressure) intraluminal pressure compared to the negative pressure in the lumen, the direction of action of the cross-wall pressure from the lumen to the extraluminal intrathoracic airway, leading to tend to expand. When patients with forced expiratory Venturi effect and turbulence of the obstruction proximal airway pressure reduces, further narrowing the airway caliber also cause obstruction site, but expiratory flow severely hampered. This patient dynamic flow - volume loops tracings, performance render breath platform expiratory flow limitation, inspiratory flow limitation lighter.Fixed upper airway obstruction fixed upper airway obstruction refers stiff upper airway obstructive lesion fixed, breathing changes in airway caliber cross-wall pressure change can not be caused by the obstruction was found in tracheal stenosis, and thyroid cancer patients . These patients, their inspiratory and expiratory airflow were limited and a similar level of dynamic flow - volume loop inspiratory flow and expiratory flow showed a platform. Most scholars believe that expiratory flow rate and inspiratory flow than 50% of vital capacity (FEF50% / FIF50%) is equal to 1 is the characteristics of the fixed upper airway obstruction. But variable type obstruction and airway obstructive lesions adjacent normal FEF50% / FIF50% certain, should be noted.Upper airway obstruction - diagnostic testsDiagnosis of upper airway obstruction: diagnosis of upper airway obstruction, the key is to take into account the possibility of upper airway obstruction. Clinical, should be timely and relevant examination: ① mainly shortness of breath, difficulty breathing, activity significantly worse, sometimes symptoms aggravated with postural after bronchodilator therapy invalid; ② exist on gas tract inflammation, injury, and in particular the history of endotracheal intubation and tracheostomy; the ③ pulmonary function tests showing maximal expiratory flow, maximal voluntary ventilation sexual decline unchanged FVC, FEV1 was not changed significantly, with the decline in maximum voluntary ventilation fails proportion; or FEV1 decreased but closing volume normal.Laboratory tests: upper airway obstruction is more common infections, such as infection, blood leukocytes may be elevated.Other laboratory examinations:Pulmonary function tests peak expiratory flow (speed) - volume curve (Central) is the preferred method of examination for the diagnosis of upper airway obstruction. Upper airway obstruction, the flow - volume curve exhibits a distinct change of diagnostic value. As mentioned earlier, can be determined according to the change of the flow - volume curve shape different upper airway obstruction. ① variable extrathoracic on, airway obstruction, its flow - volume curve showed inspiratory flow significantly restricted presented inspiratory and expiratory flow is basically normal, the therefore FEF50% / FIF50%> 1; the ② variable intrathoracic upper airway obstruction, its flow - volume curve showed expiratory flow significantly restricted render breath platform, FEF50% / FIF50%, <1; (3) fixed upper airway obstruction, its flow - volume curve showed inspiratory expiratory flow were significantly decreased, and a considerable degree of rendered as a rectangle, FEF50% / FIF50% = 1. Other indicators of lung function, such as FEV0.5, FEV1.0 reduced, PEFR, MVV progressive decline FIF50% ≤ 100L/min FEV1.0/PEFR ≥ 10 ml / (L? Min) FEVl.0/FEV0.5 ≥ 1.5. Closed volume vital capacity VC and CV normal, suggesting that the presence of upper airway obstruction. Pulmonary function tests can not be performed in patients with acute respiratory distress, and high sensitivity to upper airway obstruction.2 radiographic examination(1) plain films of the neck: plain film of the trachea, upper airway obstruction of exudative tracheitis, airway foreign body and innominate artery compression due to higher sensitivity, but on the larynx or trachea softening sensitive poor. Inspiratory neck plain film laryngotracheitis and epiglottitis has differential value. The laryngotracheitis the typical signs for the "steeple" sign. The subglottic stenosis more common in patients with laryngotracheitis, but can also be found epiglottitis. The epiglottitis the neck lateral radiographs can show swelling of the epiglottis and hypopharynx expansion. Airway plain film diagnosis of upper airway obstruction may provide important information, but less accurate, the judge should be combined with medical history and symptoms.The size and morphology of upper airway obstruction (2) Chest CT Scan: CT scan of the airway can learn obstructive lesions, the degree of airway narrowing and airway wall, as well as the situation of the lesion surrounding tissue. The enhanced scan still helps clear lesions blood supply.(3) chest MRI examination: has a good ability to distinguish, can be expected that the extent and length of the airway occlusion, as well as evaluating the mediastinal case.3 the acoustic check breathing audio spectrum analysis found that normal human peak frequency and frequency spectrum are mainly located below 200Hz.Airway obstruction in patients with chest appearance, a significant increase in the peak frequency of breath sounds, mostly three times greater than the baseline, the frequency spectrum of the group widened and moved towards the area of high-frequency greater than 200Hz. The above-mentioned changes in the inspiratory phase is greater than the expiratory phase, and the signal strength of the neck to the chest. The blocking variable thoracic breathing sound spectrum changes as compared to the expiratory than inspiratory chest signal stronger. Therefore, breathing audio spectrum analysis to determine airway obstruction has better clinical value.Endoscopy fiberoptic laryngoscope or fiberoptic bronchoscopy can directly observe the upper airway, to understand the dynamic characteristics of the lesions in the vocal cords, trachea ring the changes as well as the respiratory process, and can be collected living tissue for pathological examination, so the diagnosis decisive role. Suspected obstruction of the upper airway, should be considered for endoscopy. But the severe breathing difficulties should not be checked for biopsy and non-vascular diseases.Upper airway obstruction - Differential DiagnosisCerebrovascular accident, seizures, sleeping pill overdose, heart attack, acute laryngospasm and laryngeal edema as well as other causes of airway obstruction phase identification.Upper airway obstruction - treatment optionsUpper airway obstruction due to reasons caused by upper airway obstruction more, the choice of treatment should be determined according to its etiology and severity. Severe upper airway obstruction should take urgent measures to relieve airway obstruction, to save the lives of patients. Some type of upper airway obstruction, changes in position can make the symptoms can be alleviated; caused by infectious diseases, such as epiglottitis, pharyngeal abscess, antibiotic treatment should be timely. Acute upper airway obstruction often occurs outside the hospital can not receive timely diagnosis and treatment, lead to the death of patients. Upper airway obstruction can not allow clinical comparative study, the treatment measures are based on limited clinical observation data, and there is a big controversy.Treatment of an upper airway foreign body obstructionFirst aid techniques: (1) inhalation of foreign bodies and the first to use the dental pad or openings to open the mouth, and to clear a foreign body in the mouth; stimulate the throat with a tongue depressor or index finger, at the same time the rapid increase in patients on abdominal abdominal pressure Heimlich techniques, can be ruled out some airway foreign body; patients awake upright rescuer from the patient behind clinging to the upper abdomen, right fist, thumb pointing below the xiphoid, left hand pressed right fist rapidly up the weight several times inward; rescuer facing the patient supine patients kneeling its legs on both sides of the upper body leaning forward, right fist placed below the xiphoid, the left hand is placed on top of the right hand, rapid downward move within the weight on abdomen.(2) removal of foreign body bronchoscopy: foreign body removed by the above techniques can not remove the foreign body, or inappropriate practices such as fishbone should laryngoscope or bronchoscope peep removal of foreign body.2. Drug treatment for laryngeal or tracheal spasms caused by upper airway obstruction, and some inflammatory diseases caused by mucosal edema due to upper airway obstruction, drug therapy has a certain value. Effective drugs mainly epinephrine and glucocorticoids, these drugs poor epiglottitis treatment effect, and even lead to adverse reactions should not use this kind of upper airway obstruction.(1) adrenaline: excitable alpha adrenergic receptors causes vasoconstriction, reducing mucosal edema, throat bronchitis has good therapeutic effect, can also be used to treat laryngeal edema. Use, the use of inhalation or intratracheal instillation, each ~~ 2mg rapid onset of action, but to maintain a short time, should be repeated drug.Upper airway obstruction (2) glucocorticoids: a role in the elimination of edema, reduce local inflammation, can be used for a variety of reasons, such as endotracheal intubation edema. Viral throat bronchitis, inhaled corticosteroid effect. Durward given budesonide (budesonide) inhalation therapy, can significantly reduce the intubation rate. Hormone therapy on upper airway scar or tumor stenosis caused by invalid.3. Endotracheal intubation or tracheostomy intubation or incision can create artificial airway to keep the airway and maintain an effective respiratory conditions. Especially need referral for treatment, the intubation can significantly reduce the mortality rate of patients. Laryngeal edema, laryngospasm, functional vocal cord dysfunction, inhalation injury, angina, epiglottitis, laryngeal and tracheal tumors, etc., can be considered for endotracheal intubation or incision. Minimum nasotracheal intubation injury, the most security. But it should be marked with the meaning of airway obstruction, endotracheal intubation or incision itself can also cause upper airway obstruction, and therefore should be closely observed for patients receiving such treatment.4 mixed gas of the helium - the oxygen mixed gas of helium (80%) and oxygen (20%), its density is only 1/3 of the density of air, can reduce the resistance of the airway of turbulence to increase the gas flow rate, to improve the upper airway obstruction in patients with hypoxia. Helium - oxygen gas mixture in part, airway obstruction, such as tracheal stenosis or possession of foreign oppression, severe asthma and angioedema patients achieved a certain effect. However, this mixed gas can only relieve dyspnea, upper airway obstruction is not relieved.Surgery for laryngeal or tracheal tumor or stenosis due to upper airway obstruction, can be laryngotracheal resection and reconstruction treatment, 87% of patients receive good treatment. Airway obstruction, tonsillar hypertrophy on tonsillectomy its symptoms improve. Caused by oropharyngeal stenosis, to pharyngeal surgery has a therapeutic effect.Laser treatment laser treatment allows the tumor, granulomatous lesions carbonation, narrow, and partial resection of tracheal tumors, so as to achieve the lifting of tracheal stenosis, to relieve symptoms, has a therapeutic effect. It can be used by fiberoptic bronchoscopy.The tracheal stent use in recent years nitinol tracheal stent prepared to have a better clinical effect in experimental animal and human resettlement, and long-term placement without deformation and rust color, do not have serious airway inflammatory response and stimulation received wide attention. For tracheal granuloma, cicatricial stenosis due to benign stricture, or tumor-induced malignant stricture. General first stent placed in ice water cooling and shaping fine tubular and loaded into the inserter, the guide wire into a narrow airway by fiberoptic bronchoscopy, so patients with head thrown back as far as possible, and will be placed along the guide wire placement airway stenosis, and then pull out the guide wire. Again fiberoptic bronchoscopy determine the stent placed stenosis. After implantation, the stent body temperature, restored to its original shape and airway snug fit, the stenosis and gradually softened expansion, to achieve the lifting of the narrow effect.Upper airway obstruction - complicationsPulmonary edema.Upper airway obstruction - prognosis and prevention
Prognosis: the majority of patients with previously healthy, fully recovered after early diagnosis and effective treatment.
Prevention: aggressive treatment of the primary disease of the airway infarction.
Upper airway obstruction - Epidemiology
The disease was first upper airway obstruction Gross wrote in 1854, usually occurs in the restaurants restaurants coronary heart disease "(CafeCoronary) term to describe cause sudden death due to food asphyxiation. After 100 years in 1963 Hauqen this also described. Haugen and others, to anyone, at any time, such as swallowing, sudden loss of consciousness, upper airway obstruction should be the first suspect. If death ensuing diagnosis of "coronary heart disease" or "natural causes" should be questioned. After 20 years of development in 1974 cardiopulmonary resuscitation step description widely used, the 1976 thoracic surgeon Heimlich his operation, the lifting of a complete airway obstruction has been described as the Heimlich practices.
Upper airway obstruction (UAO) is severely hampered by a variety of reasons due to upper airway airflow medical emergency, its clinical manifestations are not specific, confused easy with bronchial asthma and obstructive pulmonary disease, and other diseases. The disease is more common in children and rare in adults. There is no specific clinical manifestations of upper airway obstruction, manifested as irritating dry cough, shortness of breath and difficulty breathing; mainly dyspnea breathing difficulties, activities can cause breathing difficulties increased significantly, and often occur due to changes in posture array onset seizures.
Upper airway obstruction - Description
Upper airway obstruction - DescriptionAirway obstruction in the upper airway obstruction (upperairwayobstruction, UAO) is severely hampered by a variety of reasons due to upper airway airflow medical emergency, its clinical manifestations are not specific, easy with bronchial asthma and obstructive pulmonary disease and other diseases confused. Clinically, the disease is more common in children is relatively rare in adults. Upper airway obstruction caused by many reasons, which derived foreign matter other than those caused by the most common, and the rest of the more common laryngeal movement disorders, infections, tumors, trauma, and iatrogenic. Timely understanding and treatment of upper airway obstruction has extremely important clinical implications, since the majority of patients with previously healthy, can be fully recovered by the effective treatment.Upper airway obstruction - symptoms and signs
Airway obstruction in the upper airway obstruction early general without any performance, often start blocking more serious symptoms. Acute upper airway obstruction abrupt onset, severe illness, and even lead to suffocation and death, often obvious signs and symptoms. There is no specific clinical manifestations of upper airway obstruction, manifested as irritating dry cough, shortness of breath and difficulty breathing; mainly dyspnea breathing difficulties, activities can cause breathing difficulties increased significantly, and often occur due to changes in posture array onset seizures. A small number of patients with snoring at night, awakened several times and dyspnea, manifested as sleep apnea syndrome. Caused by inhalation of foreign bodies, choking history, often obvious respiratory distress, looked very painful, from time to time scratching throat. Occasionally chronic upper airway obstruction caused by pulmonary edema and recurrent pulmonary edema performance. The symptoms and signs of upper airway obstruction and the extent and nature of the obstruction. The majority of upper airway obstruction seen in clinical incomplete obstruction. The main signs of inspiratory stridor, significantly more than in the neck, the lungs can also be heard and but weak, sniff can cause wheezing significantly increased. Stridor prompted more serious obstruction, airway diameter is often less than 5 mm. The inspiratory stridor multi prompted extrathoracic upper airway obstruction, more common on the vocal cords or vocal parts; biphasic stridor prompted obstruction breath of song's intensity changes and more tips in the subglottic trachea; curved neck obstruction occurred The thorax the entrance. Children are barking cough, especially at night appear more tips as bronchitis, throat, salivation, difficulty swallowing, fever but no cough is more common in severe epiglottitis. Some patients, there may be a change in sound, location and nature of its changing characteristics and disease, such as unilateral vocal cord paralysis hoarseness; bilateral vocal cord paralysis sound normal, but the wheezing; the glottis over parts lesions often appear low voice , but no hoarseness; the oral abscess contents like sound.
Upper airway obstruction - disease etiologyClinical, upper airway obstruction, although relatively rare, but may be caused by a variety of diseases, such main reasons include: ① airway cicatricial stenosis: multi-intubation or incision treatment; ② airway wall lesions: such as inflammation of the soft tissue of the throat, pharyngeal abscess, enlarged tonsils, vocal cord paralysis, laryngeal or tracheal tumor, tracheomalacia, recurrent polychondritis go far; ③ airway cavity lesions: airway foreign body is more common, and with pedicle endotracheal polyps or tumors and inflammatory granuloma; ④ airway the external oppression: around the airway space-occupying lesions such as thyroid cancer, abscess, hematoma or gas compression; ⑤ airway secretions retention: respiratory tract bleeding or a large number of sputum failed to cough up the large number of inhalation of gastric contents. The cause common cause of upper airway obstruction in adults and children of different anatomical sites, are summarized in Table 1, for reference in clinical diagnosis. A handful of cases, the functional vocal cord abnormalities or psychological factors, may also cause upper airway obstruction.
Upper airway obstruction - pathophysiologicalUpper airway obstruction airway anatomy: the conducting airways of the respiratory system, including the nose, throat, trachea, main bronchus, lobe bronchus and segmental bronchi, bronchioles until the terminal bronchioles part. Different mechanics and other respiratory physiological functions around the small airways and central airways of the respiratory tract is generally divided into three parts: (1) the small airways, airway diameter less than 2mm; ② large airways refers to Long protruding below to 2mm diameter airway; ③ The upper airway, from the nose to carina period of the respiratory tract, including the nose, pharynx, larynx and trachea. Usually pleural entrance or sternum notch is bounded by the upper extrathoracic upper airway and intrathoracic airway is divided into two parts of the upper airway. The extrathoracic on airway mandibular inferior vena (including a region of Ludwig angina), the retropharyngeal chamber (including the produce area retropharyngeal abscess) and throat. Generalized throat to the base of the tongue, down to the trachea, can be divided into the supraglottic larynx (epiglottis, aryepiglottic fold and false vocal cords), glottis (including the the arytenoid vocal cords plane structure) and subglottic area (about 1.5 ~ 2.0cm, cricoid surrounding the airways). The total length of the trachea for l0 ~ 13cm, wherein a length of about 6 intrathoracic ~~ 9cm. The extrathoracic tracheal length of about 2 ~ 4cm, the entrance to the chest from the lower edge of the cricoid, front chest about above the suprasternal notch 1 to 3cm. Normal endotracheal coronal diameter, male the l3 ~ 25mm, 10 ~ 21mm female. Cause tracheal diameter narrowing factors are the following: (1) Saber sheath trachea; ② amyloidosis; ③ recurrent polychondritis; ④ Wegener granulomatosis; the ⑤ tracheobronchial flat osteochondral angioplasty; of ⑥ rhinoscleroma disease; ⑦ complete cricoid ; ⑧ Down syndrome. Pathophysiology of upper airway obstruction: Under normal circumstances, when breathing, respiratory muscle contraction intrathoracic pressure lower airway pressure below atmospheric pressure, the gas from the outside world into the lungs; Instead, breath, respiratory muscle relaxation chest The increased pressure within the gas excreted by the lungs. Acute upper airway obstruction can directly affect the ventilation function of the body, the oxygen of the outside world can not be inhaled into the lungs, the carbon dioxide produced by the metabolism can not be eliminated from the body, causing acute respiratory failure, such as failure to obtain timely medical treatment, every serious shortage oxygen and carbon dioxide retention leads to death. Chest part of the upper airway at atmospheric pressure under the intrathoracic part in the pleural cavity under pressure role. The trachea both sides of the inside and outside pressure difference for the cross-wall pressure. Pleural cavity pressure greater than the outside pressure when the trachea, cross-wall positive pressure airway tend to close; pressure is greater than when the transmural pressure is negative, endotracheal the tracheal outside pressure, tracheal smooth. Upper airway obstruction affecting the patient's ventilatory function, due to the decrease in alveolar ventilation, airway obstruction can be produced in the patient's movement on Health hypoxemia, but its mostly normal dispersion function. Upper airway obstruction location, extent, nature (fixed or variable type) and expiratory or inspiratory pressure changes caused by patients with different pathophysiological changes produce inspiratory airflow limitation, expiratory airflow limitation, or both limited. Clinically, depending on the respiratory airflow obstruction of upper airway obstruction is divided into the following three kinds: variable extrathoracic airway obstruction, of variable intrathoracic upper airway obstruction and a fixed upper airway obstruction.A variable extrathoracic upper airway obstruction variable blocking the tracheal lumen of the size of the site of obstruction may be due to the tracheal changes in the internal and external pressures and changes in the upper airway obstruction. Variable extrathoracic upper airway obstruction found in patients suffering from diseases such as tracheomalacia and vocal cord paralysis. Under normal circumstances, the chest on the outer periphery of the airway pressure throughout the respiratory cycle are under atmospheric pressure, the inspiratory airway pressure decreases, causing the cross-wall pressure increases, and its direction of action grounds tube outward tube, causing chest on the gas Road tend to shrink. Variable extrathoracic upper airway obstruction in patients, sniff, the result of the Venturi effect and turbulence the obstruction distal airway pressure was significantly reduced, significantly increased transmural pressure caused by the obstruction site of airway caliber further narrow The inspiratory airflow serious disruption; contrary, when its forced expiratory endotracheal pressure increased, due to the cross-wall pressure decreases, the extent of blocking eased. Therefore, in this patient dynamic flow - volume loop tracings showed inspiratory flow limitation and showed inspiratory and expiratory flow limitation lighter does not appear platform, or even render normal graphics.Variable intrathoracic upper airway obstruction variable intrathoracic upper airway obstruction, seen in intrathoracic airway of tracheomalacia and tumor patients. Intrathoracic airway pressure around the pleural cavity pressure close to the external pressure (pleural cavity pressure) intraluminal pressure compared to the negative pressure in the lumen, the direction of action of the cross-wall pressure from the lumen to the extraluminal intrathoracic airway, leading to tend to expand. When patients with forced expiratory Venturi effect and turbulence of the obstruction proximal airway pressure reduces, further narrowing the airway caliber also cause obstruction site, but expiratory flow severely hampered. This patient dynamic flow - volume loops tracings, performance render breath platform expiratory flow limitation, inspiratory flow limitation lighter.Fixed upper airway obstruction fixed upper airway obstruction refers stiff upper airway obstructive lesion fixed, breathing changes in airway caliber cross-wall pressure change can not be caused by the obstruction was found in tracheal stenosis, and thyroid cancer patients . These patients, their inspiratory and expiratory airflow were limited and a similar level of dynamic flow - volume loop inspiratory flow and expiratory flow showed a platform. Most scholars believe that expiratory flow rate and inspiratory flow than 50% of vital capacity (FEF50% / FIF50%) is equal to 1 is the characteristics of the fixed upper airway obstruction. But variable type obstruction and airway obstructive lesions adjacent normal FEF50% / FIF50% certain, should be noted.Upper airway obstruction - diagnostic testsDiagnosis of upper airway obstruction: diagnosis of upper airway obstruction, the key is to take into account the possibility of upper airway obstruction. Clinical, should be timely and relevant examination: ① mainly shortness of breath, difficulty breathing, activity significantly worse, sometimes symptoms aggravated with postural after bronchodilator therapy invalid; ② exist on gas tract inflammation, injury, and in particular the history of endotracheal intubation and tracheostomy; the ③ pulmonary function tests showing maximal expiratory flow, maximal voluntary ventilation sexual decline unchanged FVC, FEV1 was not changed significantly, with the decline in maximum voluntary ventilation fails proportion; or FEV1 decreased but closing volume normal.Laboratory tests: upper airway obstruction is more common infections, such as infection, blood leukocytes may be elevated.Other laboratory examinations:Pulmonary function tests peak expiratory flow (speed) - volume curve (Central) is the preferred method of examination for the diagnosis of upper airway obstruction. Upper airway obstruction, the flow - volume curve exhibits a distinct change of diagnostic value. As mentioned earlier, can be determined according to the change of the flow - volume curve shape different upper airway obstruction. ① variable extrathoracic on, airway obstruction, its flow - volume curve showed inspiratory flow significantly restricted presented inspiratory and expiratory flow is basically normal, the therefore FEF50% / FIF50%> 1; the ② variable intrathoracic upper airway obstruction, its flow - volume curve showed expiratory flow significantly restricted render breath platform, FEF50% / FIF50%, <1; (3) fixed upper airway obstruction, its flow - volume curve showed inspiratory expiratory flow were significantly decreased, and a considerable degree of rendered as a rectangle, FEF50% / FIF50% = 1. Other indicators of lung function, such as FEV0.5, FEV1.0 reduced, PEFR, MVV progressive decline FIF50% ≤ 100L/min FEV1.0/PEFR ≥ 10 ml / (L? Min) FEVl.0/FEV0.5 ≥ 1.5. Closed volume vital capacity VC and CV normal, suggesting that the presence of upper airway obstruction. Pulmonary function tests can not be performed in patients with acute respiratory distress, and high sensitivity to upper airway obstruction.2 radiographic examination(1) plain films of the neck: plain film of the trachea, upper airway obstruction of exudative tracheitis, airway foreign body and innominate artery compression due to higher sensitivity, but on the larynx or trachea softening sensitive poor. Inspiratory neck plain film laryngotracheitis and epiglottitis has differential value. The laryngotracheitis the typical signs for the "steeple" sign. The subglottic stenosis more common in patients with laryngotracheitis, but can also be found epiglottitis. The epiglottitis the neck lateral radiographs can show swelling of the epiglottis and hypopharynx expansion. Airway plain film diagnosis of upper airway obstruction may provide important information, but less accurate, the judge should be combined with medical history and symptoms.The size and morphology of upper airway obstruction (2) Chest CT Scan: CT scan of the airway can learn obstructive lesions, the degree of airway narrowing and airway wall, as well as the situation of the lesion surrounding tissue. The enhanced scan still helps clear lesions blood supply.(3) chest MRI examination: has a good ability to distinguish, can be expected that the extent and length of the airway occlusion, as well as evaluating the mediastinal case.3 the acoustic check breathing audio spectrum analysis found that normal human peak frequency and frequency spectrum are mainly located below 200Hz.Airway obstruction in patients with chest appearance, a significant increase in the peak frequency of breath sounds, mostly three times greater than the baseline, the frequency spectrum of the group widened and moved towards the area of high-frequency greater than 200Hz. The above-mentioned changes in the inspiratory phase is greater than the expiratory phase, and the signal strength of the neck to the chest. The blocking variable thoracic breathing sound spectrum changes as compared to the expiratory than inspiratory chest signal stronger. Therefore, breathing audio spectrum analysis to determine airway obstruction has better clinical value.Endoscopy fiberoptic laryngoscope or fiberoptic bronchoscopy can directly observe the upper airway, to understand the dynamic characteristics of the lesions in the vocal cords, trachea ring the changes as well as the respiratory process, and can be collected living tissue for pathological examination, so the diagnosis decisive role. Suspected obstruction of the upper airway, should be considered for endoscopy. But the severe breathing difficulties should not be checked for biopsy and non-vascular diseases.Upper airway obstruction - Differential DiagnosisCerebrovascular accident, seizures, sleeping pill overdose, heart attack, acute laryngospasm and laryngeal edema as well as other causes of airway obstruction phase identification.Upper airway obstruction - treatment optionsUpper airway obstruction due to reasons caused by upper airway obstruction more, the choice of treatment should be determined according to its etiology and severity. Severe upper airway obstruction should take urgent measures to relieve airway obstruction, to save the lives of patients. Some type of upper airway obstruction, changes in position can make the symptoms can be alleviated; caused by infectious diseases, such as epiglottitis, pharyngeal abscess, antibiotic treatment should be timely. Acute upper airway obstruction often occurs outside the hospital can not receive timely diagnosis and treatment, lead to the death of patients. Upper airway obstruction can not allow clinical comparative study, the treatment measures are based on limited clinical observation data, and there is a big controversy.Treatment of an upper airway foreign body obstructionFirst aid techniques: (1) inhalation of foreign bodies and the first to use the dental pad or openings to open the mouth, and to clear a foreign body in the mouth; stimulate the throat with a tongue depressor or index finger, at the same time the rapid increase in patients on abdominal abdominal pressure Heimlich techniques, can be ruled out some airway foreign body; patients awake upright rescuer from the patient behind clinging to the upper abdomen, right fist, thumb pointing below the xiphoid, left hand pressed right fist rapidly up the weight several times inward; rescuer facing the patient supine patients kneeling its legs on both sides of the upper body leaning forward, right fist placed below the xiphoid, the left hand is placed on top of the right hand, rapid downward move within the weight on abdomen.(2) removal of foreign body bronchoscopy: foreign body removed by the above techniques can not remove the foreign body, or inappropriate practices such as fishbone should laryngoscope or bronchoscope peep removal of foreign body.2. Drug treatment for laryngeal or tracheal spasms caused by upper airway obstruction, and some inflammatory diseases caused by mucosal edema due to upper airway obstruction, drug therapy has a certain value. Effective drugs mainly epinephrine and glucocorticoids, these drugs poor epiglottitis treatment effect, and even lead to adverse reactions should not use this kind of upper airway obstruction.(1) adrenaline: excitable alpha adrenergic receptors causes vasoconstriction, reducing mucosal edema, throat bronchitis has good therapeutic effect, can also be used to treat laryngeal edema. Use, the use of inhalation or intratracheal instillation, each ~~ 2mg rapid onset of action, but to maintain a short time, should be repeated drug.Upper airway obstruction (2) glucocorticoids: a role in the elimination of edema, reduce local inflammation, can be used for a variety of reasons, such as endotracheal intubation edema. Viral throat bronchitis, inhaled corticosteroid effect. Durward given budesonide (budesonide) inhalation therapy, can significantly reduce the intubation rate. Hormone therapy on upper airway scar or tumor stenosis caused by invalid.3. Endotracheal intubation or tracheostomy intubation or incision can create artificial airway to keep the airway and maintain an effective respiratory conditions. Especially need referral for treatment, the intubation can significantly reduce the mortality rate of patients. Laryngeal edema, laryngospasm, functional vocal cord dysfunction, inhalation injury, angina, epiglottitis, laryngeal and tracheal tumors, etc., can be considered for endotracheal intubation or incision. Minimum nasotracheal intubation injury, the most security. But it should be marked with the meaning of airway obstruction, endotracheal intubation or incision itself can also cause upper airway obstruction, and therefore should be closely observed for patients receiving such treatment.4 mixed gas of the helium - the oxygen mixed gas of helium (80%) and oxygen (20%), its density is only 1/3 of the density of air, can reduce the resistance of the airway of turbulence to increase the gas flow rate, to improve the upper airway obstruction in patients with hypoxia. Helium - oxygen gas mixture in part, airway obstruction, such as tracheal stenosis or possession of foreign oppression, severe asthma and angioedema patients achieved a certain effect. However, this mixed gas can only relieve dyspnea, upper airway obstruction is not relieved.Surgery for laryngeal or tracheal tumor or stenosis due to upper airway obstruction, can be laryngotracheal resection and reconstruction treatment, 87% of patients receive good treatment. Airway obstruction, tonsillar hypertrophy on tonsillectomy its symptoms improve. Caused by oropharyngeal stenosis, to pharyngeal surgery has a therapeutic effect.Laser treatment laser treatment allows the tumor, granulomatous lesions carbonation, narrow, and partial resection of tracheal tumors, so as to achieve the lifting of tracheal stenosis, to relieve symptoms, has a therapeutic effect. It can be used by fiberoptic bronchoscopy.The tracheal stent use in recent years nitinol tracheal stent prepared to have a better clinical effect in experimental animal and human resettlement, and long-term placement without deformation and rust color, do not have serious airway inflammatory response and stimulation received wide attention. For tracheal granuloma, cicatricial stenosis due to benign stricture, or tumor-induced malignant stricture. General first stent placed in ice water cooling and shaping fine tubular and loaded into the inserter, the guide wire into a narrow airway by fiberoptic bronchoscopy, so patients with head thrown back as far as possible, and will be placed along the guide wire placement airway stenosis, and then pull out the guide wire. Again fiberoptic bronchoscopy determine the stent placed stenosis. After implantation, the stent body temperature, restored to its original shape and airway snug fit, the stenosis and gradually softened expansion, to achieve the lifting of the narrow effect.Upper airway obstruction - complicationsPulmonary edema.Upper airway obstruction - prognosis and prevention
Prognosis: the majority of patients with previously healthy, fully recovered after early diagnosis and effective treatment.
Prevention: aggressive treatment of the primary disease of the airway infarction.
Upper airway obstruction - Epidemiology
The disease was first upper airway obstruction Gross wrote in 1854, usually occurs in the restaurants restaurants coronary heart disease "(CafeCoronary) term to describe cause sudden death due to food asphyxiation. After 100 years in 1963 Hauqen this also described. Haugen and others, to anyone, at any time, such as swallowing, sudden loss of consciousness, upper airway obstruction should be the first suspect. If death ensuing diagnosis of "coronary heart disease" or "natural causes" should be questioned. After 20 years of development in 1974 cardiopulmonary resuscitation step description widely used, the 1976 thoracic surgeon Heimlich his operation, the lifting of a complete airway obstruction has been described as the Heimlich practices.
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