[Metabolic and organ protective properties of various infusion solutions and the choice of starting therapy in the pre-admission stage of acetic acid poisoning].

MATERIALS AND METHODS: We conducted an open prospective study in 60 patients (30 men and 30 women) with acetic acid poisoning. A randomization was performed on the groups, taking into account the tactics of infusion therapy: group I--15 patients who did not receive an infusion therapy at a pre-admission stage; group II--15 patients who received the infiusion therapy with solution of sodium chloride 0.9%; group III--15 patients who received the infusion therapy with modified gelatin (Gelofusinwn), group IV-15 patients who received the infusion therapy with reamberinum. RESULTS: We found that the most favorable results were noted in patients of group IV in the early posttraumatic period.

[Homeostasis changes during rehabilitation period after acute chemical poisoning].

The article deals with review of 78 patients of rehabilitation toxicological unit. The patients received resuscitation and detoxification. All patients were divided into three groups; 1st group--patients after poisoning with psychopharmaceuticals, 2nd group--patients after poisoning with cauterizing liquids and 3rd group--patients with encephalopathy after poisoning with neurotoxin (psychopharmaceuticals, narcotics and ethanol). Disorders of rheology, haemostasis and endotoxicosis accrued in all groups. These disorders were a signs of the erythrocytes and platelets aggregation developing and viscoelasticity disorder. Homeostasis changes during rehabilitation period need an accurate diagnostics for purposeful treatment of the defined disorders.

Neuroleptic Malignant Syndrome: A Potential Etiology of Multisystem Organ Failure in a Burn Patient.

Neuroleptic malignant syndrome (NMS) is described in the medical literature but rarely seen among acutely ill trauma patients. A 44-year-old man with burns to the hands and back after a chemical explosion was transported to an outside facility where he received treatment for presumed acute coronary syndrome after developing ventricular tachycardia and elevated serum troponins after the exposure. His cardiac catheterization was unremarkable, but an echocardiogram revealed severe cardiomyopathy, and he was also in multisystem organ failure. He was transferred to our facility after hospital day 2 for treatment of his multisystem organ failure and 2% total body surface area burns. His laboratory results were remarkable for a creatine kinase of >100 000 units/L, and he required 14 g of intravenous calcium. Upon further investigation, the patient reported taking ziprasidone for his bipolar disorder, and he had a core temperature of 103.5 °F on his initial presentation to the outside facility. As he convalesced, the unifying diagnosis was NMS. NMS is a side effect of antipsychotic therapy and is manifested by hyperpyrexia, rigidity, autonomic instability, and altered consciousness. An elevated creatine kinase >100 000 units/L is almost pathognomonic for NMS. Patients can also present with leukocytosis, organ failure, and electrolyte disturbances including hypocalcemia. We hypothesized that dehydration, the warm environmental conditions at our patient's job, and immense stress resulting in a catecholamine surge following his trauma were inciting triggers to this event. This case highlights the importance of considering alternate diagnoses in patients whose clinical presentation does not fit the most "obvious cause."

[Forensic medical evaluation of a burn injury from combustion of flammable fluids on the human body based on morphological changes in internal organs].

The author describes morphological features of splanchnic organs in the patients that suffered an injury from combustion of flammable fluids at the body surface. The burn injury is a specific form of trauma originating from a combination of several injurious factors including thermoinhalation and intoxication with combustion products in the absence of oxygen in the centre of the hot spot. A rather specific combination of morphological changes in internal organs along with results of laboratory studies provides the most reliable criterion for forensic medical diagnosis of burn injuries from combustion of flammable fluids on the human body.

Plasma nuclear DNA and mitochondrial DNA as prognostic markers in corrosive injury patients.

STUDY OBJECTIVES: Ingestion of a corrosive substance produces an injury to the gastrointestinal tract and it is often difficult to evaluate the severity and prognosis of this injury. Increased concentrations of plasma nuclear DNA and mitochondrial DNA (mtDNA) have been found to be associated with the area of corrosion. This study examined the level of plasma DNA as it relates to the severity of corrosive injury. METHODS: Forty-eight consecutive patients were enrolled prospectively. The concentrations of plasma nuclear DNA and mtDNA were measured by real-time quantitative polymerase chain reaction assay at presentation to the emergency room and 12 h later. RESULT: The median age of the patients enrolled was 55 years (20 men and 28 women) with an overall mortality rate of 21%. Nineteen patients underwent operative intervention secondary to perforation. Findings included significantly elevated plasma nuclear DNA and mtDNA in the mortality group at presentation and 12 h after injury compared to the survival group. CONCLUSION: The concentrations of plasma nuclear DNA and mtDNA were elevated within 4 h after corrosive injury. The elevated concentrations of plasma nuclear DNA and mtDNA could be useful prognostic markers to correlate with the clinical outcome in corrosive patients.

[Analysis on clinical characteristics of 316 patients with hydrofluoric acid burns].

Objective: To investigate the clinical characteristics of patients with hydrofluoric acid (HF) burns. Methods: Clinical data of 316 patients with HF burns admitted to Zhejiang Quhua Hospital from January 2004 to December 2016 were retrospectively analyzed. Patients were divided into non and mild poisoning group (NMP, n=157), moderate poisoning group (MP, n=120), and severe and fatal poisoning group (SFP, n=39) based on the severity of poisoning. Occurrences of hypocalcemia, hypomagnesemia, hypokalemia, and hyperkalemia of patients within 24 hours after admission were recorded. Values of emergency urinary fluoride of patients on admission were recorded. Values of urinary fluoride of patients admitted to hospital in 4 hours post injury in groups MP and SFP at post injury hour 4, 12, and 24 and on post injury day 2, 3, 4, 5, 6, and 7 were also recorded. Electrocardiographic abnormalities of patients within 24 hours after admission were recorded. Data were processed with chi-square test, Kruskal-Wallis H test, and Mann-Whitney U test. Results: (1) Hypocalcemia, hypomagnesemia, and hypokalemia occurred in some patients in each of the three groups, but no patient had hyperkalemia. Taking serum calcium namely total serum calcium as reference, the incidence rate of hypocalcemia of patients in group NMP was close to that in group MP (χ(2)=0.05, P>0.05). The incidence rate of hypocalcemia of patients in group SFP was significantly higher than that in group NMP or group MP (χ(2)=10.53, 7.92, P<0.01). The incidence rates of hypokalemia in the three groups were close (χ(2)=0.63, P>0.05). Taking serum ionized calcium as reference, the incidence ratio of hypocalcemia of patients in group NMP was close to that in group MP (χ(2)=0.01, P>0.05), while there were statistically significant differences in incidence ratio of hypocalcemia of patients between group SFP and each of group NMP and group MP (χ(2)=4.66, 4.47, P<0.05). Taking serum calcium as reference, the incidence rate of hypocalcemia of patients was 7.3% (23/316). Taking serum ionized calcium as reference, the incidence rate of hypocalcemia of patients was 60.0% (42/70), which was significantly higher than that of taking serum calcium as reference (χ(2)=113.74, P<0.01). The incidence rates of hypomagnesemia of patients in groups MP and NMP were close (χ(2)=0.02, P>0.05). The incidence rate of hypomagnesemia of patients in group SFP was significantly higher than that in group NMP or group MP (χ(2)=14.69, 9.94, P<0.01). (2) The urinary fluoride levels were tested in 288 patients, with the value of emergency urinary fluoride of patients on admission 0.2-590.0 mg/L. The values of urinary fluoride of 202 patients were above the normal value. The values of emergency urinary fluoride of patients in groups NMP, MP, and SFP were 2.15 (1.11, 4.30), 5.89 (1.72, 14.25), and 36.0 (13.2, 103.2) mg/L, respectively. The values of emergency urinary fluoride of patients in groups MP and SFP were significantly higher than the value in group NMP (χ(2)=23.28, 66.03, P<0.01). The value of emergency urinary fluoride of patients in group SFP was significantly higher than that in group MP (χ(2)=39.23, P<0.01). The value of urinary fluoride of 33 patients admitted to hospital within 4 hours post injury in groups MP and SFP reached the top at 4 hours post injury and then gradually declined, which returned to normal on about 5 days post injury. The values of urinary fluoride of patients in group SFP at 4, 12, and 24 hours post injury and on 2, 3, 4, 5, 6, and 7 days post injury were significantly higher than those in group MP (Z=-4.28, -4.15, -3.81, -4.21, -2.48, -2.06, -2.31, -2.68, -3.03, P<0.05 or P<0.01). (3) Twenty-seven patients had electrocardiographic abnormality. There were 12 patients with T wave changes (the most common), 8 patients with ST-T changes, 6 patients with ventricular arrhythmias, 6 patients with conduction block, and 1 patient with broadened QRS waveform. There was no patient with prolonged Q-T interval. The ratios of patients with the above electrocardiographic abnormalities in group SFP were higher than those in group NMP and group MP. Conclusions: Clinical manifestations of patients with HF burn are hypocalcemia, hypomagnesemia, hypokalemia, and electrocardiographic abnormality. In addition to routine serum electrolyte and electrocardiogram monitoring, the levels of serum ionized calcium and urinary fluoride can be helpful to evaluate the severity of illness of the patients.

Management of a Rare Case With Severe Hydrofluoric Acid Burns: Important Roles of Neutralizers and Continuous Renal Replacement Therapy.

Hydrofluoric acid (HF), a dangerous inorganic acid, is widely used in various industries and in daily life. Chemical burns caused by HF exposure occur more frequently in some regions worldwide. It has been reported that some cases with HF burns can be lethal due to the hypertoxicity of HF. In this article, we present a case of a 24-year-old worker who suffered HF burns by 53% HF solution to his face, neck, and nasal cavity. This patient quickly developed electrolyte disturbance, that is, hypocalcemia, and hypopotassemia, and myocardial injury after exposure. Multiple measures had been taken to treat this patient, including fluid resuscitation, electrolyte replacement, timely wound treatment with neutralizers, and respiratory tract care. Moreover, continuous renal replacement therapy was also employed to remove fluoride in the circulatory system and rectify the electrolyte disturbance and acid-base imbalance. The patient smoothly pulled though and survived. High fluoride levels in the dialysate solution were confirmed, indicating that continuous renal replacement therapy is an effective and potentially lifesaving treatment for acute HF poisoning.

INDICATORS OF HUMORAL IMMUNITY UNDER CHEMICAL BURNS OF ESOPHAGUS IN RATS.

It is well known that the immune system has been actively involved in the regeneration and healing processes of post burn wounds. However, unanswered questions remain concerning the role of humoral immunity in the healing mechanisms and development of burn wound complications. We have developed an experimental model of chemical esophageal burn (CEB) which corresponds to esophageal burn in 1-8 years old children. We studied the features of humoral immunity upon CEB in rats. A decrease in IgG levels and an increase in levels of medium- and low- molecular circulating immune complexes (CIC) on the first day of esophageal burns were observed. On the 21st day of burn, we observed an increase in the IgG concentration and a tendency to accumulation of medium- and low-molecular CIC. The studied indicators can be used to differentiate CEB development and create a timeline of burn wounds.

[Clinical observation on the treatment of phenol burn patients complicated by acute kidney injury with early blood purification].

OBJECTIVE: To observe the clinical effects of early blood purification in the treatment of phenol burn patients complicated by acute kidney injury (AKI). METHODS: Five phenol burn patients complicated by AKI, matched with the inclusion criteria, were hospitalized from January 2010 to July 2014. Within post injury hour 24, patients received rapid liquid support, positive wound management, and hemoperfusion (HP) combined with continuous veno-venous hemofiltration (CVVH) for 2 to 3 hours, then HP was stopped and CVVH was continued for 16 to 21 hours. HP combined with CVVH was performed for 2 to 3 times, then HP was stopped and CVVH was continued for 12 to 22 days. On post injury day (PID) 1, 3, 5, 7, 14, and 21, urea nitrogen, creatinine, ALT, AST, total bilirubin (TBIL), direct bilirubin (DBIL) in serum were determined, and the volume of liquid intake, urine, ultrafiltration, and liquid output were recorded, and the concentrations of IL-6, IL-10 and TNF-α in serum were determined by ELISA. General conditions of patients were recorded. Data were processed with one-way analysis of variance and LSD- t test. RESULTS: (1) On PID 1, the levels of urea nitrogen and creatinine were (9.0 ± 3.2) mmol/L and (115 ± 24) µmol/L respectively, which were obviously higher than normal values (with the values of 2.9-8.2 mmol/L and 45-104 µmol/L respectively). On PID 3, 5, 7 and 21, the levels of urea nitrogen were (12.5 ± 4.1), (11.2 ± 5.6), (8.7 ± 2.3) and (6.4 ± 3.9) mmol/L respectively, which were similar with the value of DID 1 (with t values 1.53, 0.76, 0.17 and 1.17 respectively, P values above 0.05). On PID 14, the level of urea nitrogen was (15.8 ± 3.3) mmol/L, which was obviously higher than the value of PID 1 (t =3 .29, P = 0.023). On PID 3, 5, 7 and 14, the levels of creatinine were (248 ± 67), (224 ± 87), (276 ± 59) and (307 ± 77) µmol/L respectively, which were obviously higher than the value of PID 1 (with t values 4.17, 2.70, 5.65 and 5.32 respectively, P values below 0.01). On PID 21, the level of creatinine was (78 ± 28) µmol/L, which was obviously lower than the value of PID 1 (t = 2.23, P = 0.041). The levels of ALT, AST, TBIL, and DBIL were higher than normal values from PID 1, and the levels were higher than normal values on PID 3, 5, 7, and 14, and they were similar with the normal values on PID 21. (2) On PID 1, 3, 5, 7, 14, and 21, the volume ratio of liquid intake to liquid output maintained from1:1 to 2:1. On PID 1, 3, 5, 7, and 14, although the volume of urine fluctuated, they were still less than 400 mL/d, and the volume for ultrafiltration showed a tendency from declining at first to a rise later. On PID 21, the volume of urine increased, and the volume for ultrafiltration decreased. (3) On PID 1, the serum concentrations of TNF-α and IL-6 increased, and the serum concentration of IL-10 decreased. On PID 3, 5, and 7, the serum concentrations of TNF-α and IL-6 decreased, and the serum concentration of IL-10 increased. On PID 14, the serum concentrations of TNF-α and IL-6 were elevated again but without a high peak value, and the serum concentration of IL-10 decreased but still higher than the value of PID 1. On PID 21, the serum concentrations of TNF-α and IL-6 obviously decreased, and the serum concentration of IL-10 obviously elevated. (4) Primary healing of the wound was achieved on PID 21 to 28. Patients were all cured and left hospital on PID 28 to 45. All the patients were followed up for 6 months to 3 years. At the last follow up, patients had no symptoms of chronic poisoning and the functions of liver and kidney were normal. CONCLUSIONS: Early blood purification treatment is effective for phenol patients phenol burn patients complicated by AKI, and wound healing and kidney function recovery were assured.

Bioactive substance accumulation and septic complications in a burn trauma patient: effect of perioperative blood transfusion?

Evidence has emerged that suggests adverse effects to perioperative homologous blood transfusion are related to the age of the blood products. Recently, time-dependent accumulation of bioactive substances in red cell suspensions, standard platelet concentrates and fresh frozen plasma during storage have been shown. The potential adverse effects of these bioactive substances were analysed in a burn trauma patient. A patient with 40 per cent second and third degree burn trauma without other injuries underwent a two-step transplantation operation. Samples for analyses of histamine, eosinophil cationic protein (ECP), eosinophil protein X (EPX), neutrophil myeloperoxidase (MPO) and interleukin 6 (IL-6) were drawn frequently from the patient before, during and after the operations, and from all transfused red cell, platelet and fresh frozen plasma units. Urine was sampled every hour during the first operation for analyses of ECP and EPX excretion. All analyses were performed by ELISA and RIA methods, and results compared to patient outcome. The patient received a total of 48 and 8 SAGM blood, 6 and 0 platelet and 12 and 4 fresh frozen plasma units at the two operations, respectively. Transfused products contained a total of 64.54 nmol and 17.50 nmol histamine, 115518 ng and 25764 ng ECP, 174457 ng and 38770 ng EPX, 6950915 ng and 1505125 ng MPO, and 14740 pg and 5600 pg IL-6 at the two operations, respectively. The accumulation of the substances in patient plasma correlated to postoperative septic reactions, without any disclosure of bacteraemia after the first operation, while the accumulation at the second operation correlated to the septic reaction and Pseudomonas aeruginosa infection. Time-dependent accumulation of bioactive substances in blood products during storage may be related to the development of post-transfusion adverse effects.

Biochemical indicators of caustic ingestion and/or accompanying esophageal injury in children.

A prospective clinical study was conducted to evaluate whether or not any biochemical predictor of caustic ingestion and complicating esophageal injury exists. Children who were admitted to the hospital within 24 hours following caustic substance ingestion between 1994 and 2000 inclusive were evaluated. The ingested substance and complaints upon admission were noted. Groups were constructed according to the ingested substances such as household bleach (HB) (Group 1), acid (Group 2) or alkali ingestion (Group 3). Full biochemical analyses, chest X-ray and blood gas estimations were obtained and children were evaluated endoscopically. Seventy-eight children were studied. There were 19, 20 and 39 children in Groups 1, 2, and 3, respectively. There were no sex or age differences among groups (p>0.05). Esophagogastric injury was not encountered in Group 1. Second degree injury was present in 12 and 11 children in Group 2 and Group 3, respectively. Blood pH level was decreased in Group 1 (p=0.013), but not different in Groups 2 and 3 (p>0.05). pH did not differ in patients with or without esophageal injury (p>0.05). While serum uric acid values were significantly increased in children with esophageal burn (p=0.001), serum phosphorus and alkaline phosphatase levels were significantly decreased in children with esophageal injury (p=0.01 and p=0.019, respectively). Blood bicarbonate and serum potassium, chloride, urea nitrogen, creatinine, glutamic-oxaloacetic transaminase, glutamic-pyruvic transaminase, lactic dehydrogenase, calcium, glucose, protein, albumin and bilirubin levels did not differ between group (p>0.05), nor between patients with or without complicating esophageal injury (p>0.05). Low serum pH level is an indicator of HB ingestion. Routine endoscopy may not be necessary in children with normal blood pH values after ingestion. Although normal values of pH, uric acid, phosphorus and alkaline phosphatase levels do not rule out ingestion of an acid-or alkali-containing substance other than HB, increase in uric acid and decreases in phosphorus and alkaline phosphatase levels point to the presence of an esophageal injury.

1976 Hanford americium exposure incident: hematologic effects.

Hematologic evaluation of an individual with an initial systemic body burden of approximately 200 mu Ci 241Am revealed a significant (P less than 0.01) reduction of total leukocytes, neutrophils and lymphocytes. This effect on total leukocytes and neutrophils was evident approximately 30 days after exposure, appeared to stabilize at about 3 months after exposure, and remained at this lower level through a 52-month observation period. The effect on lymphocytes was apparent by 3 days after exposure, stabilizing at approximately 50% of pre-exposure values for about 7 months, with a return to pre-exposure levels in the following 4 yr. There was a progressive and significant (P less than 0.001) decline in platelet counts during the 52-month post-exposure period. The pattern of response in erythrocyte parameters was complex. Immediately after the accident, these values were less than the pre-exposure mean level; they gradually increased (P less than 0.001) for approximately 2 yr and then began a progressive decline (P less than 0.001).

Intra-arterial calcium infusion for hydrofluoric acid burns.

Between March 3, 1987 and Sept. 8, 1989, intra-arterial calcium infusions were used to treat 28 patients (38 extremities) suffering hydrofluoric acid (HF) exposures that failed to respond to topical treatments. Although 18 of the injuries occurred at work, only 1 patient was using HF in a concentration greater than 12%. Many of these products were available over the counter. Most patients did not wear protective equipment and had no concept of the danger of injury from the product. Onset of symptoms (pain, erythema and edema) was delayed from 1 to 6 h after exposure. Arterial catheters were placed and the patient was begun on a protocol using 10 ml of 10% calcium chloride diluted with 40 ml normal saline and infused over a 4-h period. Each patient was allowed a 4-8 h rest period before assessing the need for additional infusions. Blood calcium, magnesium, phosphorus, PT, and PTT were monitored. Infusions were repeated until there was no tenderness. Using tenderness as an end-point increased the number of infusions compared to previous reports. The mean number of infusions was 4.1 (range, 1-10). Success (complete healing) was 100%. There was a significant rise in serum calcium, but not to dangerous levels (range 9.3-12.8). There was also a significant fall in magnesium, which reached levels requiring magnesium intravenously. There were no significant changes in phosphorus, PT, and PTT.

[Intravenous drop of calcium gluconate for phosphorus burns].

20 patients with phosphor burn (TBSA 2%-75%) were cured by i.v. drop of calcium gluconate combined with other therapies including eschar conservation. Our experimental data showed that dogs with burn by spreading 85% phosphoric acid and napalm locally increased the level of plasma phosphorus and pathological damages to the heart, lung, kidney and etc were similar to those previously reported phosphorus burns. Intravenous drop of calcium gluconate after phosphate burn reduced the level of plasma phosphorus to normal rapidly and lessened the visceral damages. We consider that i.v. drop of calcium gluconate can accelerate the elimination of phosphorus, and prevent phosphorus poisoning after phosphorus burns.

[Effect of lamellar keratoplasty time on the production of serum specific antibody in corneal alkali burns].

OBJECTIVE: To observe the production of serum specific anti-denatured corneal antibody and the effects of lamellar keratoplasty on changes of corneal histopathology in different stages after alkali burns. METHODS: 20 male New Zealand rabbits, with alkali burns in right eye were randomly divided into 5 groups including: burned group; 2 early lamellar keratoplasty group (operation at 3 or 7 days post alkali burns respectively); 2 middle and later lamellar keratoplasty groups (operation at 2 or 5 weeks after alkali burns respectively). The level of serum specific antibody in each group was detected by ELISA and the corneal structure was evaluated by light and electron microscopy in different stages after alkali burns. RESULTS: The anti-denatured corneal antibody was induced after corneal alkali burns. The level of antibody significantly increased at 2th week post, peaking burn at 5 or 6th week, then decreasing. More antibodies were detected when contralateral eye was burn at 8 week post first burn. However, only slight increasing antibody was detected in early lamellar keratoplasty group. Furthermore, no significant changes of antibody production were observed in middle and later lamellar keratoplasty group. The light and electron microscopic analysis showed that, the corneal epithelium recovered better, the fibre of corneal stroma arranged better, inflammatory cells infiltrated less and neovascularization formed less in lamellar keratoplasty groups comparing to the burned group. The early lamellar keratoplasty groups recovered better than in middle and later lamellar keratoplasty groups. CONCLUSION: Early lamellar keratoplasty after corneal alkali burns can significantly decrease the immune response. Histopathological data also indicate that early lamellar keratoplasty can improve the tissue regeneration and recovery, prevent topical inflammatory reaction, and abate corneal neovascularization. This study suggests that early lamellar keratoplasty is more effective than the conservative treatment.

[Effect of dibunol on the course of experimental sinusitis]. / Vliianie dibunola na techenie éksperimental'nogo sinusita.

Experimental sinusitis in rabbits was induced by a chemical burn of the mucous membrane. Local application of dibunol decreased the intensity of the purulent inflammation in the sinuses and that of perifocal serous inflammation. Serous inflammation of the contralateral sinus was practically absent. The amount of the lipid peroxidation products in the circulating blood in rabbits receiving dibunol was close to the control and statistically lower than in animals not treated with dibunol. The activity of local acid phosphatase, glucuronidase, marker lysosomal hydrolases and that of myeloperoxidase was lower in animals treated with dibunol, particularly at the pick of inflammation, this was probably due to the dibunol stabilizing effect on the cell membranes.

[The parameters of the body immune reactivity in applying the therapeutic keratoplasty for the treatment of ocular burn lesions of extra severity]. / Pokazateli immunologicheskoi reaktivnosti organizma pri primenenii lechebnoi keratoplastiki v lechenii ozhogovoi bolezni glaz osobo tiazheloi stepeni.

One hundred and two (128 eyes) patients with stage 4 ocular burns underwent examinations. One-stage therapeutic keratoplasty was used in 67 (67.7%) patients. Retransplantation was made in 35 (34.3%) of patients due to graft rejection. According to the study, the more severe the clinical course of burn lesions is (cases that necessitated transplantation in the present research), the more pronounced changes are observed in the body immune reactivity of victims. In particular, the below peculiarities were observed: a progressing reduction of the contents of lymphocytes' and of B-lymphocytes; and a diminishing phagocytic activity of neutrophils in the peripheral blood registered at the terminal treatment stage in the patients after retransplantation versus the 1st-group patients with a more favorable clinical course. The compensatory increase of T-lymphocytes, T-helpers and of IgA, IgG was found to be less pronounced in group 2. A notably more intense sensitization response of the body to corneal antigens was established in the patients after retransplantation, which was a basis for using this index as a prognostication test in respect to the graft rejection crisis.

Designing of mouse model: a new approach for studying sulphur mustard-induced skin lesions.

This study was planned to design a mouse model for studying sulphur mustard (SM)-induced skin injury. SM was applied dermally at dose of 5 or 10 mg kg(-1) in polyethyleneglycol-300 (PEG-300) or dimethylsulphoxide (DMSO) or acetone once. The changes in body weight, organ body weight indices (OBWI) and haematological and oxidative stress parameters were investigated over a period of 3-7 days and supported by histopathological observations. Exposure to SM in PEG-300 or DMSO resulted in a significant depletion in body weight, OBWI, hepatic glutathione (GSH) and elevation in hepatic lipid peroxidation, without affecting the blood GSH and hepatic oxidised glutathione (GSSG) levels. Interestingly, no aforesaid change was observed after dermal application of SM diluted in acetone. These biochemical changes were supported by the histological observations, which revealed pronounced toxic effect and damage to liver, kidney and spleen after dermal application of SM diluted in PEG-300 or DMSO. The skin showed similar microscopic changes after dermal application of SM in all the three diluents, however; the severity of lesions was found to be time and dose dependent. It can be concluded that dermal exposure of SM diluted in acetone can be used to mimic SM-induced skin toxicity without systemic toxicity in a mouse model.