An infectious disease should be understood as an individual case of a laboratory and/or clinically determined infectious state of a given macroorganism, caused by the action of microbes and their toxins, and accompanied various degrees homeostasis disturbances. This special case manifestations infectious process for this particular individual. About infectious disease they say when a dysfunction of the macroorganism occurs, accompanied by the formation of a pathological morphological substrate of the disease.
For infectious disease certain stages of development are characteristic:
1. Incubation period- the time that passes from the moment of infection to the onset of clinical manifestations of the disease. Depending on the properties of the pathogen, immune status macroorganism, the nature of the relationship between the macro- and microorganism, the incubation period can vary from several hours to several months and even years;
2. Prodromal period- time of appearance of the first clinical symptoms general, non-specific for this disease, for example weakness, fatigue, lack of appetite, etc.;
3. Period acute manifestations diseases- the height of the disease. At this time, symptoms typical for this disease appear: temperature curve, rashes, local lesions, etc.;
4. Period of convalescence- period of decline and disappearance typical symptoms and clinical recovery.
Clinical recovery is not always accompanied by the release of the macroorganism from microorganisms. Sometimes, against the background of complete clinical recovery, a practically healthy person continues to release pathogenic microorganisms into the environment, i.e. Acute carriage is observed, sometimes turning into chronic carriage (for typhoid fever - lifelong).
The contagiousness of an infectious disease is the ability to transmit the pathogen from an infected person to a healthy susceptible organism. Infectious diseases are characterized by the reproduction (multiplication) of an infectious agent that can cause infection in a susceptible organism.
Infectious diseases are widespread among the population. In terms of prevalence, they occupy third place after cardiovascular and oncological diseases. Infectious diseases negatively affect human health and cause significant economic damage. There are crisis infectious diseases (for example, HIV infection), which, due to their high epidemic rate and mortality, threaten all of humanity.
Infectious diseases are classified according to their prevalence in the population; They can be roughly divided into five groups:
Those with the greatest prevalence (more than 1000 cases per 100,000 population) are influenza, ARVI;
Widespread (more than 100 cases per 100,000 population) - viral hepatitis A, shigellosis, acute intestinal diseases unknown etiology, scarlet fever, rubella, chicken pox, parotitis;
Frequently occurring (10-100 cases per 100,000 population) - salmonellosis without typhoid fever, gastroenterocolitis of established etiology, viral hepatitis B, whooping cough, measles;
Relatively rare (1-10 cases per 100,000 population) - typhoid fever, paratyphoid fever, yersiniosis, brucellosis, meningococcal infection, tick-borne encephalitis, hemorrhagic fevers;
Rarely occurring (less than 1 case per 100,000 population) - polio, leptospirosis, diphtheria, tularemia, rickettsiosis, malaria, anthrax, tetanus, rabies.
A feature of an infectious disease is its cyclical nature. This means that in the development of an infectious disease there are several successive periods: incubation, initial, peak of the disease and recovery. Each period has its own characteristic features.
The period of time from the moment of infection to the first clinical manifestations of the disease is called incubation (latent). Different infectious diseases have different durations of this period (from several hours to months and even years). At this time, there are usually no visible health problems. For some diseases (measles, malaria, tonsillitis, chicken pox, etc.), the duration of the incubation period is so strictly defined that it is one of the most characteristic signs of this disease (see section “Description of clinical signs”).
The initial period is the time from the moment the first signs of the disease appear until its peak.
In the initial period, as a rule, there are no characteristic signs inherent in a particular disease. Prevail general symptoms illnesses (fever, malaise, general weakness, decreased performance, etc.).
As the infectious disease develops, signs characteristic of the disease appear. This moment marks the beginning of the period at the height of the disease. In the future, many signs can reach their maximum severity.
From the moment the severity of the manifestations of the infectious disease decreases, the period of recovery (reconvalescence) begins, the duration of which depends on many factors: the severity of the disease, concomitant diseases, characteristics of the body, as well as the quality of the treatment and the volume of rehabilitation measures performed).
Sometimes, after an infectious disease, residual effects are observed that arose during the peak period, but persist for many months, years and even a lifetime (with polio, encephalitis, diphtheria, etc.)
With most infectious diseases, a person becomes dangerous to others at the end of the incubation period. Only during the recovery period does the risk of infection from the patient decrease significantly. During this same period, the body is completely cleansed of the pathogenic agent.
1. Incubation
2. Pre-icteric with the following variants - dyspeptic, asthenovegetative, polyarthralgic, mixed, influenza-like, without manifestations.
3. The height of the period, signs - hyperfermentemia without jaundice, with jaundice, hepatomegaly, sometimes hepatosplenomegaly, endogenous intoxication.
4. Period of convalescence.
5. Outcomes – biliary dyskinesia, prolonged hepatitis, chronicization of the disease leading to cirrhosis or cirrhosis-cancer (hepatocellular carcinoma).
In the acute period of viral hepatitis, especially with hepatitis B, hepatitis B+D, acute hepatic encephalopathy (AHE) may develop.
OPE periods:
1. Prekoma I
2. Prekoma II
3. Coma I (shallow coma)
4. Coma II (deep coma, suppression of all body functions).
The clinical picture of all viral hepatitis is largely similar and differs in percentage terms in the severity of the disease and its outcome. Hepatitis A and E are characterized by a predominantly cyclical benign course with full recovery, and with hepatitis B, C and D, a moderate and severe course, protracted and chronic forms of the disease, and deaths are often observed.
It is not always easy to correctly and timely assess the severity of viral hepatitis, since clinical manifestations, sometimes even in cases resulting in death, are mild and only in the period of complete decompensation of liver function do symptoms appear that indicate a particular severity of the disease. Clinical criteria the severity of viral hepatitis is often subjective, and the indicators of functional tests do not always accurately and completely reflect the degree of damage to the liver parenchyma.
When assessing the severity of the disease, the severity of intoxication and jaundice, an increase in the size of the liver and spleen, weight loss, bilirubin level in the blood serum, aminotransferase activity, and prothrombin index are taken into account. The severity of the disease can be most reliably assessed during the height of the disease.
In this case, the length of the incubation period should be taken into account. The shorter it is, the more severe the disease. Pay attention to the nature and duration of the pre-icteric period. Severe intoxication, polyarthralgia, and a pronounced dyspeptic symptom complex are characteristic of fulminant and severe forms of viral hepatitis. Prolonged intense jaundice, hypotension, bradycardia alternating with tachycardia, lethargy, nausea, low-grade fever, decreased diuresis indicate a severe or malignant course of viral hepatitis with an uncertain prognosis.
In mild cases of viral hepatitis, the concentration total bilirubin in the blood serum is 20-80 µmol/l according to the Jendraszik method, the prothrombin index corresponds to normal values; in moderate cases, total bilirubin increases to 80-160 µmol/L, the prothrombin index does not change significantly; in severe cases, the bilirubin concentration is more than 160 µmol/l, the prothrombin index decreases, the level total protein, fibrin, albumin, the parameters of the blood coagulation system change.
Acute viral hepatitis occurs predominantly cyclically. The incubation period for acute hepatitis A is on average 15-30 days, for acute hepatitis B - 30-180 days. The pre-icteric (initial) period can occur in the following ways: 1) dyspeptic - patients complain of lack of appetite, nausea, sometimes vomiting, low-grade fever, the duration of this period is 3-7 days; 2) asthenovegetative - patients complain of weakness, headache, general malaise, loss of appetite, body temperature - subfebrile or normal; 3) flu-like - patients complain of headache, muscle pain, weakness, loss of appetite, body temperature - 37.5-39°C, and in some cases 39-40°C; The duration of the 2nd and 3rd variants of the pre-icteric period is 5-10 days. 4) the polyarthralgic variant is observed mainly in acute hepatitis B, as well as C. Patients complain of pain in the joints, sometimes muscle pain, weakness, and loss of appetite are observed. The duration of this period is 7-14 days. 5) a mixed variant of the onset of the disease is most often manifested by signs of several syndromes.
In some patients, the disease may begin without signs of intoxication.
With the appearance of clear signs of liver damage - the period at the height of the disease - the health of most patients improves. The temperature normalizes, the urine darkens, the sclera becomes subicteric, jaundice gradually increases, and the stool becomes discolored. The further course of the disease depends on the degree of damage to the liver by the virus, which determines the severity of the disease. With a mild course of viral hepatitis, jaundice increases over 3-5 days, remains at the same level for 1 week, then completely disappears by 15-16 days. Already at the end of 1-2 weeks of the icteric period, the urine becomes lighter and the feces turn yellowish-brown.
In moderate and severe cases of the disease, the icteric staining of the sclera and skin is more intense, and the icteric period is longer (20-45 days). From the outside of cardio-vascular system hypotension is observed, in most patients - bradycardia, deafness of heart sounds. In 80-90% of patients, the liver increases in size, its surface is smooth, the edge is rounded, and moderately painful. In 30-40% of patients the spleen is palpable. In severe cases of acute viral hepatitis, some patients experience bloating due to indigestion (signs of damage to the pancreas, secretory glands stomach and biocinosis disorders gastrointestinal tract). Some patients with severe viral hepatitis may experience moderate ascites. Some patients have itchy skin- the so-called cholestatic variant of the disease.
Some patients experience certain changes in the central nervous system. Even with a mild course of acute viral hepatitis, mood changes, adynamia, lethargy, and sleep disturbances may occur. With increasing severity of the disease, these phenomena occur more often and their severity is more clear.
In severe cases, clear cerebral disorders are observed due to significant degenerative changes in the liver, endogenous intoxication and increased activity of lipid peroxidation processes, as well as the accumulation of their intermediate products.
During the period of convalescence, a reverse development of the symptoms of the disease and normalization of biochemical parameters are observed.
Preliminary diagnosis acute viral hepatitis is established on the basis of an epidemiological history, data on the development of the disease, clinical picture taking into account the characteristics of transmission routes, the duration of the incubation period, the presence of a pre-icteric period, typical subjective and objective signs, taking into account the age of the patient.
The diagnosis is confirmed by routine and special laboratory tests.
IN general analysis In the blood of patients with viral hepatitis, lymphocytosis is observed with moderate anemia and leukopenia in severe cases of the disease. ESR is slightly reduced. Urobilin and bile pigments are found in urine, in feces - during the peak period - especially in moderate and severe forms disease, it is not possible to detect stercobilin.
In the blood serum throughout the entire icteric period, an increased content of total bilirubin is detected, mainly due to its direct fraction. The ratio between direct and indirect fractions is 3:1. In all patients, already in the pre-icteric period of the disease, throughout the entire icteric period and in the period of early convalescence, increased activity AlAT, AST enzymes, indicating the presence of cytolytic processes in the liver. In patients with acute hepatitis, there is an increase in the thymol test and a decrease in the concentration of total protein, which indicates a reduced protein-synthetic function of the liver. With viral hepatitis, there are disturbances in the blood coagulation and anticoagulation systems, depending on the period and severity of the disease. Using these indicators (electrocoagulograms, thrombocytograms, biochemical tests), one can judge the severity of the disease, the phase and degree of DIC syndrome.
They are widely used in the diagnosis and differential diagnosis of viral hepatitis. instrumental methods studies - ultrasound, cholangiography, computed tomography.
With the aim of specific diagnostics ELISA reactions, radioimmunoassay and various combinations thereof are used. Using these methods, specific antigens and antibodies to the antigens of all currently known hepatitis viruses are detected in the blood of patients. Detection of antibodies in the Ig M class indicates an acute disease. Detected antibodies in the Ig G class indicate a protracted or chronic course of viral hepatitis or a previous infectious process, or past illness in the past, about vaccinations.
Using polymerase chain reaction, DNA or RNA of hepatitis viruses can be detected in the blood of patients, which confirms the diagnosis.
Differential diagnosis acute viral hepatitis should be carried out with diseases such as leptospirosis, yersiniosis, mononucleosis, malaria, mechanical and hemolytic jaundice, toxic hepatosis. In this case, it is necessary to take into account the peculiarities of the clinical picture of these diseases, the possibilities of modern specific and instrumental diagnostics.
When setting clinical diagnosis The type of virus that caused the disease, the severity and course of viral hepatitis should be noted.
Leptospirosis is characterized by an acute onset of the disease, often with chills, continued fever during the height of the disease and jaundice, muscle pain, especially the calf, hemorrhagic syndrome. Leukocytosis with neutrophilia and a shift of the formula to the left is detected in the blood, and an accelerated ESR is observed. The activity of ALT and AST is moderately increased, the ratio of direct and indirect bilirubin is 1:1. The concentration of urea and residual nitrogen in the blood serum increases. Bilirubin is constantly detected in the stool, a reaction to occult blood often positive, stool is not discolored. Red blood cells, white blood cells in large quantities, granular, waxy casts are found in the urine. Diuresis is reduced, up to anuria. Possible azotemic coma. The final recognition of the disease is confirmed by the detection of leptospira in the urine sediment or blood serum and the increase in antibodies in the blood serum of patients in the agglutination-lysis reaction with a specific leptospirosis antigen.
In generalized forms of yersiniosis, jaundice can also be observed, however, it is accompanied by fever, metastatic foci in other organs, tissues, leukocytosis with neutrophilia, accelerated ESR. Exacerbations and relapses of the disease are possible. The diagnosis is confirmed serological methods with specific yersinia antigen.
The visceral form of mononucleosis is characterized by lymphadenopathy, fever at the height of jaundice, and a serious condition. Broad-plasma lymphocytes (virocytes) are found in increased numbers in the blood.
With malaria, there is a clear alternation of attacks of apyrexia with chills, followed by a feeling of heat and sweating, and a painful, enlarged spleen is often detected. It occurs in the blood hemolytic anemia, in a thick drop of blood and a smear are found various shapes malarial plasmodium. In the blood serum, the indirect fraction of bilirubin predominates.
For mechanical jaundice using the method ultrasound examination You can find stones in the gall bladder and bile ducts, dilatation of the bile ducts, an increase in the size of the head of the pancreas and other components that cause obstructive jaundice. In most patients, there may be a moderate increase in the activity of ALT, AST, leukocytosis, and accelerated ESR.
Hemolytic jaundice is characterized by anemia, accelerated ESR, and an increase in total bilirubin due to its indirect fraction. Stercobilin is always present in feces.
The differential diagnosis of acute viral hepatitis with hepatosis is complex and requires thoughtful and painstaking work from the doctor. In this case, a fully collected anamnesis is essential.
Outcomes of the disease. Acute viral hepatitis most often ends in complete recovery. Some patients may develop cholecystitis, cholangitis, pancreatitis, and biliary dyskinesia after acute hepatitis. In 5-10% of patients, a protracted course with periodic exacerbations may be observed, due to long-term persistence of the virus. In such cases, it is possible to develop chronic hepatitis, which is typical for hepatitis B and C and can ultimately lead to liver cirrhosis or hepatocellular carcinoma.
The most dangerous outcome of viral hepatitis is acute or subacute massive liver necrosis, in which the clinical picture of acute or subacute hepatic encephalopathy develops. Acute viral hepatitis is characterized by acute hepatic encephalopathy.
The mechanism of development of acute or subacute liver necrosis is extremely complex and poorly understood. As a result of intensive reproduction of the virus in hepatocytes, excessive accumulation of reactive oxygen species occurs, which in turn leads to depletion of the functional capacity of the antioxidant system. This leads to an increase in lipid peroxidation processes, destruction of the structure of cell membranes of the hepatocyte and its intracellular structures, accumulation of toxic peroxides, ammonia in tissues and blood, and inactivation of many enzyme systems of the cell. IN cell membranes additional channels appear, natural channels are destroyed, the receptor sensitivity of the cell decreases, which leads to irreversible disturbances of enzymatic reactions, uncoupling of phosphorylation processes, and the release of lysosomal proteases, leading to the complete destruction of hepatocytes.
With this destruction of hepatocytes, all liver functions are inhibited. First of all, pigment metabolism is disrupted. In the blood of patients, there is an intensive increase in bilirubin to extremely high numbers. In the peripheral blood, the concentration of lipid peroxidation products increases several times, indicating a high intensity of formation of fatty acid radicals in membrane structures. The activity of all AOS components is depleted. The synthetic function of the liver is impaired. Incomplete proteins, products of fibrin degradation, appear in the blood, and the level of total blood protein and its fractions decreases. The synthesis of components of the blood coagulation system is disrupted, which leads to the development of “consumption coagulopathy” (the third phase of DIC) and bleeding, sometimes massive, leading to the death of patients. The cycle of urea synthesis and ammonia utilization is disrupted, which leads to the accumulation of these products in the blood and deep pathological changes in the central nervous system.
As a result of inhibition of the functions of the gastrointestinal tract and the development of dysbiosis, fermentation processes are activated in the intestines, highly toxic products such as indole, skatole, ammonia and others accumulate and are absorbed into the blood. Passing through the bloodstream through the liver, they are not inactivated and are carried into the central nervous system, causing signs of encephalopathy. Reactive oxygen species circulating in high concentrations in the blood, intercellular fluid and tissues of the brain substance contribute to the destruction of myelin and other cellular structures, increase the binding of toxins circulating in the blood by cells of the nervous tissue, increasing the manifestations of encephalopathy.
Water-electrolyte, carbohydrate, protein, fat, and vitamin metabolism are disrupted. There is a complete “imbalance” of metabolism, metabolic acidosis increases, which in 2/3 of cases is the direct cause fatal outcome. 1/3 of patients die from massive bleeding.
Clinical features and methods for predicting acute hepatic encephalopathy (AHE). The term “acute hepatic encephalopathy” refers to the unconscious state of a patient with impaired reflex activity, convulsions, and disruption of vital functions as a result of deep inhibition of the cerebral cortex spreading to the subcortex and underlying parts of the central nervous system. This is a sharp inhibition of neuropsychic activity, characterized by impaired movements, sensitivity, reflexes and lack of reactions to various stimuli.
Hepatic coma is an endogenous coma caused by endogenous intoxication as a result of loss of function and breakdown of the liver.
Currently there are many various classifications APE characterizing one or another stage of the complication. EAT. Tareev, A.F. Bluger proposed to distinguish three stages of OPE - precoma 1, precoma 2 and 3 - coma itself.
Precoma 1 is characterized by intermittent disturbance of consciousness, mood instability, depression, decreased ability to orientate, mild tremor, and sleep inversion. Patients are irritable, sometimes euphoric. They are disturbed by attacks of melancholy, doom, and premonition of death. Fainting, short-term loss of consciousness, dizziness, hiccups, nausea, and vomiting may occur. Jaundice is increasing. Bradycardia gives way to tachycardia. Tendon reflexes are increased. This state lasts from several hours to 1-2 days with the transition to the second stage.
In the 2nd stage of precoma, consciousness is increasingly disturbed, memory lapses are characteristic, alternating with attacks of psychomotor and sensory agitation up to delirium. Upon awakening, there is no orientation in time, space and action. Tendon reflexes are high. Deafness of heart sounds, tachycardia, and hypotension are observed. The breathing rhythm is periodically disrupted. The size of the liver begins to shrink. 1/3 of patients experience nosebleeds, gastrointestinal, uterine and other bleeding. Diuresis decreases. The abdomen is distended, intestinal motility is reduced. This state lasts 12 hours - 2 days.
At the 3rd stage - the coma itself - there is a complete loss of consciousness and the disappearance of reflexes, first tendon, then corneal and, lastly, pupillary. Pathological Babinski reflexes, foot clonus, rigidity of the limb muscles, hyperkinesis, convulsive syndrome, and then complete areflexia may occur. Severe tachycardia, hypotension, and respiratory rhythm disturbance are observed. The abdomen is distended, intestinal motility is reduced, in some patients abdominal cavity Free fluid is detected, the liver is reduced in size. There is a significant decrease in diuresis up to anuria. Soon (6 hours - 24 hours) patients die from massive bleeding or from symptoms deep violation metabolism with symptoms of severe metabolic acidosis.
Some clinicians adhere to a different classification of hepatic coma, which provides for the following stages of its development: precoma-1, precoma-2, coma-1, coma-2. Precoma-1 is a period of harbingers. Precoma-2 - in the clinical picture of the disease there are clear clinical signs of encephalopathy. Coma-1 is a period of excitement with loss of consciousness. Coma-2 - deep loss of consciousness, areflexia, respiratory rhythm disturbance, reduction in liver size, bleeding, anuria.
Prediction of APE is possible several days before the appearance of harbingers of this formidable complication. In order to predict APE, seriously ill patients should examine the state of the blood coagulation and anticoagulation systems daily using the electrocoagulography method, which allows one to obtain a graphical record of the entire process of blood coagulation and fibrinolysis within 20 minutes.
We have developed a new method for assessing the parameters of various coagulation phases based on the degree of blood clot retraction and the time of maximum retraction. Proposed simple formula Calculation of the blood clot retraction index (BCRI):
t - duration of maximum retraction of a blood clot, sec;
h - height of oscillatory movements of the recorder, mm.
Severe viral hepatitis is characterized by a decrease in IFRS. Patients in whom it is equal to 32 conventional units. the coagulogram should be examined daily, and their condition should be regarded as a threat of coma. With IRKS equal to 9 conventional units. Patients develop signs of coma. With her further development the IRCS value decreases to 0. If the general condition of the patient improves, the IRCS increases.
This method can also be used to assess the effectiveness of therapy.
The commonly used prothrombin index is not an early prognostic test. It can only be used to document an already developing and clinically diagnosed coma. The outcomes of OPE are most often unfavorable. In case of recovery, but improper management of patients during the period of early convalescence, those who have recovered from the disease develop early cirrhosis of the liver.
With early prediction of APE at the preclinical stages and proper management of patients, recovery occurs, or APE does not occur.
Treatment. All patients with acute viral hepatitis must remain in bed during the period of acute clinical manifestations.
For the entire period of acute clinical manifestations and early convalescence, patients are prescribed table No. 5 according to Pevzner. It is forbidden to eat anything fried, fatty or spicy. Alcoholic drinks are strictly contraindicated. For meat products, white boiled chicken meat, veal and boiled rabbit meat are recommended. Patients are advised to take fresh boiled fish. Vegetable lean soups, pea, rice, and buckwheat soups should be recommended as first courses. The main courses include mashed potatoes, rice, buckwheat, oatmeal, seasoned with butter (20-30g). IN dietary food cooked sausages should be included. Among dairy products, milk, cottage cheese, kefir, and lean mild cheeses should be recommended. Patients are shown salads from fresh vegetables without onions, seasoned with refined sunflower oil (olive, corn, Provençal), vinaigrettes. Compotes, jelly from fresh and canned fruits and berries, table mineral waters, rosehip decoction, tea with lemon should be widely recommended. Patients can eat fresh apples, pears, plums, cherries, pomegranates, watermelons, cucumbers, and tomatoes.
For hepatitis A and E, which is characterized by an acute, cyclical course, prescribing antiviral agents not shown. They are advisable to use in cases of progressive (protracted) course of acute hepatitis B and D against the background of high activity pathological process with indicators of pathogen replication and in all cases of acute hepatitis C, taking into account the high probability of chronicity. Patients are prescribed alpha interferon, in particular its recombinant (intron A, roferon A, pegintron, pegasys) and native (wellferon, human leukocyte interferon) drugs. There is no consensus regarding the interferon therapy regimen for acute viral hepatitis. Most often, drugs are prescribed at a dose of 3-5 million IU 3 times a week (or every other day) for 3-6 months. With this method of therapy, the percentage of chronicity decreases by approximately 5 times in hepatitis B and 3 times in hepatitis C. Synthetic nucleosides (famciclovir, lamivudine, ribavirin, trivorin) and protease inhibitors (invirase, Crixivan) can also be used for etiotropic treatment. IN last years Inducers of endogenous interferon are effectively used - neovir, cycloferon, amiksin, kagocel, etc. Amiksin patients are prescribed 0.125 g 2 days in a row per week, for 5 weeks. In addition, leukinferon, interleukin-1, interldeikin-2 (roncoleukin), thymus preparations (thymalin, thymogen, T-activin), thymopoietins (glutoxim) may be recommended.
The above drugs are also indicated for severe acute hepatitis B with the threat of developing acute liver failure.
In the presence of intoxication, patients are prescribed detoxification intravenous therapy within 3-5 days. For this purpose, a 5% glucose solution of 200.0-400.0 is injected into a vein; rheosorbilact 200.0-400.0; 5% solution ascorbic acid 10.0-15.0; acesol and chlosol 200.0-400.0.
Throughout the icteric period, enterosorbents are prescribed orally. Starting from the first day of the disease and until the activity of aminotransferases is completely normalized, patients should receive natural antioxidants internally, such as infusion of Astragalus wooliflora and others.
If there is a threat of APE, patients should be prescribed intravenous drips of saline and colloidal solutions V total volume 1200-2400 ml per day. The solutions are administered 2 times a day (morning and evening) subclavian vein through a catheter. Reosorbilact 400.0 is prescribed; acesol - 400.0; 4% solution of glutargin - 50 ml, 5% solution of ascorbic acid - 20.0; 5% glucose solution - 400.0; donor albumin - 400.0-500.0; cocarboxylase, ATP, trasylol or gordox 100,000-200,000 units, or contrical, aminocaproic acid, heptral (800 mg per day).
When bleeding occurs, hemostatic therapy is prescribed that is adequate to the losses. For this purpose, you can use aminocaproic acid, vikasol, blood plasma, whole blood, erythrocyte suspension, fibrinogen.
Patients are shown cleansing enemas.
At psychomotor agitation patients are fixed to the bed, seduxen or sodium hydroxybutyrate is administered.
With reduced diuresis, mannitol, mannitol, and aminophylline should be administered intravenously.
When organizing and carrying out a set of therapeutic measures, it should be remembered that the effectiveness of treatment largely depends on the quality of patient care, therefore in the ward intensive care There should be specially trained personnel who are proficient in intensive care and resuscitation methods, as well as methods of care and maintenance for patients with hepatic coma.
It should also be remembered that APE recognized at the preclinical stages and properly administered treatment will save the patient’s life.
Dispensary observation of convalescents is carried out by a KIZ doctor when district clinics for viral hepatitis A and E for 3 months, for hepatitis B and C - for 6 months.
In cases where the recovery of hepatocytes is delayed (indicators of aminotransferase activity are increased), observation is extended until complete recovery.
In the development of the disease, four periods (stages) are usually distinguished: latent, prodromal, the period of the height of the disease and the outcome, or the period of the end of the disease. This periodization developed in the past when clinical analysis acute infectious diseases (typhoid fever, scarlet fever, etc.). Other diseases (cardiovascular, endocrine, tumors) develop according to different patterns, and therefore the given periodization is not very applicable to them. A.D. Ado distinguishes three stages of disease development: the onset, the stage of the disease itself, and the outcome.
Latent period(in relation to infectious diseases - incubation) lasts from the moment of exposure to the cause until the appearance of the first clinical signs of the disease. This period can be short, as with the action of chemical warfare agents, and very long, as with leprosy (several years). During this period, the body’s defenses are mobilized, aimed at compensating for possible violations, at destroying pathogenic agents or at removing them from the body. It is important to know the features of the latent period when carrying out preventive measures (isolation in case of infection), as well as for treatment, which is often effective only in this period (rabies).
Prodromal period- this is the period of time from the first signs of the disease to the full manifestation of its symptoms. Sometimes this period manifests itself clearly ( lobar pneumonia, dysentery), in other cases it is characterized by the presence of weak but clear signs of the disease. With mountain sickness, for example, this is causeless fun (euphoria), with measles - Velsky - Koplik - Filatov spots, etc. All this is important for differential diagnosis. At the same time, identifying the prodromal period in many chronic diseases is often difficult.
Period of pronounced manifestations, or the height of the disease, is characterized by the full development of the clinical picture: convulsions with insufficiency of the parathyroid glands, leukopenia with radiation sickness, a typical triad (hyperglycemia, glycosuria, polyuria) with diabetes mellitus. The duration of this period for a number of diseases (lobar pneumonia, measles) is determined relatively easily. At chronic diseases with their slow progress, the change of periods is elusive. In diseases such as tuberculosis and syphilis, the asymptomatic course of the process alternates with its exacerbation, and new exacerbations are sometimes noticeably different from the primary manifestations of the disease.
Outcome of the disease. The following outcomes of the disease are observed: recovery (complete and incomplete), relapse, transition to a chronic form, death.
Recovery- a process that leads to the elimination of disorders caused by the disease and the restoration of normal relations between the body and the environment, in humans - primarily to the restoration of working capacity.
Recovery can be complete or incomplete. Full recovery is a condition in which all traces of the disease disappear and the body completely restores its adaptive capabilities. Recovery does not always mean returning to your original state. As a result of the disease, changes in various systems, including the immune system, may appear and persist in the future.
In case of incomplete recovery the consequences of the disease are expressed. They remain for a long time or even forever (fusion of the pleura, narrowing of the mitral orifice). The difference between complete and incomplete recovery is relative. Recovery can be almost complete, despite a persistent anatomical defect (for example, the absence of one kidney, if the second fully compensates for its function). One should not think that recovery begins after the previous stages of the disease have passed. The healing process begins from the moment the disease occurs.
The idea of recovery mechanisms is formed on the basis general position that illness is the unity of two opposing phenomena - the actual pathological and the protective-compensatory. The predominance of one of them decides the outcome of the disease. Recovery occurs when the complex of adaptive reactions is strong enough to compensate for possible disturbances. Recovery mechanisms are divided into urgent (emergency) and long-term. Urgent ones include such reflex protective reactions as changes in respiratory rate and heart rate, the release of adrenaline and glucocorticoids during stress reactions, as well as all those mechanisms that are aimed at maintaining the constancy of the internal environment (pH, blood glucose, blood pressure, etc.). d.). Long-term reactions develop somewhat later and last throughout the disease. This is primarily the inclusion of backup capabilities of functional systems. Diabetes mellitus does not occur when even 3/4 of the pancreatic islets is lost. A person can live with one lung, one kidney. A healthy heart can perform five times more work under stress than at rest.
Enhanced function increases not only as a result of the inclusion of previously non-working structural and functional units of organs (for example, nephrons), but also as a result of an increase in the intensity of their work, which in turn causes activation of plastic processes and an increase in organ mass (hypertrophy) to a level when the load for each functioning unit does not exceed normal.
The activation of compensatory mechanisms, as well as the cessation of their activity, depends primarily on the nervous system. P.K. Anokhin formulated the idea of functional systems that specifically compensate for a functional defect caused by damage. These functional systems are formed and operate according to certain principles:
Signaling of a violation that has occurred, leading to the activation of appropriate compensatory mechanisms.
Progressive mobilization of spare compensatory mechanisms.
Reverse afferentation about the successive stages of restoration of impaired functions.
The formation in the central nervous system of such a combination of excitations that determines the successful restoration of functions in a peripheral organ.
Assessing the adequacy and strength of final compensation over time.
The collapse of the system as unnecessary.
The sequence of stages of compensation can be traced using the example of lameness when one leg is damaged:
signaling of imbalance from the vestibulocochlear organ;
restructuring the work of motor centers and muscle groups in order to maintain balance and the ability to move;
caused by a stable anatomical defect, constant combinations of afferentations entering the higher parts of the central nervous system, and the formation of temporary connections that provide optimal compensation, i.e., the ability to walk with minimal lameness.
Relapse- a new manifestation of the disease after its apparent or incomplete cessation, for example, the resumption of attacks of malaria after a more or less long interval. Recurrences of pneumonia, colitis, etc. are observed.
Transition to chronic form means that the disease progresses slowly, with for long periods remission (months and even years). This course of the disease is determined by the virulence of the pathogen and mainly by the reactivity of the body. Thus, in old age, many diseases become chronic (chronic pneumonia, chronic colitis).
Terminal states- the gradual cessation of life even with seemingly instantaneous death. This means that death is a process, and in this process several stages (terminal states) can be distinguished: preagony, agony, clinical and biological death.
Preagonia can be of varying duration (hours, days). During this period, shortness of breath, a decrease in blood pressure (up to 7.8 kPa - 60 mm Hg and below), and tachycardia are observed. The person experiences a blackout of consciousness. Gradually the pre-agony turns into agony.
Agony(from the Greek agon - fight) is characterized by a gradual shutdown of all body functions and at the same time extreme tension of protective mechanisms that are already losing their expediency (convulsions, terminal breathing). The duration of the agony is 2 - 4 minutes, sometimes more.
Clinical death is a condition when all visible signs of life have already disappeared (breathing and heart function have stopped, but metabolism, although minimal, still continues). At this stage, life can be restored. That is why the stage clinical death attracts special attention from clinicians and experimenters.
Biological death is characterized by irreversible changes in the body.
Experiments on animals, primarily on dogs, made it possible to study in detail the functional, biochemical and morphological changes at all stages of dying.
Dying represents the disintegration of the integrity of the organism. It ceases to be a self-regulating system. In this case, the systems that unite the body into a single whole are first destroyed, first of all - nervous system. In the same time lower levels regulations are preserved to some extent. In turn, there is a certain order of dying various departments nervous system. The cerebral cortex is most sensitive to hypoxia. In case of asphyxia or acute blood loss, activation of neurons is first observed. In this regard, motor agitation occurs, breathing and heart rate increase, and blood pressure increases. Then inhibition occurs in the cortex, which has a protective significance, since for some time it can save cells from death. With further dying, the process of excitation, and then inhibition and exhaustion, spreads lower, to the stem part of the brain and to the reticular pharmacy. These phylogenetically more ancient parts of the brain are most resistant to oxygen starvation (centers medulla oblongata can tolerate hypoxia for 40 minutes).
Changes in other organs and systems occur in the same sequence. With fatal blood loss, for example, within the first minute breathing sharply deepens and becomes more frequent. Then its rhythm is disrupted, the breaths become either very deep or superficial. Finally, the excitation of the respiratory center reaches a maximum, which is manifested by especially deep breathing, which has a pronounced inspiratory character. After this, breathing weakens or even stops. This terminal pause lasts 30–60 s. Then breathing temporarily resumes, acquiring the character of rare, first deep, and then increasingly shallow sighs. Together with the respiratory center, the vasomotor center is activated. Vascular tone increases, heart contractions intensify, but soon stop and vascular tone decreases.
It is important to note that after the heart stops working, the system that generates excitation continues to function for quite a long time. On the ECG, biocurrents are observed within 30 - 60 minutes after the disappearance of the pulse.
In the process of dying, characteristic metabolic changes occur, mainly due to ever-deepening oxygen starvation. Oxidative metabolic pathways are blocked, and the body obtains energy through glycolysis. The inclusion of this ancient type of metabolism has a compensatory value, but its low efficiency inevitably leads to decompensation, aggravated by acidosis. Clinical death occurs. Breathing and blood circulation stop, reflexes disappear, but metabolism, although at a very low level, still continues. This is enough to maintain the “minimal life” of nerve cells. This is precisely what explains the reversibility of the process of clinical death, i.e., revival is possible during this period.
The question of the time period during which resuscitation is possible and advisable is very important. After all, revival is justified only if mental activity is restored. V. A. Negovsky and other researchers argue that positive results can be achieved no later than 5 - 6 minutes after the onset of clinical death. If the dying process continues for a long time, leading to depletion of creatine phosphate and ATP reserves, then the period of clinical death is even shorter. On the contrary, with hypothermia, revival is possible even an hour after the onset of clinical death. In the laboratory of N. N. Sirotinin, it was shown that a dog can be revived 20 minutes after death as a result of bleeding, followed by a complete restoration of mental activity. It should, however, be borne in mind that hypoxia causes greater changes in the human brain than in the brain of animals.
Resuscitation, or revitalization, of the body includes a number of measures that are aimed primarily at restoring blood circulation and breathing: cardiac massage, artificial ventilation, cardiac defibrillation. The latter event requires the availability of appropriate equipment and can be carried out under special conditions.
Etiology. The concept of the causes and conditions of the disease. Classification of causes of diseases. The role of heredity and constitution in the occurrence and development of the disease.
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From the moment the pathogen enters the body until the clinical manifestation of symptoms of the disease, a certain time passes, called the incubation (latent) period. Its duration varies. For some diseases (influenza, botulism) it lasts for hours, for others (rabies, viral hepatitis B) - weeks and even months, for slow infections - months and years. For most infectious diseases, the incubation period is 1–3 weeks.
Length of incubation period due to several factors. To some extent, it is related to the virulence and infectious dose of the pathogen. The higher the virulence and the higher the dose of the pathogen, the shorter the incubation period.
It takes a certain time for a microorganism to spread, reproduce, and produce toxic substances. However the main role belongs to the reactivity of the macroorganism, which determines not only the possibility of the occurrence of an infectious disease, but also the intensity and pace of its development.
From the beginning of the incubation period, the body changes physiological functions. Having reached a certain level, they are expressed in the form of clinical symptoms.
Prodromal period, or period of precursors of the disease
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With the appearance of the first clinical signs of the disease, the prodromal period, or the period of warning signs of the disease, begins.
Its symptoms(malaise, headache, weakness, sleep disorders, loss of appetite, sometimes slight increase body temperature) are characteristic of many infectious diseases, and therefore establishing a diagnosis during this period causes great difficulties.
The exception is measles: detection of a pathognomonic symptom (Belsky–Filatov–Koplik spot) in the prodromal period allows us to establish an accurate and final nosological diagnosis.
Length of symptom onset usually does not exceed 2–4 days.
The peak period of the disease
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The height of the period has a different duration - from several days (for measles, influenza) to several weeks (for typhoid fever, viral hepatitis, brucellosis).
During the peak period, the symptoms characteristic of this infectious form most clearly manifest themselves.
Period of extinction of the disease
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The height of the disease is replaced by a period of extinction of clinical manifestations, which is replaced by a period of recovery (convalescence).
The period of recovery (reconvalescence) of the disease.
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The duration of the convalescence period varies widely and depends on the form of the disease, severity, effectiveness of therapy and many other reasons.
Recovery may be full, when all functions impaired as a result of the disease are restored, or incomplete, if residual (residual) phenomena persist.
Complications of the infectious process
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At any period of the disease, complications are possible - specific and nonspecific.
Specific complications include, caused by the causative agent of this disease and resulting from the unusual severity of the typical clinical picture and morphofunctional manifestations of the infection (perforation of an intestinal ulcer in typhoid fever, hepatic coma in viral hepatitis) or atypical localization of tissue damage (Salmonella endocarditis).
Complications caused by microorganisms of other types are not specific to this disease. Of exceptional importance in the clinic of infectious diseases are life-threatening complications that require urgent intervention, intensive observation and intensive care. These include hepatic coma (viral hepatitis), acute renal failure(malaria, leptospirosis, hemorrhagic fever with renal syndrome, meningococcal infection), pulmonary edema (influenza), cerebral edema (fulminant hepatitis, meningitis), and shock.
In infectious practice, the following types of shock are encountered:
- circulatory (infectious-toxic, toxic-infectious),
- hypovolemic,
- hemorrhagic,
- anaphylactic.
