How do I Tell the Difference Between Food Poisoning and Stomach Flu?

Fast absorption, small local fixation, uniform distribution throughout the body, rapid disappearance in blood circulation, non-toxic metabolites, mainly excreted in urine, etc.

Figure 13-1 Hydrocarbonation of nucleophilic center and mustard gas

Mustard poisoning

Mustard gas was first used extensively by the Germans in the late WWI (July 1917), after which the military forces of various countries followed suit, causing a large number of casualties. Its casualty rate accounts for 88.7% of the total poisonous casualties of 1.3 million, so it is known as the "king of poisons". From the WWI to the "Iraq-Iraq" war, mustard gas is one of the most effective chemical warfare agents that have passed the "test of war."

Metabolic characteristics of mustard gas poisoning in vivo

Fast absorption, small local fixation, uniform distribution throughout the body, rapid disappearance in blood circulation, non-toxic metabolites, mainly excreted in urine, etc.

Figure 13-1 Hydrocarbonation of nucleophilic center and mustard gas

Figure 13-1 Hydrocarbonation of nucleophilic center and mustard gas

Mustard gas remained on the body surface 2 to 3 minutes after contact with the skin and mucous membranes (at this time, it can be removed with a disinfectant), and most of it was absorbed in 10 to 15 minutes. The absorption rate is 1 to 4 g / (cm2 · min). About 12% of the mustard gas is "fixed" locally and causes damage, and most of the rest enters the blood circulation and distributes throughout the body. The kidney, lung, and liver contents are high, which may be related to the blood supply. Systemic absorption is related to the sensitivity of tissues and organs. The free state of mustard gas in the blood does not exceed 30 minutes (the half-value period is 14 minutes). But recently Drasch et al reported that mustard gas can stay in the tissues and organs of the body for 7 days after severe poisoning. At present, the absorption of mustard gas is different from that of nitrogen mustard, mainly due to its passive absorption of fat-soluble diffusion.

Mustard gas poisoning metabolites and excretion pathways

1. It reacts with various biological macromolecules in the body (such as DNA, RNA, protein, amino acid, etc.) to form hydrocarbon products.

2. Most of them are combined with glutathione (50%) or cysteine to produce non-toxic metabolites and are excreted.

3 Hydrolyzed or oxidized to form dihydroxydiethyl sulfide, mustard sulfone or mustard sulfoxide. Determination of the former content can assist diagnosis.

4 A small amount of mustard gas is converted into isethionate, glycolic acid, and inorganic sulfate.

5. Most metabolites are excreted in the urine. Urinary radioactivity measurements indicate that rats and mice excrete about 50% at 6h and 80% at 24h.

Mechanism of mustard gas poisoning

Although the mechanism of mustard gas poisoning has been studied for a long time, it has not been fully elucidated so far. At present, it is believed that mustard gas is mainly combined with nucleic acids, enzymes, proteins and other biological macromolecules in the body. The hydrocarbonation of DNA is the biological basis of extensive damage to the body. ) Has similar pharmacological and toxicological properties.

Mustard gas poisoning

Mustard gas is a typical bifunctional alkylating agent, which has a wide range of alkylation effects. The sulfur atom in the mustard gas molecule has two unshared electrons; chlorine is a more electronegative atom. Due to the induction effect of the chlorine atom, the unshared electron pair on the sulfur atom moves in the direction of the chlorine induction effect, promoting the separation of the chlorine atom. Therefore, the mustard gas dissolved in polar solutions such as water or body fluids rapidly dissociates, and the internal electrons rearrange to form normal carbon ions or normal sulfur ions. Orthosulfide ions, also known as sulfonium ions, have a strong electrophilicity and are easily reacted with nucleophilic atoms S, N, O, etc. of biological macromolecules to form Different reversed alkylation products (Figure 13-1).

Many important components in the cell contain nucleophilic centers such as S, N, and O. They have different affinities for the hydrocarbylating agents, and their order is S> N> O. Under physiological conditions, mustard gas reacts with many nucleophilic groups in the body, such as amino, mercapto, hydroxyl, carboxyl, phosphate, and imidazolyl groups. Therefore, mustard gas has a wide range of complex biological effects.

Effects of mustard gas poisoning on nucleic acids

DNA is extremely sensitive to mustard gas and is the main target of mustard gas attack. It is also the material basis of genotoxicity and cytotoxicity of mustard gas. Bases in DNA are easily hydrocarbonated by mustard gas. This effect occurs mainly in guanine.

N7, O6, N2 and N1, N6 of adenine. Under basic conditions, O2 of cytosine can also be hydrocarbonated. Among them, the alkylation at the N7 and O6 positions of guanine is the most important. Hydrocarbonation of a phosphodiester in a nucleic acid chain can form an unstable phosph triester.

Figure 13-1 Hydrocarbonation of nucleophilic centers (Y-, Z-) and mustard gas

Mustard gas is a bifunctional hydrocarbonating agent with two hydrocarbonating functional groups (or arms). Therefore, it may be bifunctional alkylation and monofunctional alkylation. Dihydrocarbonation is divided into interstrand crosslinking and intrastrand crosslinking. The former occurs between two complementary strands, while the latter occurs within the same strand (Figure 13-2). Dihydrocarbonation can also occur between DNA and proteins. As for monohydrocarbonation, the connection between the single arm of mustard gas and the DNA component.

The guanine N7 alkylation product of DNA is unstable. It is detached from the deoxyribose-phosphate bond (depurination reaction) by inherent or enzymatic action to form purine-free DNA. Then, under the action of purine-free endonuclease, the purine-free site was excised, which caused the deoxyribose-phosphate main bond to break, resulting in single- or double-strand breaks in the two helix strands of DNA.

There are two main toxicological effects of DNA alkylation damage: cytotoxicity and genetic information disorders.

Figure 13-2

Figure 13-2 The possible connection between mustard gas (H) and guanine (G) in the DNA strand

a Monohydrocarbonation b Intra-chain crosslinking c Inter-chain crosslinking d Hydrocarbonation products of H and G

Due to the DNA alkylation reaction and strand breaks, DNA molecules are distorted and DNA templates are damaged. Especially the existence of inter-strand cross-linking, which severely affects the cleavage of the two paired strands during DNA replication, thereby hindering the normal semi-retained replication process (that is, the DNA loses template function), or the DNA molecular structure and biochemical function after replication change. As a result, cell mitosis is inhibited (DNA replication is a prerequisite for cell mitosis) and cell division and proliferation are inhibited. In severe cases, cell death is caused (Figure 13-3). It is generally believed that cross-linking of DNA strands is the main cause of cytotoxicity, while intra-strand cross-linking and DNA-protein cross-linking are secondary factors of cytotoxicity. Some people think that the DNA guanine N7 position alkylation is the origin of cytotoxicity, and the O6 position alkylation is closely related to genetic disorders such as carcinogenesis, carcinogenesis and teratogenesis.

Figure 13-3 Mechanism of cytotoxicity caused by DNA alkylation damage

It has been proven that DNA double-hydrocarbonation (inter-chain cross-linking) mainly causes cytotoxicity and causes cell death; single-hydrocarbonation is less likely to cause cell death, but can cause DNA genetic information obstacles, such as the single-hydrocarbonation of DNA guanine N7 position After the product is dropped, a gap is left. This gap may cause the incorporation of wrong bases during replication and transcription, which may cause genetic information obstacles such as mutation, canceration and aberration.

Mustard gas has a similar effect on RNA as it does on DNA, and also mainly acts on the N7 position of guanine. RNA alkylation affects amino acid condensation, causing protein anabolic disorders to interfere with cell function (Figure 13-3). Experiments have shown that both prokaryotic and eukaryotic cells themselves have DNA repair capabilities, and to a certain extent, they can excise DNA damage sites and restore the normal structure and function of DNA.

Effect of mustard gas poisoning on protein

In addition to affecting protein synthesis through the action of nucleic acids, mustard gas can also directly hydrolyze with nucleophilic groups in the protein peptide chain, and it has important toxicological significance, especially with the hydrolyzation of structural proteins in cells. The main functional groups of mustard gas hydrocarbonation are: amino group of lysine, carboxyl group of glutamic acid, and thiol group of glutathione and cysteine. Experiments with labeled mustard gas (35S) and yeast showed that 50% and 35S bound to glutathione, 10% to 35S bound cell membranes, and the remaining 40% to cell microcellular structures. Mustard gas also easily interacts with serum proteins and nuclear proteins. The dehydrogenated protein undergoes denaturation, complement inactivation, and decreased immune function.

Effect of mustard gas poisoning on enzymes

Mustard gas has an inhibitory effect on at least 30 kinds of enzymes such as hexokinase, cholinesterase, pepsin, and some dehydrogenases and oxidases. Inhibition of hexose phosphokinase can affect the fermentation and conversion of sugar, leading to impaired glucose metabolism and tissue nutrition disorders. Skin damage may also be related to this process. Mustard gas significantly inhibited the activity of lactate dehydrogenase. Nitrogen mustard poisoning increased the activity of lysosomal glucuronidase (-glucuronidase) in rat small intestine crypt cells by 8 times. Inhibition of nucleotide kinases and polynucleotide phosphorylases involved in nucleic acid polymerization can aggravate nucleic acid metabolic disorders. It is believed that the effect of mustard gas on enzymes is a direct hydrocarbonation reaction and an indirect induction effect through DNA damage. The enzyme is not very sensitive to mustard gas and its specificity is not strong, so it is far less important than DNA.

Cytotoxic effects of mustard gas poisoning

The cytotoxic effect of mustard gas is one of the important characteristics of mustard gas damage. Cells in different growth cycles have different sensitivities to mustard gas; cells in the S phase (DNA synthesis phase) and G2 (late synthesis) are most sensitive to mustard gas, and cells in the division phase (M phase) are relatively insensitive. Therefore, vigorously proliferating lymphocytes, bone marrow hematopoietic cells, intestinal mucosal epithelial cells, and testicular spermatogenic cells are the most sensitive to mustard gas, making them appear "reproductive". It also determines the specific damage site of mustard gas poisoning. In addition, the sensitivity of blood cells at different stages of differentiation is also different. That is, hematopoietic stem cells are the most sensitive, followed by naive cells, and mature cells are less sensitive.

Mustard gas inhibits cell mitosis and causes chromosomal damage, including breaks, deletions, exchanges and aberrations, as well as mutations, cancers and aberrations of various cells. Under certain conditions, timely and correct DNA repair can maintain the integrity of the chromosome structure.

Experiments have shown that DNA and protein synthesis have different sensitivities to mustard gas. DNA synthesis is significantly inhibited, cell division is delayed, and protein formation is still ongoing. The two are out of balance, so the cells grow larger, eventually leading to cell disintegration and death. The use of protein synthesis to inhibit cycloheximide restores the biosynthesis of the two to reduce or eliminate the cytotoxic effect of mustard gas.

The occurrence and development of mustard gas skin cytotoxicity include: Mustard gas hydrocarbonated cells DNA guanine leads to the formation of purine-free nucleic acid, purine-free endonuclease cuts off the purine-free site of DNA, so the DNA chain is broken and activated by the enzyme activation Poly (ADP-ribose) polymerase [PADPRP], which uses NAD + as a matrix to synthesize poly-ADP-ribosomes, and therefore consumes a large amount of NAD + in the cell, resulting in a decrease or loss of NAD + content, glycolysis Desuppression inhibits and activates the monophosphate hexose bypass, which leads to the mutually beneficial release of proteins and ultimately causes pathological changes in the cells.

The cytotoxic effect of mustard gas is different from common acid-base caustics, protein coagulants or burns. The latter can quickly kill cells. Although the former interacts quickly with cell biochemical components, it has a process that causes cell damage and death. This is related to clinical There is an incubation period that is consistent. Therefore, it is often difficult to determine the extent of cellular damage in the early stages of mustard gas damage.

Effects of mustard gas poisoning on the nervous system

In the case of high-dose mustard gas poisoning, changes in the activity of higher-level parts of the central nervous system appear earliest. Excitement and convulsions occur early, especially in the lower extremities, and sometimes paroxysmal seizures, which quickly turn into suppressive paralysis. In addition, there are obvious parasympathetic nervous system excitation symptoms, such as salivation, intestinal smooth muscle spasm, and so on. The course was rapid and severe, and death was rapid. Symptoms of poisoning in animals under anaesthesia were significantly reduced compared with non-anesthetized animals.

Mustard gas acts on the skin and mucous membrane receptors, and quickly causes pathological reflexes. Blocking this reflex pathway can prevent the development of pathological processes. Experiments have shown that the surrounding of the infected skin with nofcaine not only has a lighter degree than the control, but also has a slower course and heals faster. In addition, the use of mustard gas to stimulate the sciatic nerve to the heart end can cause contralateral lower extremity ulcers, and does not heal externally.

Pathological changes of mustard gas poisoning

Local damage

In the erythema stage, dermal papillary capillaries and small blood vessels are dilated and congested, and plasma, white blood cells, and a small amount of red blood cells exudate. The basal layer of the skin showed cell separation and contained serous cellulose exudates. Edema and necrosis can affect the dermis and subcutaneous tissue. In the necrotic ulcer stage, in addition to the infiltration of leukocytes and pus cells at the base of the necrotic tissue, there are a large number of disintegrating nuclear fragments, and fibroblast proliferation can be seen, and extensive inflammatory cell infiltration and edema can be seen after infection. Eye damage mainly manifested as serous inflammation and purulent hemorrhagic inflammation. In severe cases, corneal ulcers, perforations, or pancreatitis. Irisitis or iridocyclitis is sometimes seen. Respiratory tract injury pathology is characterized by mucosal inflammation and pseudo-membrane formation. Pseudomembrane is a necrotic mucosa, in which a large number of neutrophils are infiltrated, the surface is covered with cellulose, and it is grayish white. It is more widely distributed than the diphtheria pseudomembrane and is easy to fall off. Gastrointestinal poisoning can cause mucosal bleeding, edema, necrosis, and acute submucosal cellulitis. Ulcers can form in the later stages, reaching the submucosa or muscle layer.

Mustard poisoning

Mustard gas poisoning hematopoietic system

Hematopoietic tissue is sensitive to mustard gas. When the poisoning is severe, the bone marrow is empty, and the hematopoietic cells are destroyed and disappeared. Only a few primitive hematopoietic cells, reticulocytes, and sinusoids are seen. Lymph node follicles and lymphocytes in the spleen and spleen body disappear and acute atrophy. Peripheral blood leukocytes decreased sharply and neutrophils shifted to the right. In severe cases, red blood cells and platelets are also reduced.

Mustard gas poisoning digestive system

Small intestinal mucosa epithelium, especially crypt cells, is the most sensitive. Animal experiments showed that crypt cells had nuclear shrinkage, nuclear fragmentation, and cell division phase disappeared. The villi epithelium of the small intestine exfoliated, and no new epithelial cells moved from the crypt to the villi. Intestinal mucosal barrier defect, a large amount of plasma exuded from the intestinal wall, diarrhea, bloody stool, and sepsis or toxemia can be seen.

Mustard gas poisoning nervous system

The animals were poisoned by ultra-lethal amount, and excitement and convulsions quickly appeared, and parasympathetic nervous system excitement such as drooling and intestinal smooth muscle spasm were seen. Nerve cells showed changes in Nissl bodies and vacuoles.

Mustard gas poisoning gonad

Testicular spermatogenic cells are also more sensitive. In severe poisoning, seminiferous seminiferous spermatocytes are greatly reduced, mature sperm are reduced, and spermatocyte division is rare. Generally recoverable.

Mustard poisoning other

In terms of metabolism, severe poisoning can cause a lot of tissue damage, increased protein breakdown, vomiting and diarrhea leading to water loss, imbalance in electrolysis, loss of appetite, increased negative metabolism and weight loss. In terms of circulatory function, large-dose poisoning may have bradycardia, arrhythmia, and decreased blood pressure, leading to hypovolemic shock.

Clinical manifestations of mustard gas poisoning

Mustard gas can cause various damage to the body. In the absence of protection during wartime, eye, respiratory tract and skin injuries often occur at the same time. Through absorption and can cause systemic poisoning. The incidence of vaporous mustard gas on various parts of the body is shown in Table 13-5.

Table 13-5 Incidence of vaporous mustard gas in various parts of the body

(According to the statistics of 6,980 mustard wounded in World War I)

Injury site

Incidence rate (%)

Injury site

Incidence rate (%)

eye

86.1

Wrist

11.7

Respiratory tract

75.3

chest

11.5

scrotum

42.1

Calf

11.4

Facial

26.6

Hips

9.8

anus

23.9

thigh

7.0

Back

12.9

abdomen

6.4

armpit

12.5

palm

4.3

neck

12.0

foot

1.5

Mustard poisoning skin damage

The skin is a frequent site of mustard gas damage. Moist and sweaty, limbs flexion, and other sensitive skin. The process and degree of mustard gas damage are related to the dose, external conditions and body conditions. High temperature and high humidity can significantly enhance the toxicity of mustard gas. Mustard gas can penetrate the skin quickly, most of it enters the blood, and a small part (about 12%) is "fixed" in the epidermis and dermis, forming a combined mustard gas. The degree of skin damage is related to this "fixed amount".

The degree of skin damage was indexed according to the three-degree quarter method of thermal burns.

I degree

For mild damage, the germinal layer of the epidermis was not damaged, and erythema and edema appeared;

Shallow degree

Injury, reaching the superficial layer of the dermis, part of the germinal layer of the epidermis is still present, with superficial blisters; deep second-degree injury, reaching the deep layer of the dermis, leaving only skin attachment residues, showing deep blisters;

degree

Damage to the entire layer of the skin, necrosis and ulcers.

Figure 13-4

1. Droplet damage:

The typical clinical course of droplet mustard gas skin injury can be divided into incubation period, erythema period, blister period, ulcer period and healing period. Vapor-like skin poisoning usually occurs only with erythema.

(1) Incubation period: Generally 2 to 6 hours, which may vary depending on dosage, skin condition and temperature. The hot and humid season can be shortened to 1 hour. The subjective and objective manifestations were not obvious at this stage, and the skin was thin and tender, and moist parts could have itching.

(2) Erythema stage: localized erythema with obvious boundaries, burning and itching, with mild edema, sensitive to touch pressure. Blisters do not occur when the injury is mild, and the erythema fades and desquamates and heals itself.

(3) Blister period: It usually appears 12 to 24 hours after exposure. Depending on the degree of infection, the blisters are shallow and deep. If uncompressed, the superficial blisters can remain unbroken for several days. Dispersed fine vesicles first appear in the erythema area, arranged in a ring shape, and then merge into bullae (Figure 13-4).

Figure 13-4 Redness and blistering in skin lesions with droplet mustard gas

The skin around the blister is congested and edema. The blister fluid is yellow and clear at first, which is easy to draw and attract, and then becomes cloudy and jelly. The amount of poisoning was severe. The center of the erythema showed a gray-white necrotic area, and many blisters of various sizes appeared around them. These blisters merged with each other to form a bad blister. Large doses of poisoning can form coagulative necrosis, no blister formation.

(4) Ulcer: small blister absorbs itself. The superficial blisters have high tension and are easy to rupture, revealing pink erosive surfaces, generally without infection, and can be healed within 7 to 10 days; deep blisters often rupture after a few days, and there are ulcers deep in the dermis, which can be covered with a layer Milky white necrotic membrane. Due to the slower shedding of necrotic tissue, purulent secretions are susceptible to infection. Healing begins after 3 to 4 weeks.

(5) Healing period: The speed of healing can vary depending on the degree of poisoning, the location of the injury, and whether there is infection. Skin wounds have an itching sensation during healing, pigmentation after healing, and scar formation on deep wounds.

Mustard gas poisoning vapor damage

The incubation period is 6 to 12 hours or 1 to 2 days. Non-irritating at the initial stage of exposure, diffuse erythema generally only appears on exposed areas of the skin (such as face, neck, hands, etc.). It can also damage non-exposed skin through clothing. Sensitive parts such as perineum, waist, armpits, popliteal fossils, etc., are sensitive to thin and sweaty skin. In the absence of protection during wartime, eye and respiratory tract injuries may occur at the same time.

Mustard poisoning eye damage

In the absence of protection, the incidence of eye damage was the highest (Table 13-5). Among them, mild accounted for 75%, moderate 15%, severe 10%. Serious corneal injuries accounted for 0.1%. Severe damage is mostly caused by liquid mustard aerotin. Mustard gas droplets enter the eye through the corneal epithelium and enter the parenchyma for 2 to 3 minutes, and penetrate the iris for 6 to 7 minutes.

The main lesions of eye damage are conjunctivitis and keratitis, and even pancreatitis. Perforated corneal necrosis is permanently blind. Mild to moderate injuries are usually cured in 1 to 2 or 3 to 4 weeks.

Mustard gas poisoning respiratory tract damage

The incubation period is 6 to 12 hours or longer. No obvious irritation during initial contact. The degree of local damage gradually reduced from top to bottom. The clinical manifestations are similar to those of severe cold or bronchitis, and are often accompanied by systemic absorption poisoning.

A few severely intoxicated patients developed symptoms quickly, and a few days later, extensive necrosis from the nose to the bronchial mucosa formed a pseudomembrane (consisting of necrotic tissue, fibrin, and inflammatory exudates). The lower lumen of the bronchus is narrow, and pseudomembrane obstruction can easily cause atelectasis, which causes severe ventilation disorders. Therefore, suffocation due to laryngeal edema, pseudo-membrane loss and obstruction often cause bronchial pneumonia and death. However, severe poisoning is rare, unless it is inhaled at high concentrations or is more likely to occur in hot, jungle areas.

Severe respiratory tract poisoning usually causes death 3 to 4 days or 9 to 10 days after poisoning. Early death is due to severe systemic poisoning or suffocation. Late death is due to secondary pulmonary infection (pneumonia, pulmonary gangrene, lung abscess, etc.) or cardiopulmonary function obstacle.

Mustard gas poisoning

Mainly caused by ingestion of poisoned water or food. Digestive tract damage can also be seen in severe skin infections and respiratory tract poisoning. Oral poisoning mainly damages the upper digestive tract, mainly the stomach. Non-oral absorption poisoning mainly damages the lower digestive tract, mainly the small intestine.

Oral poisoning has a short incubation period (mostly 15 minutes to 1 hour), and the severity of the injury is related to the dose of gastric poisoning and food filling. The initial symptoms are similar to general acute gastritis and gastroenteritis. Drooling soon appeared after the incubation period, with severe pain in the upper abdomen and spread to the entire abdomen. Nausea and vomiting, anorexia, diarrhea, and tar-like stools. If the emergency treatment is not timely, it often causes hemorrhagic gastritis, gastric ulcer and even gastric perforation. The oral mucosa is widely congested with edema, blistering, and ulcers, and has difficulty swallowing and speech disorders. In severe cases, systemic symptoms such as weakness, apathy, tachycardia, shortness of breath, spasms, and coma.

After recovery, indigestion, abdominal distension, abdominal pain, low gastric acid, gastric motility, and emptying disorders can be left. The prognosis is poor when severe poisoning occurs, and it can die due to systemic absorption poisoning and severe shock.

Mustard poisoning

In field situations, severe poisoning is rare. It may be caused only when a large area of the skin is poisoned by droplets without timely disinfection or prolonged exposure to high-concentration poison vapors without timely protection. It is also possible to ingest severely contaminated water and food, but this situation is relatively rare.

1. Nervous system: Early onset of nausea and vomiting followed by headache, dizziness, and restlessness. Followed by depression, depression, indifferent expression, slow response, weakness and lethargy. Some scream, slang and dance-like movements at night. After being poisoned for a long time, it was in a state of suppression, and the wounded lay quietly, unwilling to participate in surrounding activities.

Figure 13-5

Severe poisoning wounds may occur similar to shock; extremely severe poisoning wounded in paroxysmal convulsions, delirium and unconsciousness, and then the whole body muscles relax, paralyze and die.

2. Hematopoietic system: Bone marrow and lymphoid tissue are sensitive to mustard gas. Generally, the skin infection area is above 1% or the systemic symptoms of moderate or higher respiratory tract poisoning, and the white blood cell count is mild and moderately reduced.

The total number of white blood cells and the number of neutrophils increased within 1 to 2 days after poisoning, and the total number could reach (10-20) × 109 / L or more, and neutrophils accounted for more than 80% -90%. It can suddenly drop to a few hundred or even zero in the future (Figure 13-5). The degree of reduction is often consistent with the severity of the poisoning. Lymphocyte poisoning decreases significantly in the early stages, and the relative and absolute values increase when they improve. Most of the wounded leukocytes rebounded quickly, and they recovered from the beginning to basically returned to normal, usually no more than 2 weeks.

Figure 13-5 Changes in the number of peripheral blood leukocytes in mustard gas poisoning

In addition, neutrophils can appear poisonous granules, excessive nuclear defoliation, and nuclear filament breakage; vacuoles and abnormalities of lymphocytes (Figure 13-6). If the peripheral blood image continues to shift to the right, the eosinophils and basophils in the lobular nuclei disappear, often indicating that the disease is serious.

Figure 13-6

Figure 13-6 Morphological changes of peripheral blood leukocytes in severe mustard gas poisoning (focused field of view)

1. Neutral lobulated nucleus cells: enlarged cell body with too many nucleated lobes; 2. Monocytes: enlarged corpus soma, nucleus break, nuclear chromatin dissolution, nuclear vacuole vacuole; 3,5. Nuclear cells: nuclear filaments break; 4. Mononuclear cells: enlarged cell bodies, nuclear plasma vacuoles, nuclear spinous processes; 6,9. Neutrophil nucleated cells: plasma toxic particles; 7. Lymphocytes: nuclear enrichment and Partial nuclear dissolution; 8. Lymphocytes: nuclear concentration and nuclear plasma vacuoles

Platelets: A few days after intoxication, they begin to decrease. In severe cases, they decrease significantly (below 5 × 109 / L). The bleeding time is prolonged and there is a tendency to bleed, such as skin bruising, epistaxis, hemoptysis, and blood in the stool.

Red blood cells: Initially increased temporarily due to blood concentration, and then decreased due to obstacles, but the decline rate is not as obvious as that of white blood cells, which generally rises around 3 weeks. In severe cases, there may be anemia in the late stage. In addition, diffuse intravascular coagulation may sometimes be associated with the course of the disease.

3 Digestive system: In addition to oral poisoning, gastrointestinal symptoms such as nausea, vomiting, loss of appetite or disappearance, and constipation can be seen early in non-oral absorption poisoning. In severe cases, the small intestinal mucosal epithelial crypt cell division is inhibited, the villous epithelium is stripped, and the plasma-like liquid penetrates into the intestinal cavity. There may be thin stools, diarrhea, and blood or tarmaca. In addition, severe dehydration, electrolyte imbalance, and mild liver enlargement were seen.

4 Cardiovascular system: early heartbeat, hypercardia, increased blood pressure, and extrasystole. In severe cases, the heartbeat slows down, arrhythmias, splanchnic vasodilation and dilatation appear, blood pressure drops or collapses, and even severe circulatory failure.

5. Urinary system: severe poisoning can be seen in acute toxic nephritis, renal tubular epithelial cells and glomerular degeneration. Reduced urine output with protein, cast urine and hematuria.

6. Substance metabolism: Impaired glucose metabolism results in increased blood sugar and diabetes, increased protein and fat breakdown, and increased total excretion of nitrogen, ammonia, creatine, creatinine, and phosphorus in the urine. Increased blood lactic acid and ketone bodies can cause acidosis. Severe cases show severe weight loss and weakness after the acute phase, showing a state of "mustard gas cachexia".

7. Body temperature: Mild poisoning The temperature is normal or there is a low fever within a few days. The first few days of moderate poisoning can reach 38-39 ° C or higher, and then decrease slightly for 2 to 3 weeks. Co-infection can rise again. Due to the decrease of white blood cells, the body is weakened and the immune function is reduced, and it is easy to be complicated by lung infection.

Prognosis and sequelae of mustard gas poisoning

Mustard gas is a lethal poison, which can cause a high injury rate, but a low lethal rate. According to WWI statistics, the mortality rate of mustard gas poisoning is 1% to 3%. However, due to the high injury rate, the number of deaths is also considerable. In the event of the Bari port, 617 wounded with mustard gas were killed, 81 of whom died, with a mortality rate of 13.1%. Therefore, the lethal effect of mustard gas should also be taken seriously.

Both WW and the Iran-Iraq War proved that respiratory tract injury and its secondary infections, such as bronchial pneumonia and pulmonary edema, were the main causes of death from mustard gas poisoning, and death usually occurred 9 to 36 days after poisoning. In the Bayeri incident, poisoned wounded showed a second death peak after 9-10 days, mainly due to secondary infection. Secondly, those who suffer from severe systemic absorption poisoning and die from shock syndrome often die within a few hours to 1 to 2 days after the poisoning. In addition, high-dose mustard gas systemic poisoning accompanied by cardiovascular, central nervous, renal and gastrointestinal dysfunction or functional failure, repeated vomiting, massive diarrhea, visceral bleeding and extensive skin blister exudation, fluid loss, or shock can also lead to death. In general, if the injured person has severe central nervous system depression, shock, persistent high fever, or the total number of white blood cells in peripheral blood drops below 1000 × 106 / L, the prognosis is poor.

Many sequelae can be left after poisoning mustard gas. Such as skin damage can cause allergies, produce a variety of dermatitis, scar formation can cause dysfunction. Chronic bronchitis, bronchiectasis, and emphysema can occur after respiratory tract injury. Moderate and severe eye damage can leave conjunctivitis, keratitis, corneal ulcers, vision loss, and even blindness. The delayed effect of mustard gas can increase the rate of canceration and distortion.

Diagnosis and differential diagnosis of mustard gas poisoning

Diagnosis of mustard gas poisoning

1. History of poisoning: length of stay in the poisoned area, drinking or eating, smell of garlic, protection and first aid, skin and clothing poisoning and disinfection, and whether others are poisoned and signs of poisoning area, etc. .

2. Symptoms and characteristics: Mustard gas poisoning usually has no obvious pain and discomfort at that time, and often has an incubation period of several hours to ten hours. After the incubation period, the clinical manifestations of eye, respiratory tract, skin, or digestive tract injuries occur successively.

3 Laboratory tests: Blood tests include continuous observation of the total number and classification of white blood cells and determination of urinary diethylene disulfide, which is helpful to diagnose and judge the degree of poisoning and prognosis.

4 Poison test: In addition to knowing the results of the poison test, a sample of wounded clothing, early vomit, or suspicious drinking water and food can be used to help diagnose.

Differential diagnosis of mustard gas poisoning

1. Louise's poisoning: Louise's agent has severe pain when in contact with skin and mucous membranes, short incubation period, rapid development of symptoms, severe skin congestion and edema, wide range, bleeding points, early arsenic can be detected in blisters, urine and feces .

2. Nitrogen mustard poisoning: skin damage is lighter than mustard gas, and rarely causes large blisters; it has a strong stimulating effect on the upper respiratory tract, and has a greater systemic absorption effect. Nitrogen mustard has a fishy smell, and the poison test has a positive reaction to nitrogen mustard.

In addition, mustard gas skin poisoning should be distinguished from general physical factors (such as burns, frostbite, sunburn), contact dermatitis, and erysipelas; eye poisoning should be distinguished from bacterial or viral conjunctivitis; inhalation poisoning should be different from upper respiratory infections And influenza identification; oral poisoning and food poisoning and acute gastroenteritis are distinguished.

Mustard gas poisoning prevention, first aid and treatment

Mustard gas poisoning prevention

1. Use gas masks and skin protection equipment in a timely manner, and perform local and systemic decontamination as soon as possible, and evacuate the affected area when conditions permit.

2. Comply with the rules of action for poisoned areas.

3 Prevent cross-contamination. When the wounded are contained, the wounded's poisoned clothing, equipment, weapons, stretchers, etc. shall not be brought into the room.

4 Items, equipment, vehicles, etc. from the poisoned area should be inspected and disinfected in a timely manner.

First aid for mustard gas poisoning

The contents mainly include: organizing self-rescue and mutual rescue as soon as possible, timely local disinfection, using protective equipment, removing poisoned clothing, and evacuating the poisoned area.

1. Skin poisoning: Disinfect the area with the provided skin disinfectant (or powder). When disinfecting, you should first dip visible droplets with gauze, handkerchief, etc., avoid rubbing back and forth to expand the scope of exposure, and then disinfect with disinfectant. When there is no standard disinfectant, the following disinfectants can be used: 20% monochloramine ethanol solution or deep water solution; 1:10 three-in-two suspension; 1:10 calcium hypochlorite suspension; 1: 5 bleaching powder slurry; 5% Dichloroamine alcohol solution or 1: 1 bleach and talc.

Chloramine compounds (such as chloramine T and chloramine B) are oxidizing and chlorinating disinfectants. They can interact with mustard gas and Louis's agent to form non-toxic compounds, which have better disinfection effect. Commonly used for skin disinfection.

Monochloramine

Benzenesulfonyl dichlorodiethylthioimine

The disinfectant has some irritation to the local skin. After disinfecting for 10 minutes, rinse the local area with water. Without the above disinfectants, soapy water, alkaline water, clear water, etc. can be used for emergency disinfection. When localized treatment of large-area skin intoxication is not thorough, a body wash should be performed.

2. Wound poisoning: Immediately remove the droplets of poison in the wound, and put a tourniquet on the upper end of the extremity wound to reduce the absorption of the poison. Rinse the wound repeatedly with a few times of water or a lot of water with a disinfectant solution, simply bandaging, and loosen the tourniquet after half an hour.

3 Eye poisoning: Rinse immediately with 2% sodium bicarbonate solution, 0.5% chloramine aqueous solution or water.

4 Oral poisoning: Immediately prick the throat (or tongue) with your fingers and cause repeated vomiting. It is best to use 2% sodium chloride carbonate, 0.02% to 0.05% potassium permanganate or 0.3% to 0.5% chloramine aqueous solution, repeated gastric lavage more than ten times each time. Water temperature and pressure should be appropriate, and movement should be light, so as not to aggravate gastric mucosal damage. After gastric lavage, 15-20g of medicinal activated carbon powder is mixed and swallowed in a glass of water. Washed out gastric juice and vomit should be disinfected in time.

Mustard gas poisoning treatment

Mustard gas absorption poisoning, although there is no effective anti-drug, but according to the location, degree and different stages of injury, the combination of traditional Chinese and western medicine, comprehensive treatment measures, still have good results.

1. Skin injury: The treatment principle is similar to the general treatment of thermal burns or contact dermatitis, and the corresponding treatment is performed according to the injury stage.

(1) Erythema: apply anti-inflammatory, swelling, cool and antipruritic external medicine or wet compress to avoid using irritating drugs. Hormonal drugs (0.05% anti-inflammatory pine cream, 0.1% dexamethasone cream, or skin hydrocortisone cream), non-hormonal drugs (0.1% indomethacin cream or 5% diphenhydramine cream), compound snake bed Lotions, cooling creams, etc. If the swelling range is large or external application is inconvenient, prednisone 5 to 10 mg (or dexamethasone 2 to 5 mg) can be taken orally 2 to 3 times a day. If necessary, hydrocortisone is intravenously infused, 100 to 200 mg daily, available for 1 to 3 days. Others such as 3% boric acid water, 0.05% potassium permanganate water, compound calamine lotion and 5% menthol alcohol solution can be used. The vulva is exposed as much as possible. Prevent skin infections caused by rupture. When the erythema is irritable, if the area is not large, it can be rinsed with cold water, soaked and cold compress.

(2) Blisters: Try to retain the blister skin, protect the wound surface, and prevent infection. The small blister should be absorbed by itself as much as possible, and the large blister will be full or painful. After disinfection with 75% alcohol, puncture and drain the fluid at a low position. If the blister skin is difficult to retain or the blister fluid cannot be extracted, the blister skin and the contents of the blister can be completely eliminated, and the wound surface should be washed with soap and water, and then washed with 0.1% Xinjieer solution. Wounds are treated as burns. Exposure therapy is generally used to keep them clean and dry.

(3) Ulcers: prevent infection, remove saprophytic, preserve epithelium and promote healing. Specific measures are taken as burns. Debridement and drainage, dressing with antibiotic oil gauze. Can also use cod liver oil, egg butter and other gauze bandaging to accelerate wound healing. Slow healing ulcers can be irradiated with infrared. For functional sites or deeper degree wounds, strive for early skin grafting.

Vulvar ulcer wounds can be bathed or rinsed with 1: 5000 potassium permanganate solution several times a day, and coated with an antibiotic solution wet or 1% gentian tincture, which should not be bandaged. Take care to prevent urine from contaminating the wound.

When there is dry death, it can be eaten away or removed by surgery. Bromelain preparations can also be used for drug dehydration.

2. Eye damage: The principle is to prevent infection and reduce sequelae.

(1) Anti-infection: Use antibiotic eye drops or ointments as early as possible, such as 0.25% chloramphenicol, or 15% sulfamethoxazole eye drops and 0.5% cortisone eye drops. Antibiotic eye ointment is available at night.

(2) Anti-inflammatory: 0.5% cortisone acetate eye drops are used for mild and moderate eye damage. If there are purulent secretions and severe edema, the eyes can be washed with 2% sodium bicarbonate or 1% sodium chloride in the early stage. Cortisone combined with antibiotic eye drops can promote healing. To prevent eyelid adhesion in the morning, you can apply chlortetracycline eye ointment before going to bed.

(3) Symptomatic treatment: during eyelid spasm closure, pain, edema, and a large number of tears and secretions affecting the examination and treatment, 0.5% decaine or 1% dionine can be dripped into the conjunctival sac. Morphine was given in severe pain and treated as corneal injury. Dilate pupils with 1% atropine solution or eye ointment to prevent iris adhesion. When you are afraid of light, you can wear colored glasses or cover with gauze. Cold compresses within one week after injury can reduce congestion and edema. In the recovery period, 0.25% zinc sulfate eye drops can be used for accelerated healing. Ocular poisoning suffers blindness due to eye spasms, pain, edema, and visual impairment, so they should be relieved of their ideological concerns and actively cooperate with treatment.

3 Respiratory tract

(1) Infection control: mild and moderate injuries are treated according to upper respiratory tract inflammation and acute bronchitis. For severe poisoning, infection should be strictly controlled, and anti-infective drugs should be applied locally (aerosolized inhalation) and systemically as early as possible. And pay attention to isolation from respiratory infection patients. Prevent cross infection. The temperature and humidity in the ward should be appropriate, and the ventilation should be good to prevent colds. Clean your mouth often to prevent ulcers and infections.

(2) Symptomatic treatment: early symptoms of respiratory tract irritation, inhalable anti-smoke agents, spray inhalation cooling agent or 5% procaine solution. Use codeine for severe cough, take expectorants, and give sedatives for irritability. Inhale oxygen when breathing is difficult. To relieve bronchospasm and give bronchodilators, intravenously inject 0.25 gm of aminophylline or 20-50 mg of promethazine, once every 4 to 6 hours, alternately. Local instillation or nebulization of inhaled isoproterenol or dexamethasone. Suction the mouth and throat at any time.

(3) Promote necrotic pseudomembrane cough: Inhale a large amount of hot vapor, inhale 4% sodium bicarbonate or 0.05-chymotrypsin 3 ~ 5ml, 2 ~ 3 times a day, which can promote the softening or liquefaction of the pseudomembrane and facilitate cough Out. When the pseudo-membrane falls off and blocks and causes suffocation or severe breathing difficulties, tracheotomy is performed immediately, and the pseudo-membrane is removed.

4 Digestive tract injury: When vomiting or abdominal pain, subcutaneously inject 0.5 to 1 mg of atropine or give belladonna preparations. Use sedatives when you are restless. Pay attention to maintain water and electrolyte balance and control infection. When there is ulcer disease, take aluminum hydroxide orally. The lip and oral mucosa can be applied with 5% cocaine solution and 2% beauty blue. The first few days should be fasted, then changed to liquid, semi-liquid, infusion to supplement nutrition.

5. Systemic absorption poisoning: The treatment principles of systemic absorption poisoning are mainly anti-shock, anti-infection, anti-toxic and symptomatic treatment.

(1) Early application of antidote: In the early stage of poisoning (within 1 to 2 hours), intravenously inject 50ml of 25% sodium thiosulfate at a rate of 5ml / min. When the heartbeat slows down, blood pressure drops, or nausea and vomiting occur, the application is suspended and the slow injection is continued after the reaction. Early applications have some effect. The anti-drug principle is as follows:

Sodium thiosulfate does not easily penetrate cell membranes and has a poor antiviral effect; large doses require intravenous injection, which is inconvenient to apply; the timing of medication is also difficult to grasp. It is believed that sodium thiosulfate is of little practical significance as an anti-mustard agent.

Recently, foreign reports have reported that in addition to sodium thiosulfate, sodium dimercaptopropanesulfonate or sodium dimercaptosuccinate has a certain effect on the treatment of systemic poisoning of mustard gas. The use of cysteine in wounded gas poisoning during the Iran-Iraq war has achieved certain results. Experimental treatment studies have shown that the combination of sodium thiosulfate with sodium dimercaptopropanesulfonate, dexamethasone, atropine, and promethazine has a positive effect on meson gas poisoning animals, and it is worth further research.

(2) Anti-shock: toxic or stress shock occurs early, and it develops into low hemolytic shock 3 to 5 days later. For toxic shock, 5% glucose saline can be infused intravenously, plus dexamethasone 5 to 10 mg or hydrocortisone 100 to 200 mg, once or twice a day. Discontinued after the critical period. For hypovolemic shock, if the blood is isotonic, an intravenous infusion of 1.5% sodium bicarbonate and glucose-containing normal saline should be performed, and the fluid replacement rate and fluid volume should be appropriate. Depending on the condition, consider infusion of an appropriate amount of low-molecular dextran, plus potassium chloride and oxygen. Maintain water and electrolyte balance. Booster medications for circulatory failure.

(3) Anti-infection: antibiotics or other anti-infective drugs should be used early. In the future, antibiotics should be replaced in a timely manner based on bacteriological examination, blood culture, and clinical conditions. Drugs that inhibit hematopoietic function should be avoided. In severe sepsis, hormones and antibiotics can be used in combination, and the amount of antibiotics should be increased. But beware of dysbiosis, dual infections, and mold infections. In the prevention and anti-infection, Chinese medicine and gamma globulin for clearing heat and detoxifying, cooling blood and nourishing yin are beneficial for the recovery of the disease course.

(4) Restore hematopoietic function: when the surrounding blood phase is low, appropriate transfusion of whole blood or white blood cells, platelet suspension, vitamins B4, B6, B12, nucleotides and folic acid. Hematopoietic drugs for clinical recovery are rarely used, with few positive effects.

(5) Symptomatic treatment: give sedatives when irritable; use phenytoin sodium or barbitur in severe excitement or convulsions; inject atropine subcutaneously in abdominal pain; use hemostatic agents as needed to correct acidosis in time; Intravascular coagulation (DIC), low-molecular dextran can be used; to strengthen nutrition and care.