Food poisoning: how to give yourself first aid

An unsuccessful trip to a cafe or a party with a lot of alcohol can cause malaise and indigestion. We tell you how to alleviate the condition of poisoning and when you should consult a doctor. We talked about how to avoid them with Alexey Golovenko, candidate of medical sciences, gastroenterologist at GMS Clinic.

Food poisoning can be caused by many factors: food contaminated with bacteria or their toxins, excess alcohol, various toxic substances in foods. Whatever the cause, at first the symptoms of the diseases are very similar and it is quite difficult to distinguish what is happening.

Causes and types of food poisoning

In general, there are 2 main causes of food poisoning:

• The body's reaction to foods that differ from the daily diet2.
• pathogenic flora (bacteria, fungi), viruses and toxins that enter the body mainly with contaminated food.

Every corner of the world has its own infectious agents, and they are ready to instantly attack the human gastrointestinal tract, if you just gape.

During the hot season, the chance of getting poisoned increases many times over, because food is stored less and bacteria multiply much faster. Food poisoning is especially common when traveling, so there is a separate concept - “traveler's diarrhea.” Going south, to Asia, the Middle East, Africa, South America or hot islands, we endure a sharp change in climate zone, try unusual national cuisine and drink local water. All this, combined with bacteria and viruses new to our body, can cause food poisoning.

In the US, it has been estimated that out of 1,000 people who become ill after traveling, 1/3 always suffer from diarrhea and food poisoning. E. coli is becoming the most common cause of severe diarrhea abroad1.

A child's body is even more vulnerable. For a fragile body, the cause of poisoning can be anything, especially when traveling: unwashed hands, playing in the sand, unusual sweets or fruits. An accidental sip of water from a pool or sea can also affect a child's intestinal health.

What medications are needed

In the first hours after poisoning, any enterosorbents will be useful: they help remove toxins and quickly cleanse the intestines of bacterial waste products. If more than a day has passed since the poisoning, there is no need to take these drugs.

Important! It is better to refrain from the usual activated charcoal: it turns stool and vomit dark, which can mask traces of blood and prevent you from seeing a doctor in time.

Another important rule: do not take antiemetic or antidiarrheal medications without consulting your doctor. Firstly, by blocking vomiting or stool, we prevent the body from eliminating toxins, and secondly, these drugs have a number of serious side effects. Antidiarrheal drugs, for example, can make some types of diarrhea worse and even cause damage to the intestinal wall.

“Most intestinal infections are of viral etiology. Therefore, running for antibiotics for indigestion is not only wrong (only a doctor can prescribe these drugs), but also pointless,” the expert warns.

Signs of food poisoning and possible complications

Despite the fact that food poisoning occurs due to various reasons, its manifestations at first are always the same, and the symptoms are similar.

The main feature of any poisoning is the speed with which it occurs. Everything happens very rapidly and quickly - within a few hours or in the next 24 hours the body signals a problem1.

The human body is a self-regulating system and therefore tries to get rid of pathogens in any way. This may include general malaise, diarrhea and abdominal pain3:

• Abdominal pain varies in nature, but is often sharp and quite severe. The intestines react to most toxins and bacteria with a spasm.
• Intoxication of the body - headache, weakness, muscle pain and joint aches.
• Diarrhea is also a striking symptom of food poisoning, manifesting itself in almost every case.

In case of severe poisoning, other symptoms may be added - nausea, vomiting and fever3:

• Nausea is one of the clearest examples of how the body tries to resist a food infection and eliminate bacteria. Nausea may be accompanied by belching and a feeling of heaviness in the stomach.
• Vomiting is another of the body’s defense mechanisms against infectious agents. In case of severe and progressive poisoning, vomiting must be controlled, otherwise severe dehydration may occur.
• Dehydration syndrome. Conditions for such a symptom would be active vomiting or diarrhea. The human body loses a huge amount of fluid in a short period of time, which can be expressed by severe thirst and dizziness, up to loss of consciousness. Dehydration is especially dangerous in children, who, with severe poisoning, instantly lose all water reserves in the body.
• Increased body temperature. The body reacts to any attack in a similar way. Food poisoning is no exception, the body tries to fight, which is manifested by an increase in temperature from 37.5º C to 40.0º C - it all depends on the specific type of virus or bacteria.

Symptoms of alcohol poisoning

Experts divide body intoxication into three categories:

– mild alcohol poisoning;

– average degree;

– severe intoxication.

If a person has experienced a mild degree of poisoning from alcohol-containing drinks, then he may experience the following symptoms:

– hyperpigmentation of the skin;

– increased excitability, and sometimes aggressiveness;

– being in a euphoric state;

– the appearance of hypertrophied character traits (increased level of conflict, stinginess, generosity, etc.);

– a significant decrease in self-control and the appearance of inflated self-esteem;

– loss of coordination of movements.

If you stop drinking alcoholic beverages at this stage, you may only experience a hangover. In cases where drinking continues, a moderate degree of poisoning may occur, which is accompanied by the following symptoms:

– slowdown of intellectual processes;

– unintelligible speech;

– violation of orientation in space and time;

– the occurrence of dyspeptic disorders (nausea, pain in the stomach area, diarrhea, vomiting);

- appearance of drowsiness.

Having stopped consuming products harmful to the body at this stage, the drinker falls into deep sleep. In some cases, immediate first aid may be required, which will allow the person’s condition to normalize after 12 hours.

Severe alcohol poisoning is accompanied by more pronounced symptoms:

1. Being in an unconscious state.
2. Lack of response to painful and tactile stimuli.
3. Disturbances in the functioning of the cardiac, vascular, and respiratory systems (rare pulse, shortness of breath, drop in blood pressure, etc.).
4. Decreased body temperature.

In such situations, it is impossible to do without qualified medical care, since severe poisoning can cause alcoholic coma. In the absence of proper procedures, which are carried out exclusively by professionals, everything will end in death.

Poisoning can occur not only due to the use of ethyl, but also other alcohols that are used in the creation of surrogates. As a rule, in such cases, wood or methyl alcohol is used. Poisoning with these substances is extremely dangerous and leads to human death. When they are consumed, pathological intoxication is observed, the level of which differs significantly from the dose consumed. The main manifestations of methanol intoxication are similar to those mentioned above, but the difference is that after 2-4 days after consuming the drinks, vision problems appear, leading to irreversible consequences (blindness, blurring, double vision).

Treatment of food poisoning

First of all, to restore the body, you need dietary nutrition, which will help restore normal functioning of the gastrointestinal tract (GIT).

When resuming nutrition after poisoning, general recommendations must be followed3:

• You need to eat often and in small portions.
• Fried, stewed, spicy, salty and fatty foods are strictly prohibited.
• Alcohol and carbonated sweet drinks should be forgotten during treatment and further recovery.

• It is important to maintain the serving temperature of the food - it should remain neutral - neither cold nor hot.
• The predominant cooking method is boiling and steaming.
• Dishes should be light, mostly lean and familiar to the body.

A home or traveler's first aid kit should always include anti-poisoning medications.

The most popular products3,4:

• Adsorbent preparations or sorbents. No first aid kit should be without such a product. The task of the sorbent is to absorb the toxin and its further removal from the body.
• Drugs to improve digestion. They help the body fully absorb food and will be especially relevant after defeating poisoning.

• Antispasmodics or painkillers. Spasms and pain in the stomach or intestines can also be the body’s reaction to an external “attack”. The task of such medications is to relax the internal muscles and relieve spasms, as a result of which the pain goes away.

When faced with food poisoning, it is first of all important to cope with the acute period of the problem, but it is equally important to think about the period of rehabilitation of the digestive system, because the inflammatory process disrupts its normal functioning. One of the consequences of such a disorder may be a lack of digestive enzymes, which are responsible for the breakdown and absorption of food in the body. As a result, the body experiences a deficiency of nutrients, and a person, even after recovery, may still experience unpleasant symptoms for some time - discomfort in the abdomen, heaviness after eating, periodic bowel movements, etc.

Pancreatin enzyme preparations may be useful to maintain digestion after poisoning5. They are called enzymatic because they contain digestive enzymes identical to those produced by the body and are included in the standard treatment of foodborne infections6.

Digestive enzymes are a special type of compound designed to break down carbohydrates, proteins and fats for subsequent absorption in the body.

First aid: normalize water balance

“For the first three days after poisoning, we recommend maintenance therapy: it is important to prevent dehydration and ensure sufficient calorie intake,” says Alexey Golovenko.

With vomiting and diarrhea, we lose a large amount of fluid that needs to be replenished. When losses are not very abundant, just drinking water is enough.

Drink small sips, but often - this will help cope with nausea without provoking the gag reflex. If you can't drink, you can start by sucking ice cubes.

With excessive fluid loss, signs of dehydration begin to appear: dry mouth and dry skin, weakness, dizziness, decreased amount of urine or its darkening, increased heart rate or breathing rate. In this case, you will need to replace the glucose and electrolytes that have left the body - potassium and sodium necessary to maintain the water-salt balance.

“You can prepare a solution according to a simple recipe: dilute half a teaspoon of salt and 6 teaspoons of sugar in one liter of water and drink a glass. If you don’t have anything suitable on hand, sweet sodas or sports drinks with electrolytes, but without caffeine, will do,” the expert adds.

The most reliable solution would be to buy rehydrating preparations at the pharmacy - powders that contain all the necessary microelements in a balanced composition. You can purchase any ORS (oral rehydration salt preparations), or ORS, oral rehydration solution, if you are abroad.

For children, special solutions are sometimes replaced with apple juice diluted twice - with this treatment it will be easier for the child to drink more liquid.

“We advise you to follow a simple principle: as much liquid comes out, so much should return. Therefore, you should drink a glass of water after each episode of loose stools or vomiting. If the malaise continues for more than a day, it is better to replenish fluid in a larger volume. It is especially important to pay attention to the child’s well-being: children become dehydrated faster and it is more difficult to force them to drink, so if the condition worsens, medical intervention and perfusion therapy may be required,” comments Alexey Olegovich.

Joint syndrome in chronic inflammatory bowel diseases: a rheumatologist's view

The study of chronic inflammatory bowel diseases (CIBD) is an urgent problem not only in pediatric gastroenterology, but also in pediatric rheumatology due to the frequent onset of these pathological conditions with articular manifestations and the further course of clinically related intestinal and articular syndromes.

The prevalence of CIBD among the pediatric population is 2.2–6.8 per 100 thousand children [1, 2]. The most common diseases diagnosed in childhood are Crohn's disease and ulcerative colitis. It has been noted that ulcerative colitis is more common in boys, and Crohn's disease is more common in boys and girls with approximately the same frequency [2].

Crohn's disease (regional enteritis, granulomatous ileitis) is an inflammatory disease involving all layers of the intestinal wall; characterized by an intermittent (segmental) nature of damage to various sections of the gastrointestinal tract. It is characterized by diarrhea mixed with mucus and blood, abdominal pain (often in the right iliac region), weight loss, and fever.

Ulcerative colitis (nonspecific ulcerative colitis, idiopathic colitis) is an ulcerative-destructive lesion of the colon mucosa, which is localized mainly in its distal parts. The clinical picture is characterized by: bleeding from the rectum, frequent bowel movements, tenesmus; abdominal pain is less intense than with Crohn's disease, most often localized in the left iliac region. In approximately 30% of adolescent patients, ulcerative colitis begins suddenly with the onset of abdominal pain and bloody diarrhea.

According to various authors, extraintestinal manifestations of CIBD are observed in 5–25% of cases. Their largest share falls on total forms of ulcerative colitis (87.5%) and Crohn's disease involving the colon (29%) or large and small intestine (58.1%) [3]. Systemic manifestations of CIBD are divided into three groups based on pathogenetic principles. The first group includes manifestations that arise as a result of systemic hypersensitization - damage to the joints, eyes, skin, and oral mucosa; to the second - caused by bacteremia and antigenemia in the portal system - damage to the liver and biliary tract. There are also phenomena that develop secondary to long-term disorders in the colon - anemia, electrolyte disorders.

The pathogenesis of articular manifestations remains unclear. The significance of the increased permeability of the intestinal wall, observed in patients with ulcerative colitis and Crohn's disease, is discussed, as a result of which components of the bacterial wall membrane enter the blood in large quantities. These components act as peptide antigens that can lead to the development of arthritis. By binding to molecules of histocompatibility complexes and subsequently activating T-lymphocytes, peptides lead to inflammation of the joints [3].

From the point of view of a rheumatologist, the articular manifestations of CIBD are classified as so-called. seronegative spondyloarthropathy. This is a large heterogeneous group of clinically overlapping, chronic inflammatory rheumatic diseases [4]. In addition to arthritis associated with inflammatory bowel diseases, this group includes such rheumatic diseases of childhood as juvenile spondyloarthritis, juvenile reactive arthritis, juvenile psoriatic arthritis, as well as undifferentiated spondyloarthropathy (dactylitis, uveitis, sacroiliitis in the absence of a full set of criteria). Despite the heterogeneity of diseases in this group, clinically seronegative spondyloarthropathies have common features and are characterized by:

• pathological changes in the sacroiliac region and/or other joints of the spine;
• syndrome of peripheral inflammatory arthropathy, manifested by asymmetric arthritis mainly of the lower extremities;
• enthesopathic syndrome;
• association with the histocompatibility antigen HLA-B27;
• the tendency for these diseases to accumulate in families;
• frequent presence of extra-articular symptoms (damage to the eyes, aortic valves, skin) [5, 6]. In ICD-10, joint lesions in the diseases we are considering are coded as follows: M07.4 Arthropathy in Crohn's disease (K50); M07.5 Arthropathy in ulcerative colitis (K51).

Joint lesions in CIBD occur in 20–40% of cases and occur in the form of arthritis (peripheral arthropathy), sacroiliitis and/or ankylosing spondylitis [3].

Arthritis

Arthritis is one of the most common articular manifestations of chronic inflammatory bowel diseases. They are often combined with skin lesions in the form of erythema nodosum. The incidence of arthritis and the prevalence of colon damage correlate with the inflammatory activity of the underlying disease. In some cases, arthritis can precede intestinal manifestations by many months or even years, and also persist in remission [7].

The clinical picture of arthritis in Crohn's disease and ulcerative colitis is identical. Characterized by asymmetric, migrating damage to the joints, most often in the lower extremities. The knee and ankle joints are predominantly affected, followed by the elbow, hip, interphalangeal and metatarsophalangeal joints. The number of affected joints usually does not exceed five. Articular syndrome occurs with alternating periods of exacerbations, the duration of which does not exceed 3–4 months, and remissions. Enthesopathies and thalalgias may be detected. Arthritis usually begins acutely. However, patients often complain only of arthralgia, and no changes are detected during an objective examination. Over time, exacerbations of arthritis become less frequent. In most patients, arthritis does not lead to joint deformation or destruction.

There are two types of peripheral joint damage. The first is characterized by damage to a small number of large joints, asymmetric articular syndrome, and an acute course. Often in this type, articular syndrome precedes the clinical picture of the underlying disease, is associated with its exacerbations and is combined with other extraintestinal manifestations of CIBD. The second type occurs as a symmetrical polyarthritis; its exacerbations do not coincide in time with exacerbations of the main process in the intestine and other systemic manifestations of the disease [7, 8].

Colectomy in patients with ulcerative colitis helps to stop recurrent arthritis [3].

Sacroiliitis

According to X-ray examination, sacroiliitis is found in approximately 50% of patients with CIBD. Moreover, in 90% it is asymptomatic. It is not associated with an increased detection rate in patients with HLA-B27. Also, the presence of sacroiliitis does not correlate with the activity of inflammatory bowel disease. Existing for several years, it may be a precursor to ulcerative colitis or Crohn's disease. Sacroiliitis may be the only localization of changes in the joints, but is often combined with the first type of arthritis. It must be remembered that sacroiliitis can be an early symptom of ankylosing spondylitis. Therapy for intestinal syndrome does not lead to a change in the clinical picture of sacroiliitis [7].

Ankylosing spondylitis

Ankylosing spondylitis (AS) in CIBD clinically, like sacroiliitis, does not differ from idiopathic ankylosing spondylitis. More common in males. According to observations, in females, damage to the cervical spine manifests itself at a younger age and is more severe. Symptoms of AS usually precede the onset of Crohn's disease or ulcerative colitis and do not correlate with inflammatory activity in the intestine. There is pain in the spine, a feeling of morning stiffness, and increasing limitation of mobility in the cervical, thoracic, and lumbar spine. Active therapy of the underlying disease does not lead to a change in the clinical picture of spondylitis [3, 7, 9, 10].

Clinical observation

An illustration of the above material can be a clinical observation of the course of Crohn's disease with extraintestinal articular manifestations in a teenage patient.

Clinical diagnosis: Crohn's disease (damage to the small, large intestine, stomach, esophagus), remission phase, extraintestinal manifestations (history of fever, lymphadenopathy, hepatomegaly, iron deficiency anemia). Complications: stenosis of the mouth of the bauginian valve, narrowing of the entrance to the cecum.

Juvenile spondyloarthritis, activity stage I, radiological stage I–II, NF-1.

From the life history, it should be noted that the boy is from the 2nd pregnancy, which proceeded physiologically, from the first urgent birth, complicated by the weakness of labor (obstetric aid - application of passing forceps). Was on early artificial feeding. In the first year of life, he was observed by a neurologist. In the future, rare ARVI. Vaccinated according to the calendar. I did not suffer from childhood infections. Heredity is burdened with diseases of the cardiovascular system.

Medical history: in September 2008, after an injury to the left ankle joint, the child experienced swelling and tenderness in the left ankle joint. He received topical ointments with non-steroidal anti-inflammatory drugs (NSAIDs). Physiotherapeutic treatment was also used, which caused a worsening of the condition: low-grade fever appeared, arthralgia in the left ankle joint intensified, and pain in the temporomandibular joints also appeared with limited mobility in them. In three months the boy lost 12 kg. Examined at the place of residence: blood test showed erythrocyte sedimentation rate (ESR) 47–55 mm/h, leukocytosis, biochemical analysis showed increased aspartate aminotransferase (AST) to 2 norms, C-reactive protein (CRP)++. An intestinal infection was detected: the titer to S. flexneri was 1:400. The therapy (NSAIDs, antibiotics - cefazolin, ceftriaxone, amikacin) had no effect. While taking antibiotics, she developed unstable, liquefied stools and pain in the umbilical area. Tuberculosis was excluded at the Phthisiology Research Institute. Computed tomography of the left ankle joint revealed: narrowing of the joint space, marginal ulcer in the medial malleolus, effusion into the joint cavity. Orthopedic pathology was excluded. Since January 2009, she has been observed at the University Children's Clinical Hospital (UDCH) of the First Moscow State Medical University named after. I. M. Sechenov. On admission the condition was of moderate severity. Pale, symptoms of intoxication are pronounced. Dystrophy. Joint syndrome in the form of effusion, limited mobility, increased local temperature and pain in the left ankle joint, Achilles bursitis on the left, moderate atrophy of the muscles of the left leg, gait is impaired. Rigidity of the thoracic spine (+ 1 cm), limited mobility in the temporomandibular joints. Abdominal pain and loose stools are noted. High humoral activity: ESR up to 50 mm/h, leukocytosis up to 22,000 in 1 μl with a band shift up to 24%, anemia - hemoglobin (Hb) 109 g/l, single increase in AST and alanine aminotransferase (ALT) levels up to 1.5– 2 normal Examined for arthritogenic infections: the result is negative. Immunogenetic examination revealed HLA class 1: A2, B 64 (14), B38 (16). The child was given a preliminary diagnosis: juvenile spondyloarthritis. Pulse therapy with glucocorticoids, intravenous immunoglobulin, NSAIDs were used, and intra-articular puncture of the left ankle joint was performed with the administration of Depo-Medrol. The child was prescribed sulfasalazine 1500 mg/day as a basic drug. During the therapy, positive dynamics were noted, laboratory activity decreased slightly, abdominal pain was relieved, stool normalized, range of motion in the left ankle joint increased, but swelling and morning stiffness in it persisted. In March 2009, there was another exacerbation of the articular syndrome, fever up to 37.8 °C, abdominal pain, unstable stool, and swelling of the right ankle joint. The child was again hospitalized at the UDCH in May-June 2009: ESR 29 mm/h, hypochromic anemia, thrombocytosis, CRP ++, IgG 2150 mg/dl, in the coprogram there were up to 40 red blood cells per field of view once. Sigmoidoscopy was performed: sigmoiditis, proctitis, endoscopic signs of colitis. On esophagogastroduodenoscopy: erosive gastritis, duodenitis, jeunitis. A colonoscopy was recommended, but the child’s parents refused. The boy's dose of sulfasalazine was increased to 1750 mg/day. But the patient’s condition remained unstable: unstable stool, swelling, pain and dysfunction of the left ankle joint persisted. In October 2009, he was again hospitalized at the UDKB: ESR 34 mm/h, hypochromic anemia increased, Hb 90 g/l, thrombocytosis, leukocytosis up to 16 thousand in 1 μl, CRP ++. The child underwent a colonoscopy: Crohn's disease, deep ulcers in the colon, ulcerative terminal ileitis, proctitis, colitis, sigmoiditis. According to magnetic resonance imaging of the iliosacral joints, there is left-sided sacroiliitis. The boy's therapy was adjusted: sulfasalazine was discontinued, Salofalk 2000 mg/day was prescribed, and he continued to receive NSAIDs. During therapy, the condition showed a positive effect - intestinal syndrome was relieved, stool returned to normal. However, in December 2009, after ARVI, the underlying disease again worsened: temperature increased to febrile levels, ESR 50 mm/h, swelling of the ankle joints, and stiffness in them. Since the end of December 2009, cramping pain in the abdomen and loose stools have been noted. In January 2010, due to high laboratory and clinical activity of the underlying disease, ineffectiveness of traditional therapy (Salofalk monotherapy), and progressive disability of the patient, infliximab therapy was started. On February 3, 2010, the first administration was carried out, against the background of which pronounced positive dynamics were noted, intestinal syndrome was relieved, the range of movements in the ankle joints increased, exudation in them decreased, and the activity of laboratory parameters decreased. On 02/17/2010 and 03/17/2010, the second and third intravenous administration of Remicade, 100 mg per injection, was performed. During treatment, there was a clear positive dynamics, intestinal syndrome was completely relieved, weight gained 7 kg, but the decrease in Hb remained to 87 g/l. During hospitalization in May-July 2010, ESR was 23 mm/h, Hb 91 g/l. A repeat colonoscopy revealed a narrowing of the transverse colon that was not passable by the endoscope. Irrigoscopy was performed: the blind, ascending, 1/2 of the transverse colons are deformed, with severe spasm, with poststenotic expansion of the transverse and descending colon. Infliximab therapy was continued; taking into account the patient's weight gain, the dose was increased. In total, the boy received 24 injections of infliximab. His condition has completely stabilized. He gained 22 kg and grew 25 cm. Intestinal and joint syndromes were completely relieved. Laboratory indicators of ESR of 5–14 mm/hour were completely normalized. Hb 151 g/l. The boy leads an active lifestyle.

Literature

1. Yablokova E. A. Clinical features and impaired mineralization of bone tissue in children with inflammatory bowel diseases. Diss. Ph.D. honey. Sci. M., 2006. 185 p.
2. Tourtelier Y., Dabadie A., Tron I., Alexandre JL, Robaskiewicz M., Cruchant E., Seyrig JA, Heresbach D., Bretagne JF Incidence of inflammatory bowel disease in children in Britani (1994 –1997). Breton association of study and research on digestive system diseases (Abermad) // Arch Pediatr. 2000 Apr; 7 (4): 377–384.
3. Guido Adler. Crohn's disease and ulcerative colitis. M.: GEOTAR-MED, 2001.
4. Shostak N. A., Pravdyuk N. G., Abeldyaev D. V. Seronegative spondyloarthropathy - improving approaches to early diagnosis and treatment // Breast Cancer. 2013, no. 6, 1002–1008.
5. Handbook of Rheumatology / Hakim A., Clooney G., Hak I.; lane from English N.I. Tatarkina. M.: GEOTAR-Media, 2010. 560 p.
6. Dougados M., Hermann KG, Landewe R. et al. Assess spondyloarthritis to international Society (ASAS) handbook: a guide The Assessment of spondyloArthritis // Ann Rheum Dis. 2009. Vol. 68. R. 1–44.
7. Rheumatology. National Leadership, ed. E. L. Nasonova, V. A. Nasonova. M.: GEOTAR-Media, 2008. 720 p.
8. D'Incà R., Podswiadek M., Ferronato A., Punzi L., Salvagnini M., Sturniolo GC Articular manifestation in inflammatory bowel disease patients. A prospective study // Dig Liver Dis. 2009, Mar 9.
9. Rodriguez VE, Costas PJ, Vazquez M., Alvarez G., Perez-Kraft G., Climent C., Nazario CM Prevalence of spondyloarthropathy in Puerto Rican patients with inflammatory bowel disease/Ethn Dis. 2008, Spring; 18(2 Suppl 2):S2–225–9.
10. Guide to pediatric rheumatology / ed. N. A. Geppe, N. S. Podchernyaeva, G. A. Lyskina. M.: GEOTAR-Media, 2012. 720 p.

A. V. Meleshkina1, Candidate of Medical Sciences S. N. Chebysheva, Candidate of Medical Sciences E. S. Zholobova, Doctor of Medical Sciences, Professor M. N. Nikolaeva

GBOU VPO First Moscow State Medical University named after. I. M. Sechenova Ministry of Health of the Russian Federation, Moscow

1 Contact information

Abstract. The article covers specifics of development of articular manifestations under chronic inflammatory bowel diseases and provides clinical example of crohn's disease development starting with un-bowel manifestations in forn of articular syndrome.

What to do if your whole body ache due to poisoning

First of all, in case of poisoning, it is necessary to clearly identify the probable toxic agent that caused the symptom complex - this procedure will make the treatment as effective and targeted as possible.

It makes no sense to separately deal with body aches during poisoning - this condition is only one of the symptoms of systemic intoxication, which must be eliminated comprehensively as part of detoxification conservative therapy.

In case of a mild form of toxicity and the absence of life-threatening and health-threatening manifestations, therapy can be carried out at home.

In cases of severe forms of poisoning with the development of obvious neurological symptoms, respiratory, renal, cardiovascular and other insufficiencies, hospitalization in a hospital is necessary.

Possible actions may include:

• Abundant gastric lavage (with soda solution), taking enterosorbents and laxatives. In case of alkali poisoning, laxatives are prohibited. In case of acid toxicity, soda should not be used (it is replaced with milk). If affected by cauterizing poisons (including organophosphorus compounds), it is undesirable to perform manual gastric lavage followed by inducing artificial vomiting,
• Cleaning the skin from surface poisons using a cotton swab,
• Immediately transport the victim from the contaminated area to fresh air,
• Carrying out artificial respiration and chest compressions in critical cases,
• Monitoring the condition of the victim until the medical team arrives.

It is better not to use medications in cases of unknown etiology of poisoning - this can aggravate the patient’s condition or even cause irreversible pathological consequences in him.

When accurately identifying a pathological agent, this information should be immediately reported to doctors - in some situations it is possible to use classical antidotes and serums.

Body aches and weakness without fever are the main causes

As mentioned above, poisoning can be caused by various bacterial, viral or fungal infections, chemicals, poisons of synthetic, animal and plant origin. These exogenous toxins cause a number of pathological manifestations in the human body.

Body aches are a clinical symptom of the first period of a generalized reaction in the initial reactive stages of poisoning. Depending on the specific pathological agent affecting various parts of internal organs and systems, the physiology of the process itself differs. The three main causes of muscle and bone aches in this context include :

• A reverse reaction of acute loss of nutrients and minerals during rapid dehydration with a slowdown in metabolic processes in the cellular structures of muscles,
• Direct toxic effect of a pathogenic agent on nerve endings,
• Consistent accumulation of special mediators in soft tissues, formed as a result of a strong inflammatory reaction.

In general, toxins have a negative effect on the peripheral and central nervous system, also affecting the tone of vascular structures. When pathogenic agents enter the systemic bloodstream through the gastrointestinal tract, the predominant modulator of the pain syndrome is the liquid contents of the veins, capillaries and arteries.

In addition to purely local reactions of narrowing, expansion or even collapse of the conductive structures of the blood flow, toxins carried by the blood during the nutrition of soft tissues cause the breakdown of individual protein muscle structures, as well as the breakdown of glycogen, loss of electrolytes and glucose, which together leads to the formation of a characteristic pain syndrome all over the body.

Another reason why the body aches without fever is oxygen deficiency , which nourishes muscle structures through the bloodstream due to the accumulation of ketone bodies during the breakdown of fats against the background of an acute lack of glucose.

As clinical practice shows, body aches and weakness disappear after some time with the beginning of the active development of the second phase of the reactive period of poisoning, when the body, on its own or with the help of medicinal support, restores the electrolyte balance, reserves of glucose and other substances. In the latter case, acute localized pathological processes come to the fore, or the victim’s condition worsens, resulting in a toxic-septic systemic syndrome.