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."

[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.

[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.

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.

[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.

Hexafluorine vs. standard decontamination to reduce systemic toxicity after dermal exposure to hydrofluoric acid.

INTRODUCTION: Dermal exposure to hydrofluoric acid (HF) may cause severe burns and systemic toxicity. Hexafluorine (Prevor, France) is a product marketed as an emergency decontamination fluid for HF skin and eye exposures. Documentation concerning Hexafluorine is scanty, and a recent study indicates that its ability to reduce HF burns is at most equal to that of water. OBJECTIVE: The present study was conducted to evaluate Hexafluorine's capacity to reduce HF-induced systemic toxicity. METHODS: Sprague Dawley rats were anesthetized, catheterized in the left femoral artery, and shaved on their back. A filter paper (3.5 x 6 cm) was soaked in 50% HF and applied on the back of each rat for 3 min. Thirty seconds after removal of the paper, a 3-min rinsing with either 500 mL Hexafluorine (group H), 500 mL water (group W), or 500 mL water followed by a single application of 2.5% calcium gluconate gel (group Ca) was carried out. Blood samples were analyzed for ionized calcium and potassium (before injury and 1, 2, 3, and 4 h after) and also for ionized fluoride (1, 2, and 4 h after injury). RESULTS: The animals developed hypocalcemia, hyperkalemia, and hyperfluoridemia after the HF exposure. The only significant difference observed among the groups was in serum potassium at 1 h between group Ca and group W. However, there was a constant trend toward milder hypocalcemia and less pronounced hyperkalemia in group Ca compared to the other groups. There were no differences in the electrolyte disturbances between the Hexafluorine-treated animals and those treated with water only. Five of 39 animals died before completion of the experiment as a result of the HF exposure, one from group Ca and two from each of the other two groups. CONCLUSION: In this experimental study, decontamination with Hexafluorine was not more effective than water rinsing in reducing electrolyte disturbances caused by dermal exposure to hydrofluoric acid.

[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.

[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.

Arterial blood gas analysis in acute caustic ingestion injuries.

PURPOSE: Quickly differentiating patients who need emergency salvage operation for caustic ingestion injury from those who do not remains difficult. We thus conducted a retrospective study to assess whether arterial blood gas (ABG) analysis is helpful for deciding on the best management plan. METHODS: We divided 129 patients with caustic ingestion injuries into two groups according to treatment. Group 1 consisted of 30 patients who underwent surgery and two who should have. Group 2 consisted of 97 patients treated conservatively. The 30 operated patients in group 1 were further divided into two groups according to whether they survived (group 3) or died (group 4). We analyzed and compared ABG data between groups 1 and 2, and between groups 3 and 4. RESULTS: In groups 1 and 2, the mean pH was 7.22 +/- 0.12 and 7.38 +/- 0.06, respectively, and the mean base excess (BE) was -12.0 +/- 5.2 and -1.8 +/- 3.7, respectively. Both these values were significantly different between groups 1 and 2 (P < 0.001). In groups 3 and 4, the mean pH was 7.27 +/- 0.09 and 7.11 +/- 0.11, respectively, and the mean BE was -10.3 +/- 4.7 and -16.1 +/- 4.6, respectively. Both these values were significantly different between groups 3 and 4 (P < 0.001 and P < 0.005, respectively). CONCLUSIONS. ABG data can help make the right decision about treatment. An arterial pH lower than 7.22 or a BE lower than -12.0 indicates severe injury, and an emergency salvage operation should be seriously considered.

Predictors of esophageal stricture in children with unintentional ingestion of caustic agents.

BACKGROUND: Prediction of the severity of esophageal injury following ingestion of a caustic substance is a challenging problem for clinicians. It was hoped that risk factors for the early prediction of esophageal stricture in such patients could be identified in this study. METHODS: This study comprises an evaluation of 32 children with esophageal injury due to ingestion of caustic materials. Patients' signs and symptoms as well as laboratory data including leukocyte counts and C-reactive protein level were reviewed. RESULTS: Patients who presented with a greater number of symptoms and signs were inclined to have more severe esophageal injury and stricture. The frequency of symptoms and signs in patients with serious esophageal injury was higher than that in patients with low-grade injury. Patients with severe injury were more significantly associated with the occurrence of stricture. The characteristic of caustic ingestion was associated with esophageal stricture, but not esophageal injury. There was no statistically significant difference in leukocyte counts relative to severity of esophageal injury. The mean of leukocyte counts of patients with esophageal stricture was close to that of patients without esophageal stricture. There was also no statistically significant difference in C-reactive protein values between the 2 groups of patients. CONCLUSIONS: Leukocyte counts and C-reactive protein are not useful parameters for predicting the severity of esophageal injury and occurrence of stricture following injury to the esophagus by caustic materials. Alkali ingestion more probably leads to esophageal stricture than acid ingestion. After caustic ingestion, the presence of a greater number of symptoms and signs suggests a more-severe injury, which necessitates more-aggressive management.

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.

Systemic effects and skin injury after experimental dermal exposure to monochloroacetic acid.

There have been many fatal occupational accidents of skin exposure to monochloroacetic acid (MCA). However, there have been no reports of dermatological findings and the lethal consequences have not yet been demonstrated. Therefore, harmful local and systemic effects were investigated after dermal exposure to MCA. A 0.5 mL aliquot of MCA solution (40% w/w) was applied to the abdominal skin of ten 10-week-old male SD rats under anesthesia. The exposure area (25 x 25 mm2) was 1.6% of the total surface area. The dose of MCA per area was 34.1 mg/cm2. Saline was similarly administered to 10 control rats. Histopathological findings after 10 min were observed by light microscopy. Blood samples were collected by exsanguinations from the carotid arteries after 4 h. Skin samples were collected 10 min after the initial exposure. Histological findings showed severe degeneration of collagen bundles in the epidermis and subcutaneous tissues. P(CO2), HCO(3)-, TCO2, BE and glucose levels were decreased in the MCA group. AST, m-AST, ALT, BUN, Cr, NH3, lactic acid, pyruvic acid, RBC, Hb, Hct, total protein and albumin were increased in the MCA group. The burn was determined to be a third-degree burn on the basis of the histopathological findings. The severe toxicity was probably a consequence of the rapid permeability. Biochemical parameters were a consequence of hepatocellular injuries, renal dysfunction, dysglyconeogenesis and dysfunction of ammonia metabolism. MCA reportedly enters the TCA cycle and inhibits aconitase. MCA metabolites also inhibit pyruvate carboxylase in the gluconeogenesis pathway. Therefore, the important serum biochemical abnormalities such as hypoglycemia and lactic acidosis should be monitored to find the acute systemic disorders.

[The influence of the change in postburn erythrocyte membrane viscoelasticity on the regional myocardial blood flow].

OBJECTIVE: To explore the characteristics of the dynamic change in postburn erythrocyte membrane viscoelasticity and its influence on the regional myocardial blood flow. METHODS: Wistar rats inflicted with 30% TBSA III degree scalding on the back were employed as the model. The mechanical indices of erythrocytic membrane, such as elastic modulus and the coefficient of viscosity, were determined with micro-pipe sucking methods at preburn and 1, 3, 6, 12, 24 and 48 postburn hours (PBHs). The regional myocardial blood flow was simultaneously monitored with hydrogen clearance methods. RESULTS: The erythrocyte membrane viscoelasticity increased sharply at 3 PBH, reached the peak level at 6 PBH and decreased gradually thereafter to near normal level at 24 PBH. The regional myocardial blood flow decreased obviously at 1 PBH, it reached the lowest level at 6 PBH and bounced back to near normal level at 48 PBHs. The change in the viscoelasticity was significantly and negatively correlated to that of the regional myocardial blood flow. CONCLUSION: The deformability of postburn erythrocyte membrane decreased, leading to the decrease in the regional myocardial blood flow. This might be one of the important reasons of postburn myocardial injury.

Interpretation of accelerants in blood of cadavers found in the wreckage after fire.

Accelerants in the blood of 73 cadavers found in wreckage after fire were analyzed by gas chromatography (GC) and a combination of gas chromatography-mass spectrometry (GC-MS) to decide whether accelerants containing petroleum components had been used and whether the cadavers had been exposed to fire before or after death. In 16 of 26 cases in which accelerants were used to start a fire before death, accelerants were detected in the blood. In 7 cases in which accelerants were used to start a fire, the victims were determined to have been exposed to the vapor of accelerants after death because no accelerants were detected in the blood, no soot was found in the airways, and carboxyhemoglobin (COHb) concentrations were not higher than those found in smokers. In 9 of 34 cases in which accelerants were suspected to have been used to start a fire before death, accelerants were detected in the blood. When soot is not detectable by the unaided eye in the airways of a victim found in debris of a fire in which the use of accelerants is suspected, or the COHb concentration in the blood is no higher than in a smoker, analysis of accelerants in the blood seems to be helpful in determining the cause of death and whether inflammable were used.