Acetylsalicylic acid: in what cases is it taken?

How to drink acetylsalicylic acid correctly

An adult patient with active rheumatism is prescribed to take about 6-7 g of ASA per day. Frequency of administration – up to 5 times a day. The duration of the treatment course is 1.5 months. Throughout the course, the dose remains unchanged.

Discontinuation of the drug in adults and children should occur gradually, over 8-12 days.

If a person suffers from headaches or has an increased body temperature, then the medicine is taken in smaller quantities. For fever and pain of various origins, it will be enough to take up to 1 g at a time. Up to 5 doses are allowed per day.

It is worth noting that aspirin will help cope with headaches if they were caused by increased intracranial pressure.

The treatment course should not last more than 14 days.

In order to prevent thrombosis, you need to drink the medicine up to 3 times a day, 0.5 g.

Instructions for use ACETYLSALICYLIC ACID

Occurs when taking single high doses of acetylsalicylic acid (more than 100 mg/kg) or long-term use of acetylsalicylic acid in high doses (salicylicism).

When taking acetylsalicylic acid at a dose of 150-200 mg/kg (or when the level of salicylates in plasma is 50-80 mg/dl), mild poisoning develops. Typical symptoms include ringing in the ears, hyperventilation due to stimulation of the respiratory center, and respiratory alkalosis due to loss of CO2.

When taking acetylsalicylic acid at a dose of 200-300 mg/kg (or when the level of salicylates in plasma is 80-110 mg/dl), moderate poisoning develops. Severe shortness of breath, hypertemia due to uncoupling of phosphorylation oxidation (a poor prognostic sign in adults), and metabolic acidosis due to increased anaerobic glycolysis appear.

When taking acetylsalicylic acid at a dose of 300-500 mg/kg (or when the level of salicylates in plasma is 110-160 mg/dl), severe poisoning develops. Collapse, coma, convulsions, and hypoprothrombinemia occur.

When taking acetylsalicylic acid in a dose of > 500 mg/kg (or when the level of salicylates in plasma > 160 mg/dl), extremely severe poisoning develops with renal and respiratory failure.

Helpful measures include discontinuing the drug, inducing vomiting or gastric lavage with activated charcoal, and prescribing saline laxatives to prevent absorption of the drug in the stomach and intestines. Introduction of alkalizing agents to maintain urine pH values ​​at 7.5-8.0. When the level of salicylates in plasma exceeds 300 mg/l (2.2 mmol/l) in children and 500 mg/l (3.6 mmol/l) in adults, forced alkaline diuresis is indicated (provided by intravenous infusion of sodium bicarbonate 88 mEq/l and 5 % glucose at a rate of 10-15 ml/kg/h with furosemide 40-60 mg). Restoration of bcc and correction of acid-base balance are carried out. When the level of salicylates is more than 1000 mg/l, as well as with refractory acidosis, hemodialysis is indicated. In case of cerebral edema, mechanical ventilation with an oxygen-enriched mixture in positive end-expiratory pressure mode is indicated. For cerebral edema, hyperventilation is performed in combination with the administration of osmotic diuretics.

There is no specific antidote.

It is not recommended to use acetazolamide to alkalinize urine in the treatment of intoxication due to the possibility of developing acidemia and increasing the toxic effect of salicylate on the patient's body.

How to take acetylsalicylic acid for children

The optimal dose for children is determined taking into account weight (approximately 100-120 mg per 1 kg per day). For active rheumatism, it should be taken up to 5 times a day. After 10-15 days from the start of the therapeutic course, the dosage can be reduced by 1.5 times. Treatment continues for up to 5-6 weeks.

In case of fever and various pains, the child can be given 15 mg per 1 kg up to 5 times a day.

You should not give your child aspirin if there is a high body temperature caused by a viral infection. This can trigger the development of a serious disease - Reine's syndrome, which can threaten the child's life.

The active substance penetrates perfectly into body tissues and fluids.

Composition and effectiveness

In its pure form, ASA is a white, finely crystalline powder with a noticeably sour taste. It is an acetic ester, soluble in water and alcohols. The drug quickly relieves pain and has a pronounced antipyretic, anti-inflammatory, and antiplatelet effect. Its effectiveness is similar to other NSAIDs - non-narcotic analgesics.

1. The analgesic properties of ASA are due to its effect on the central nervous system, the activity of prostaglandins and other mediators of pain sensitivity.
2. A decrease in body temperature occurs due to the correction of the thermoregulation center, vasodilation and a pronounced diaphoretic effect.
3. Inflammatory reactions are eliminated due to the effect of acetylsalicylic acid on the capillary network: reducing the permeability of vascular walls, blocking enzymatic and energetic activity in pathological foci.
4. Aspirin has the ability of an anticoagulant: it prevents platelet aggregation (sticking together), slows down the synthesis of prothrombin, which is responsible for blood clotting. This reduces the risk of thrombosis and associated life-threatening conditions.

Acetylsalicylic acid is absorbed almost completely into the bloodstream from the stomach cavity within 10–15 minutes. Severe symptoms of the disease subside immediately:

• dizziness, headache, joint and muscle pain decreases;
• temperature indicators decrease;
• the feeling of heat and other signs of malaise disappear.

As a result of taking aspirin, a decrease in temperature in patients is often accompanied by profuse sweating.

The decay period of acetylsalicylic acid in the body is about 1–2 hours. Metabolites are excreted in the urine. The therapeutic effect of the drug persists for some time.

Due to its rapid therapeutic effect and effectiveness in treating a variety of diseases, acetylsalicylic acid is classified as an emergency medicine and is on the list of vital drugs.

Contraindications

The use of aspirin should be discontinued in the following conditions:

• bleeding in the stomach or intestines;
• kidney and liver diseases;
• gout;
• aortic dissection;
• exacerbation of erosive and ulcerative lesions of the digestive system;
• period of bearing a child;
• breast-feeding;
• increased sensitivity to the elements included in the composition.

Indications and doses

Acetylsalicylic acid is prescribed for the following pathologies:

• febrile symptoms of inflammatory and infectious diseases;
• mild and moderate pain syndromes of various origins: migraine, neuralgic manifestations, myalgia;
• rheumatic joint damage;
• risk of thrombosis and thromboembolism;
• the risk of development and consequences of myocardial infarction;
• acute ischemic stroke;
• in complex therapy: alcohol withdrawal syndrome.

The recommended dose of the drug depends on the type and severity of the disease:

• for high fever, ARVI, pain - 100–500 mg three times a day;
• for intense fever - up to 1.5 g per day;
• for rheumatoid polyarthritis, other joint inflammations, myocardial diseases - up to 4 g daily.

Acetylsalicylic acid should be taken after meals. It is recommended to grind the non-coated tablets into powder and wash them down with plenty of warm water. You can use a slightly alkaline mineral one. The effervescent drug must first be dissolved in 50–60 ml of liquid. In liquid form, acetylsalicylic acid is absorbed faster into the blood and has less contact with the gastric mucosa.

Adverse reactions and overdose

Taking the drug can sometimes be accompanied by negative reactions in the form of: nausea, stomach upset, weight loss, allergies, liver or kidney failure.

With prolonged use, you may experience tinnitus, hearing problems, blurred vision, dizziness, and headache. In rare cases, vomiting and bleeding occur.

With prolonged use or use of the drug in a large dose, an overdose may occur, which is manifested by increased adverse reactions. With severe intoxication, convulsions, shock, severe dehydration and even coma may begin.

In this case, the person should be immediately taken to the hospital. It is necessary to rinse the stomach and take activated charcoal.

Pharmacodynamics and pharmacokinetics

The main component of the medicine is acetylsalicylic acid (some mistakenly call it acetylic acid). The pharmaceutical drug belongs to anti-inflammatory medications.

It is useful to know that Aspirin and acetylsalicylic acid are the same thing.

C9H8O4 is the chemical formula of Aspirin.

Taking Aspirin in a dosage of 300 mg to 1 mg helps eliminate joint and muscle pain. In addition, a similar dose of the drug helps to improve well-being during colds and flu, and helps with fever.

Acetylsalicylic acid is suitable for the treatment of acute and chronic inflammatory diseases.

It is advisable to take aspirin for:

• Bekhterov's diseases
• Osteoarthritis
• rheumatoid arthritis

For the above diseases, doctors prescribe higher doses of the drug than when fighting colds and high body temperature. Based on the specific course of the disease, patients are prescribed 4-8 g of medication per day.

Aspirin is also useful to take in the presence of many vascular diseases. In such cases, doctors recommend taking from 75 g to 300 mg of the substance daily (depending on the nature and danger of the disease).

Pharmacokinetics

After consuming the medicine, the active substance is rapidly and completely absorbed from the stomach. During and after absorption, it is converted to salicylic acid (the main active metabolite).

Decomposition products are primarily excreted through the kidneys.

Can pregnant women take acetylsalicylic acid?

Pregnancy and breastfeeding are contraindications for the use of aspirin. This is especially true for the 1st and 3rd trimesters. Using the medicine in the early stages can increase the risk of birth defects, and taking it in recent months can lead to post-term pregnancy.

The active substance can pass into breast milk in small quantities. When children accidentally took the drug, no adverse reactions appeared, but it is still worth refraining from taking it. If a woman is prescribed long-term use of aspirin, then breastfeeding must be interrupted for the entire course of treatment.

When else should you not take aspirin?

- With high blood pressure.

Because taking it may increase the risk of hemorrhagic stroke in this case. If you have hypertension, you should take aspirin only when your blood pressure is adequately controlled.

- If you suspect a stroke.

If we are dealing with a suspected stroke (a person suddenly developed severe weakness in an arm or leg, speech, motor disturbances, the corner of the mouth is drooping, he cannot smile, etc.), in no case should aspirin be given in this situation. There are no objective signs that allow one to clearly differentiate between hemorrhagic (associated with cerebral hemorrhage) and ischemic (associated with blockage of a cerebral artery by an atherosclerotic plaque) type of stroke. And if the stroke is hemorrhagic, and we give such a person aspirin, then it’s scary to imagine how it could end...

All you need to do if you suspect a person is having a stroke is to lay him in a horizontal position, try to calm him down and call an ambulance as soon as possible.

Acetylsalicylic acid for primary prevention in patients with arterial hypertension

The true prevalence of arterial hypertension (AH) is difficult to estimate; according to various estimates, it is 30–45% in the general population, with a tendency to increase with age. According to the updated recommendations for the treatment of hypertension of the European Society of Cardiology (ESC) from 2013, over the past decades, positive changes in the level of mean arterial pressure (BP) have been noted in various countries, but no consistent trend towards a decrease in its values ​​has been recorded [1] .

The lack of information about the frequency and severity of hypertension has led to the use of so-called “surrogates” to assess the prevalence of hypertension [2]. It is believed that one of the most informative “surrogates” is mortality from acute cerebrovascular accident (ACVA), since at the moment hypertension is the most significant condition against which stroke develops. A strong correlation has been proven between the prevalence of hypertension and mortality from stroke [3]. When assessing the mortality rate from stroke by the World Health Organization (WHO), it was revealed that in the countries of Western Europe there has recently been a trend towards a decrease in the prevalence of hypertension, in contrast to the countries of Eastern Europe, where there has been a clear increase in the number of deaths from stroke [4].

Thus, at present, hypertension remains the most common cardiovascular disease (CVD), which in itself serves as a significant risk factor for the development of severe, often fatal complications.

High blood pressure, as a cause of serious cardiovascular and renal damage, has been described in a large number of large observational studies. These data have been covered in detail in the ESC clinical guidelines since the first editions [5, 6]. Office blood pressure (BP measured at a doctor's appointment or in a hospital) is directly related to the incidence of many cardiovascular events (CVE), including stroke, acute myocardial infarction (AMI), sudden death, heart failure and atherosclerosis of peripheral arteries (APA), as well as severe renal failure [7, 8]. This relationship persists across all age and ethnic groups [9, 10].

The development of complications in patients with hypertension is observed both against the background of high blood pressure values ​​and at relatively low values ​​(systolic blood pressure (SBP) 110–115 mm Hg, diastolic blood pressure (DBP) 70–75 mm Hg). In individuals over 50 years of age, SBP has been shown to have a greater prognostic value than DBP [11]. In addition, pulse BP is of additional importance in the elderly, and patients with isolated systolic hypertension are at high risk of cardiovascular complications [1].

It should be noted that ambulatory blood pressure values ​​(self-measurement of blood pressure and 24-hour blood pressure monitoring) are of greater importance in determining the risk of complications and patient prognosis, since they more objectively reflect the patient’s true level of hypertension in the context of his usual lifestyle.

The association of blood pressure with CVD morbidity and mortality varies greatly depending on the presence of additional risk factors. Metabolic disorders (carbohydrate and lipid metabolism disorders, hyperuricemia), which are closely associated with hypertension, are of great importance [1].

For a long time, recommendations for the treatment of hypertension were aimed at reducing blood pressure, which was considered the only or one of the main goals determining both the need and the type of therapy chosen. This approach was based on the fact that lowering blood pressure itself, regardless of the methods used to achieve it, can significantly reduce the risk of CV events. However, in 1994, the ESC, the European Society of Hypertension (ESH) and the European Atherosclerosis Society (EAS) developed recommendations for the prevention of coronary heart disease (CHD) in clinical practice. They noted that all patients should take measures to prevent coronary artery disease and its analogues in accordance with the overall cardiovascular risk (CVR). Currently, this approach is universally accepted and is included in the ESC recommendations for the treatment of hypertension in 2003, 2007, 2013. [1, 5, 6]. This concept is based on the fact that only a small proportion of patients with hypertension have an isolated increase in blood pressure - the majority of patients have additional CV risk factors. In addition, in the presence of concomitant pathology, blood pressure and other CV risk factors can mutually reinforce each other, and the resulting CV risk will be greater than the sum of the risks for each condition. As a result, patients with high CV risk may have a very different antihypertensive treatment strategy than those at low risk. Thus, the therapeutic approach should be based both on determining the degree of increase in blood pressure and on assessing the overall cardiovascular risk [1].

Determining the degree of overall CVD is not difficult in certain patient populations, including those with a history of CVD, diabetes mellitus, congenital heart disease, or the presence of one of the risk factors (RFs). In all of the described conditions, the cardiovascular risk is assessed as high or very high, which requires intensive risk reduction measures. However, a large number of patients with hypertension cannot be classified into any of these categories. In such cases, the use of special models is required to determine the SSR [1].

Based on large European cohort studies, the SCORE (Systematic COronary Risk Evaluation) model was developed. This well-known model allows us to estimate the risk of death from CVD within 10 years and includes assessment of age, gender, smoking, total cholesterol and SBP [12]. In table 1 shows examples from which it is clear that, depending on the combination of these factors, people of the same age can have a fundamentally different prognosis.

When assessing cardiovascular risk, special attention should be paid to identifying target organ damage, since asymptomatic dysfunctions in the functioning of individual organs that occur during hypertension signal the progression of the cardiovascular continuum, which significantly worsens the prognosis even with a small number of risk factors [1].

Thus, preventing CVD in patients with hypertension is a complex task, which includes not only the need to lower blood pressure, but also the impact on additional risk factors. Methods for solving it are measures to change lifestyle, as well as the prescription of additional medications, including hypoglycemic agents for carbohydrate metabolism disorders, lipid-lowering drugs for dyslipidemia (primarily statins), as well as antiplatelet agents.

In 2009, a large meta-analysis was published on the secondary prevention of CVD, which found that the administration of acetylsalicylic acid (ASA) leads to an absolute reduction in the incidence of cardiovascular events (CVD), while major bleeding is observed relatively rarely [13]. However, with primary prevention, the harm-to-benefit ratio is not so significant: the absolute reduction in the incidence of cardiovascular events is only slightly greater than the incidence of major bleeding. However, in certain groups of patients during primary prevention, a more pronounced effect of ASA is observed. And although studies completed to date in patients with diabetes mellitus have not yet shown a significant benefit of antiplatelet therapy, a subanalysis of the HOT study (Hypertension Optimal Treatment, 1998) revealed that the administration of ASA significantly reduced the incidence of CVD and death in patients with reduced glomerular velocity. filtration (GFR) [14]. The best results were observed in patients with GFR < 45 ml/min/1.73 m2. In this group, the risk of bleeding was moderate compared with the high effectiveness in preventing the development of CVD [15].

The HOT study was the first attempt to study the effect of ASA administration in patients with hypertension on the development of CVD [14]. We recruited 18,790 patients from 26 countries aged 50–80 years (mean age 61.5 years) with hypertension and DBP 100–115 mmHg. Art. (average 105 mmHg). Of these, 9399 patients were prescribed ASA at a dose of 75 mg per day, and 9391 received placebo. As a result, it was shown that ASA reduced the risk of developing major CV events (non-fatal AMI, non-fatal stroke, cardiovascular death) by 15% (p = 0.03) and myocardial infarction by 36% (p = 0.02). However, no positive preventive effect against stroke was observed (Table 2).

A total of 129 non-fatal bleedings were recorded in the ASA group and 70 in the placebo group, while fatal ones were observed in only 7 and 8 patients, respectively (Table 3).

A study of the effectiveness of low doses of ASA compared with placebo in patients with controlled hypertension allowed to prove the positive effect of the drug on the development of fatal and non-fatal AMI, the frequency of which decreased by 36%, which prevents 1.5 cases of AMI per 1000 treated patients in 1 year (2 .5 AMI per 1000 patients with diabetes) in addition to the effect of the antihypertensive therapy itself. This is achieved without increasing the risk of stroke, which was observed in the ASA and placebo groups with the same frequency. In addition, a significant positive effect was observed for major CV events, the incidence of which was reduced by 15%. Also, while taking ASA in patients with hypertension, a statistically insignificant trend towards a decrease in cardiovascular and overall mortality was revealed. For asymptomatic AMI, the preventive effect is less pronounced, however, the authors propose to regard asymptomatic AMI as a milder version of prevented symptomatic AMI.

Although the incidence of fatal bleeding was similar in the ASA and placebo groups, the overall incidence of bleeding (mainly gastrointestinal and nasal) was 1.8 times higher in the Aspirin group, p < 0.01. And the number of bleedings against the background of ASA in the HOT study did not exceed that in secondary prevention studies at the same doses of ASA.

The benefits of antiplatelet therapy with ASA have been shown in patients with well-controlled hypertension, so these results cannot be generalized to patients with unstable blood pressure. To reduce the likelihood of hemorrhagic stroke, it is necessary to select adequate antihypertensive therapy before starting antiplatelet therapy.

To translate the HOT findings into clinical practice, an additional study (sub-analysis) [16] was conducted to determine which patient groups benefit most from ASA. Patients included in the study were divided according to the degree of overall risk according to the WHO scale, as well as other risk factors presented in Table. 4.

This study showed that a significant benefit of ASA therapy was observed in the subgroup of patients with creatinine levels greater than 150 mmol/L. In this group, the relative risk (RR) for major CV events was 0.595 (95% CI 0.387–0.913), RR for AMI was 0.193 (95% 0.056–0.670). In Fig. it was shown that in patients with elevated creatinine levels during ASA therapy, there was a significant reduction in the incidence of major CV events (by 86%), AMI (by 86%), cardiovascular (45%) and overall (39%) mortality. In addition, a statistically insignificant trend towards a decrease in the incidence of stroke was noted.

The number of fatal AMIs in the HOT study was small and therefore not separately assessed.

A subanalysis of the effect of ASA on the incidence of fatal and non-fatal bleeding did not reveal significant differences between the subgroups, which means that hemorrhagic complications during ASA therapy occurred randomly, regardless of the baseline level of cardiovascular risk.

The absolute benefits (reduction in the incidence of major CV events and AMI) and risks (increased risk of bleeding) during treatment with ASA were also assessed. A more pronounced reduction in the number of major CV events than in the study as a whole was observed in the subgroup of patients at high and very high risk, with a baseline SBP of more than 180 mmHg. Art. or baseline DBP more than 107 mm Hg. Art. and in patients with high creatinine levels (Table 5).

In addition, a decrease in the incidence of AMI was observed in these subgroups. In contrast, the risk of major bleeding was 1.0 to 2.0 (mean, 1.4) bleeding events/1000 patient-years and was independent of baseline CVD and SBP/DBP at study entry.

In absolute terms, the use of low doses of ASA for primary prevention of CV events showed moderate effectiveness and prevented only 1.6 major CV events per 1000 patient-years; i.e., 176 patients would need to be treated for 3.8 years to prevent one event. However, in patients at high and very high risk and with high BP at enrollment, aspirin use was associated with a significant benefit (3.1–3.3 CVD/patient-years prevented); in these subgroups, a total of 82–91 patients would need to be treated for 3.8 years to prevent the event. The most significant benefit from ASA therapy was found in the subgroup of patients with creatinine levels > 150 mmol/l, in which the drug allowed to prevent 13 major CV events/1000 patient-years (7 of which were cardiovascular death), and to prevent one event only 22 patients need to be treated for 3.8 years.

Since the development of bleeding was independent of CV risk, the benefits of ASA administration clearly outweigh the risk in patients in the subgroup with a high baseline CV risk.

Thus, in the course of the subanalysis, it was concluded that ASA therapy as primary prevention in patients with hypertension has an advantage in cases where, despite adequate antihypertensive therapy, the patient remains at a high risk of CV events (at a level of 11–15 events/1000 patients). years). Based on this, the researchers suggested that the recommendations include information that low-dose ASA is indicated for patients with moderate increases in creatinine levels, and it may also be considered in the case of high and very high total CV risk or in patients with higher blood pressure levels. Once CVR is reduced by intensive antihypertensive therapy, the absolute benefit of ASA therapy decreases, while the absolute risk of bleeding complications (except possibly intracranial hemorrhage) remains the same regardless of the level of blood pressure achieved.

The results of the HOT study and, in particular, its sub-analysis were soon included in updated guidelines for the treatment of hypertension. Currently, according to European recommendations [1], ASA can be prescribed only if target blood pressure is achieved. Antiplatelet therapy, preferably at a low dose, should be given to all patients with a history of CVD (Class IA) and should also be considered in patients with reduced renal function or high CVD (Class IIA-B). The use of ASA is not recommended in patients with low and intermediate risk, since in this case the benefits of treatment do not outweigh its negative effects (Class IIIA). It should be noted that, according to the latest meta-analysis, with primary prevention with low doses of ASA, a decrease in cancer incidence and overall mortality was observed [17].

Domestic recommendations, based on European ones, also suggest the use of ASA in low doses (75–150 mg per day) after an AMI, stroke or transient ischemic attack, if there is no threat of bleeding [18]. A subanalysis of the HOT study is also reflected here: low-dose ASA is indicated for patients over 50 years of age with a moderate increase in serum creatinine or with a very high risk of CVD, even in the absence of other CVD [18]. It was noted that the benefit of reducing the risk of cardiovascular complications when using ASA exceeds the risk of bleeding. To minimize the risk of hemorrhagic stroke, treatment with ASA should be started only after achieving target blood pressure values ​​[18].

At the same time, American recommendations for the prevention of CVD [19] suggest prescribing ASA at a dose of 75–100 mg per day to all patients over 50 years of age without signs of CVD (level 2B). At the same time, the comments note that the effect of ASA on overall mortality over a 10-year period is insignificant and does not depend on the level of cardiovascular risk. In patients at moderate and high risk, the benefit of reducing the risk of AMI with therapy is offset by the increased risk of major bleeding. Regardless of the degree of risk, there is no point in long-term prescribing to a patient a drug whose benefits are insignificant. Thus, ASA should probably be prescribed only to those patients in whom the prevention of AMI is significantly more important than the risk of bleeding complications.

Literature

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A. V. Melekhov1, Candidate of Medical Sciences E. E. Ryazantseva

GBOU VPO RNIMU im. N. I. Pirogova Ministry of Health of the Russian Federation, Moscow

1 Contact information

Abstract. As HOT research has shown that taking acetylsalicylic acid by patients with arterial hypertension (AH) reduced the risk of development of cardiovascular complications and myocardial infarction. Research results and the results if its subanalysis have already been accounted for in updated recommendations on AH treatment.