S2k guideline for diving accidents.

For the purposes of this guideline, a diving accident is defined as an event that is either potentially life-threatening or hazardous to health as a result of a reduction in ambient pressure while diving or in other hyperbaric atmospheres with and without diving equipment. This national consensus-based guideline (development grade S2k) presents the current state of knowledge and recommendations on the diagnosis and treatment of diving accident victims. The treatment of a breath-hold diver as well as children and adolescents does not differ in principle. In this regard only unusual tiredness and itching without visible skin changes are mild symptoms. The key action statements: on-site 100% oxygen first aid treatment, immobilization/no unnecessary movement, fluid administration and telephone consultation with a diving medicine specialist are recommended. Hyperbaric oxygen therapy (HBOT) remains unchanged as the established treatment in severe cases, as there are no therapeutic alternatives. The basic treatment scheme recommended for diving accidents is hyperbaric oxygenation at 280 kPa.

S2k guideline diagnosis and treatment of carbon monoxide poisoning.

Carbon monoxide (CO) can occur in numerous situations and ambient conditions, such as fire smoke, indoor fireplaces, silos containing large quantities of wood pellets, engine exhaust fumes, and when using hookahs. Symptoms of CO poisoning are nonspecific and can range from dizziness, headache, and angina pectoris to unconsciousness and death. This guideline presents the current state of knowledge and national recommendations on the diagnosis and treatment of patients with CO poisoning. The diagnosis of CO poisoning is based on clinical symptoms and proven or probable exposure to CO. Negative carboxyhemoglobin (COHb) levels should not rule out CO poisoning if the history and symptoms are consistent with this phenomenon. Reduced oxygen-carrying capacity, impairment of the cellular respiratory chain, and immunomodulatory processes may result in myocardial and central nervous tissue damage even after a reduction in COHb. If CO poisoning is suspected, 100% oxygen breathing should be immediately initiated in the prehospital setting. Clinical symptoms do not correlate with COHb elimination from the blood; therefore, COHb monitoring alone is unsuitable for treatment management. Especially in the absence of improvement despite treatment, a reevaluation for other possible differential diagnoses ought to be performed. Evidence regarding the benefit of hyperbaric oxygen therapy (HBOT) is scant and the subject of controversy due to the heterogeneity of studies. If required, HBOT should be initiated within 6 h. All patients with CO poisoning should be informed about the risk of delayed neurological sequelae (DNS).

Application of MR diffusion imaging for non-invasive assessment of acute kidney injury after lung transplantation.

To assess whether MR diffusion imaging may be applied for non-invasive detection of renal changes correlating with clinical diagnosis of acute kidney injury (AKI) in patients after lung transplantation (lutx).Fifty-four patients (mean age 49.6, range 26-64 years) after lutx were enrolled in a prospective clinical study and underwent functional MR imaging of the kidneys in the early postoperative period. Baseline s-creatinine ranged from 39 to 112 µmol/L. For comparison, 14 healthy volunteers (mean age 42.1, range 24-59 years) underwent magnetic resonance imaging (MRI) using the same protocol. Renal tissue injury was evaluated using quantification of diffusion and diffusion anisotropy with diffusion-weighted (DWI) and diffusion-tensor imaging (DTI). Renal function was monitored and AKI was defined according to Acute-Kidney-Injury-Network criteria. Statistical analysis comprised one-way ANOVA and Pearson correlation.67% of lutx patients (36/54) developed AKI, 47% (17/36) had AKI stage 1, 42% (15/36) AKI stage 2, and 8% (3/36) severe AKI stage 3. Renal apparent diffusion coefficients (ADCs) were reduced in patients with AKI, but preserved in transplant patients without AKI and healthy volunteers (2.07 ±â€Š0.02 vs 2.18 ±â€Š0.05 vs 2.21 ±â€Š0.03 × 10 mm/s, P < .05). Diffusion anisotropy was reduced in all lutx recipients compared with healthy volunteers (AKI: 0.27 ±â€Š0.01 vs no AKI: 0.28 ±â€Š0.01 vs healthy: 0.33 ±â€Š0.02; P < .01). Reduction of renal ADC correlated significantly with acute loss of renal function after lutx (decrease of renal function in the postoperative period and glomerular filtration rate on the day of MRI).MR diffusion imaging enables non-invasive assessment of renal changes correlating with AKI early after lutx. Reduction of diffusion anisotropy was present in all patients after lutx, whereas marked reduction of renal ADC was observed only in the group of lutx recipients with AKI and correlated with renal function impairment.

[Evaluation and assessment of the health care process in patients with carbon monoxide poisoning in Germany]. / Evaluation und Beurteilung des Versorgungsprozesses von Patienten mit Kohlenmonoxidvergiftung in Deutschland.

BACKGROUND: Carbon monoxide poisoning (COP) is the most common cause for poisoning by inhalation in Germany. In the past 8 years, a marked increase in the number of COP-related deaths has been registered nationwide. A national German guideline is missing. METHODS: The national and international literature was screened systematically. Existing international guidelines and expert recommendations for the diagnosis and treatment of COP were compared and evaluated. Furthermore, quality of health care was analyzed by a prospective preclinical dataset of emergency rescue services and retrospective analysis of routine data from 2014 to 2016 in Germany. RESULTS: There is not a single evidence-based guideline worldwide. We determined 8 key performance indicators based on the five recommendations available for treatment of COP. These indices were subdivided into prehospital terms, hospital facilities, and diagnostic and therapeutic measures performed; they act as indicators for quality of care. In particular, the key figure "start oxygen" revealed that up to 41 % of the patients had not been treated with inhaled oxygen. In summary, data capture showed considerable incompleteness that is mainly due to missing time stamps. CONCLUSION: In order to achieve a consistent treatment of patients with COP which meets the standard of recommended care, there is an urgent need for a consented national guideline. Another objective is to establish a nationwide prospective registry evaluating the treatment of carbon monoxide poisoning.

Carbon monoxide poisoning from waterpipe smoking: a retrospective cohort study.

OBJECTIVE: Waterpipe smoking may increasingly account for unintentional carbon monoxide poisoning, a serious health hazard with high morbidity and mortality. We aimed at identifying waterpipe smoking as a cause for carbon monoxide poisoning in a large critical care database of a specialty care referral center. METHODS: This retrospective cohort study included patients with a history of exposure to waterpipe smoking and carbon monoxide blood gas levels >10% or presence of clinical symptoms compatible with CO poisoning admitted between January 2013 and December 2016. Patients' initial symptoms and carbon monoxide blood levels were retrieved from records and neurologic status was assessed before and after hyperbaric oxygen treatment. RESULTS: Sixty-one subjects with carbon monoxide poisoning were included [41 males, 20 females; mean age 23 (SD ± 6) years; range 13-45] with an initial mean carboxyhemoglobin of 26.93% (SD ± 9.72). Most common symptoms included syncope, dizziness, headache, and nausea; 75% had temporary syncope. Symptoms were not closely associated with blood COHb levels. CONCLUSION: CO poisoning after waterpipe smoking may present in young adults with a wide variability of symptoms from none to unconsciousness. Therefore diagnosis should be suspected even in the absence of symptoms.

The Diagnosis and Treatment of Carbon Monoxide Poisoning.

BACKGROUND: The symptoms of carbon monoxide (CO) poisoning are nonspecific, ranging from dizziness and headache to unconsciousness and death. A German national guideline on the diagnosis and treatment of this condition is lacking at present. METHODS: This review is based on a selective literature search in the PubMed and Cochrane databases, as well as on existing guidelines from abroad and expert recommendations on diagnosis and treatment. RESULTS: The initiation of 100% oxygen breathing as early as possible is the most important treatment for carbon monoxide poisoning. In case of CO poisoning, the reduced oxygen-carrying capacity of the blood, impairment of the cellular respiratory chain, and immune-modulating processes can lead to tissue injury in the myocardium and brain even after lowering of the carboxyhemoglobin (COHb) concentration. In patients with severe carbon monoxide poisoning, an ECG should be obtained and biomarkers for cardiac ischemia should be measured. Hyperbaric oxygen therapy (HBOT) should be critically considered and initiated within six hours in patients with neurologic deficits, unconsciousness, cardiac ischemia, pregnancy, and/or a very high COHb concentration. At present, there is no general recommendation for HBOT, in view of the heterogeneous state of the evidence from multiple trials. Therapeutic decision-making is directed toward the avoidance of sequelae such as cognitive dysfunction and cardiac complications, and the reduction of mortality. Smoke intoxication must be considered in the differential diagnosis. The state of the evidence on the diagnosis and treatment of this condition is not entirely clear. Alternative or supplementary pharmacological treatments now exist only on an experimental basis. CONCLUSION: High-quality, prospective, randomized trials that would enable a definitive judgment of the efficacy of HBOT are currently lacking.

Olive Oil-Based Lipid Emulsions Do Not Influence Platelet Receptor Expression in Comparison to Medium and Long Chain Triglycerides In vitro.

Lipid emulsions influence platelet aggregation and receptor expression. However, the effect on platelet function is not fully explained. Therefore, the aim of this study was to examine the influence of the lipids Lipofundin®, Lipidem® and ClinOleic® on surface expressions of P-selectin, GPIb and GPIIb/IIIa on platelets in vitro. Whole blood was incubated in two different concentrations (0.06 and 0.6 mg/ml) of LCT/MCT, n-3/LCT/MCT and LCT-MUFA for 30 min, followed by activation with TRAP-6 or ADP for flow-cytometric assay. Rates of P-selectin, GPIb and GPIIb/IIIa expression were analyzed. There was a significant increase in GPIIb/IIIa- and P-selectin-expression after incubation with LCT/MCT and n-3/LCT/MCT at the concentration of 0.6 mg/ml, without and after stimulation with TRAP-6 and ADP. GPIb was significantly decreased. Accordingly, LCT-MUFA had no effect on receptor expression of platelets in vitro. We demonstrated that LCT-MUFA did not activate receptor expression of platelets whereas LCT/MCT significantly increased platelet aggregation in vitro. This finding should be noted for parenteral nutrition of intensive care patients and, in the future, might provide further insight into the pathogenic pathways of acute thromboembolic events. However, prospectively designed clinical studies are needed to support our results.

[Hyperbaric therapy and diving medicine - hyperbaric therapy part 1: evidence-based emergency care]. / Hyperbare Therapie und Tauchmedizin - Hyperbare Therapie Teil 1: evidenzbasierte Akutversorgung.

Hyperbaric oxygen therapy (HBOT), i. e. breathing pure oxygen at elevated ambient pressure, remains the gold standard of care in treating air or gas embolism and decompression illness. Guidelines are less clear on the value of HBOT in acute management of carbon monoxide (CO) poisoning or clostridial necrosis. To evaluate the evidence of clinical efficacy of HBOT we performed a systematic literature review. Part 1 assesses acute indications such as air or gas embolism, decompression sickness, CO-poisoning, clostridialmyonecrosis, necrotizing problem wounds, acute traumatic wounds and arterial retinal occlusion. Part 2 discusses further uses of HBOT as adjuvant treatment and highlights problems in assessing the value of HBOT using evidence-based medicine criteria.

[Hyperbaric therapy and diving medicine - hyperbaric therapy part 2: adjuvant therapy]. / Hyperbare Therapie und Tauchmedizin - Hyperbare Therapie Teil 2: adjuvante Therapieoptionen.

Hyperbaric oxygen therapy (HBOT), i. e. breathing pure oxygen at elevated ambient pressure, remains the gold standard of care in treating air or gas embolism and decompression illness. Guidelines are less clear on the value of HBOT in acute management of carbon monoxide (CO) poisoning or clostridial necrosis. To evaluate the evidence of clinical efficacy of HBOT we performed a systematic literature review. Part 1 assesses acute indications such as air or gas embolism, decompression sickness, CO-poisoning, clostridialmyonecrosis, necrotizing problem wounds, acute traumatic wounds and arterial retinal occlusion. Part 2 discusses further uses of HBOT as adjuvant treatment and highlights problems in assessing the value of HBOT using evidence-based medicine criteria.

Neoadjuvant targeted therapy in a primary metastasized renal cell cancer patient leads to down-staging of inferior vena cava thrombus (IVC) enabling a cardiopulmonary bypass-free tumor nephrectomy: a case report.

BACKGROUND: We report on a 62-year-old gentleman presenting at our urological department with an advanced renal cell cancer of the right kidney (10 cm in diameter), with an extensive caval vein thrombus (level IV) and bilateral pulmonary metastases. Another suspicious lesion at the left hemithorax was radiologically described. METHOD: A presurgical, neoadjuvant systemic therapy with sunitinib, a tyrosine kinase inhibitor, was initiated for 4 cycles in total (50 mg/day; 4 weeks on/2 weeks off). The cytoreductive nephrectomy was performed following the fourth cycle of sunitinib and after a 14-day break. Transesophageal echocardiography was used for intraoperative monitoring of the caval vein thrombus. Systemic treatment with sunitinib was continued 4 weeks after surgery. RESULTS: A significant reduction in tumor size, metastatic sites and down-staging of IVC from level IV to level III according to Novick classification was achieved. CONCLUSION: Significant down-staging of the tumor caval vein thrombus which initially reached the right atrium enabled us to perform surgery limited to the abdominal cavity without extracorporeal circulation nor hypothermia.

Paediatric airway management in mucopolysaccharidosis 1: a retrospective case review.

CONTEXT: Airway management in children suffering from mucopolysaccharidosis 1 (Hurler syndrome) remains challenging despite advances in both treatment and airway management techniques. OBJECTIVES: Forty-one anaesthetic charts following ten children over a 6-year period (2004-2010) were reviewed with emphasis on airway problems. RESULTS: All children had early stem cell transplantation at the age of 2 years or earlier. Mean (SD) age was 5 (4.3) years. Mask ventilation was difficult in five of 41 (12%) anaesthetics or in three of ten children. There were 29 intubations. Direct laryngoscopy was described as difficult (Cormack and Lehane ≥3) on 11 occasions in five of ten children. There were three of 26 (12%) failed intubations with direct laryngoscopy. These situations were resolved by a fibre-optic procedure, by laryngeal mask airway (LMA) insertion or by use of a videolaryngoscope. A laryngeal mask airway was used 11 times to avoid invasive airway management and once when direct laryngoscopy was impossible. CONCLUSION: The airway management of children with mucopolysaccharidosis 1 remains critical, despite advances in both treatment and airway management techniques. Problems did not seem to increase as children grew older. We assume that technical improvements such as standardised use of the laryngeal mask airway or attached tube channel videolaryngoscopes as well as a stem cell transplantation treatment of the disease helped the management of older children with mucopolysaccharidosis 1.

Thyroid gland rupture: a rare case of respiratory distress.

BACKGROUND: Rupture of a normal thyroid gland after blunt cervical trauma is a rare case of airway compression. This case report describes the case of a 79-year-old woman who developed severe respiratory distress after a bicycle crash. CASE REPORT: Presenting about 2 h after the crash, the patient noted cervical swelling and increasing dyspnea. The diagnosis of thyroid gland rupture was made with a combination of computed tomography scan, cervical radiography, and bronchoscopy. Invasive airway management was required in the first few hours after the crash. The patient underwent a left hemithyroidectomy, and recovered without complications. CONCLUSION: This case report highlights the fact that thyroid gland rupture can be a threatening complication of blunt cervical trauma.

Potential of whole blood coagulation reconstitution by desmopressin and fibrinogen under conditions of hypothermia and acidosis--an in vitro study using rotation thrombelastometry.

BACKGROUND: Desmopressin (DDAVP) and fibrinogen improve platelet function and clot stability. We investigated the influence of DDAVP and fibrinogen on whole blood coagulation in an in vitro model of hypothermia and acidosis. METHODS: After IRB approval and written consent blood samples were taken from 10 healthy volunteers. Samples were prepared with hydrochloric acid to maintain--beside normal pH--reduced pH (∼7.2) and severely reduced pH (∼7.0), and were assigned to four treatment groups: addition of either isotonic saline for compensation of dilutional effects (ISO), desmopressin (DDAVP+), fibrinogen (FIB+), or both substances (DDAVP+FIB+). Baseline was ISO at 37°C and normal pH. Remaining samples were incubated for 30 min and measured at 32°. Rotation thrombelastometry (ROTEM) after extrinsically activation and fibrin polymerization was tested. Repeated measures ANOVA were performed (p < 0.05). RESULTS: Hypothermia and acidosis synergistically impaired whole blood coagulation. DDAVP+ normalized maximum clot firmness (MCF) at normal pH. Coagulation time (CT) was not affected. FIB+ normalized MCF at pH 7.35 and pH 7.2. CT was normalized independently of pH. DDAVP+FIB+ did not show additional effects to FIB+. Fibrin polymerization was increased by FIB+ and DDAVP+FIB+ independently of pH. DDAVP+ did not alter fibrin polymerization. CONCLUSION: DDAVP and fibrinogen increased whole blood coagulation under hypothermia. Acidosis diminished this effect. Thus, acidosis should be corrected first and then both substances could be used for bridging until normothermia can be achieved. In combination, the effects of fibrinogen were overwhelming DDAVP effects. Thus, combined administration did not show any benefit compared to fibrinogen administration alone.

Adrenoceptor stimulation does not affect ICAM-1 and VCAM-1 expression in vitro.

BACKGROUND: Endothelial adhesion molecules ICAM-1 (CD54) and VCAM-1 (CD106) mediate cellular adhesion and transcellular migration. Cell adhesion and diapedesis have a key role in the course of shock and sepsis. During severe sepsis, adrenoceptor agonist levels may be increased due to endogenous production or due to intensive care treatment. As yet, the influence of ß1 or ß2 agonists on adhesion molecule formation on endothelial cells has remained unclear. METHODS: Cultured human umbilical vein endothelial cells were stimulated with E. coli. Following bacterial stimulation the cells were incubated with either ß2 receptor agonist terbutaline or ß1 agonist norepinephrine. ICAM-1 and VCAM-1 expression were examined using flow cytometry. RESULTS: Administration of norepinephrine did not cause increases of both CD54 and CD106 in stimulated HUVEC. Compared to negative controls the bacterial stimulation itself led to an increase of adhesion molecules. Following administration of terbutaline no significant increase in CD54 expression was found. CONCLUSIONS: Bacterial stimulation led to an increase of adhesion molecule expression. Adrenoceptor stimulation of activated endothelial cells did not cause significant increases of cellular adhesion molecules.

Dependence of platelet function on underlying liver disease in orthotopic liver transplantation.

OBJECTIVE: The purpose of the present study was to explore the platelet function during the perioperative period of orthotopic liver transplantation (OLT) due to the underlying liver disease. METHODS: The blood coagulation parameters, platelet surface markers and the determination of platelet aggregation were analyzed in 34 patients who underwent OLT. Blood samples were drawn preoperatively, anhepatic, 10 min and 1 hour after reperfusion, 1 day, 3 and 7 days postoperatively. Conventional coagulation screens, thrombopoietin (TPO) serum levels, P-selectin, GPIIb/IIIa and GPIb binding sites on the surface of platelets as evaluated by flow cytometry and platelet aggregation response were measured. RESULTS: Coagulation factors, maximum aggregation and rate of aggregation were significantly different before transplantation due to the underlying liver disease. Further we found a markedly depressed GPIIb/IIIa and P-selectin expression and a reduced rate of aggregation in all patients throughout the study. In contrast maximum aggregation of platelets was restored on the third day after reperfusion without intergroup differences and almost comparable to healthy controls. An inverse correlation was found between peripheral platelet count pre-transplantation and peak TPO concentrations one weak post-transplantation. CONCLUSIONS: In the entire process of OLT, coagulation factors, maximum aggregation and rate of platelet aggregation depend on the surgical phases during transplantation and on the underlying liver disease. The data obtained in this study might contribute to a better understanding of the pathophysiology and assessment of bleeding risk in OLT.

Reduced post-operative neutrophil activation in liver transplant recipients suffering from post-hepatitic cirrhosis.

BACKGROUND: It has been supposed that liver transplant recipients with hepatitis C virus infection have a higher incidence of infectious complications after transplantation. This study was designed to investigate whether neutrophil function is immediately affected by liver transplantation. METHODS: Biochemical values, plasma levels of myeloperoxidase (MPO), hydrogen peroxide production of neutrophils and neutrophil-platelet complexes were analyzed in 32 patients who underwent liver transplantation and 20 healthy volunteers. RESULTS: MPO levels were significantly increased 24 h after reperfusion. In post-hepatitic patients levels were significantly lower three d up to one wk post-transplant than in patients due to other liver diseases. One wk post-operatively the respiratory burst activity following N-formyl-methionyl-leucylphenylalanine (fMLP) or (tumor necrosis factor-alpha) TNF-alpha/fMLP stimulation was depressed in post-hepatitic recipients. Respiratory burst stimulated with phorbol 12-myristate 13-acetate in these patients was increased one wk after transplantation. One d after transplantation the neutrophil-platelet complexes decreased significantly throughout the post-operative period. CONCLUSIONS: The results of this study suggest a reduced post-operative neutrophil activation in liver transplant recipients suffering from post-hepatitic cirrhosis compared to cirrhosis due to other causes. We hypothesized that neutrophil dysfunction in those patients depends on the underlying disease with an increased susceptibility to bacterial or fungal infections.

Alteration of anion gap and strong ion difference caused by hydroxyethyl starch 6% (130/0.42) and gelatin 4% in children.

BACKGROUND: Synthetic colloid administration is a common practice for preventing perioperative hypovolemia and consecutive circulatory failure in children. This prospective, randomized study was conducted to investigate the effects of two different unbalanced synthetic colloid solutions on acid-base equilibrium in children. METHODS: Fifty pediatric patients (aged 0-12 years) scheduled for major pediatric surgery were randomized to receive either 10 ml x kg(-1) of 6% hydroxyethyl starch solution 130/0.42 (HES) or 4% modified fluid gelatin (GEL) to maintain adequate systemic hemodynamics. Before and after colloid administration, a blood sample was collected to analyze hemoglobin, hematocrit, electrolytes, and acid-base parameters. The anion gap and the strong ion difference (SID) were calculated using standard formulas. RESULTS: Both HES and GEL administration caused a significant increase in plasma chloride concentration (P < 0.01) and an accompanying decrease in SID (P < 0.01). In the HES group, the anion gap decreased significantly (P < 0.01) whereas the anion gap remained stable in the GEL group. In both groups, initial actual base excess and pH did not change significantly after colloid administration. CONCLUSIONS: Moderate intraoperative plasma replacement with unbalanced synthetic colloids HES and GEL leads to a decrease in SID and, in the case of HES, to a significant decrease in the anion gap in children. These alterations may result in a possible misinterpretation when the anion gap and SID are used for differential diagnosis of metabolic disturbances during major pediatric surgery.

Unsaturated long-chain fatty acids induce the respiratory burst of human neutrophils and monocytes in whole blood.

BACKGROUND: It is increasingly recognized that infectious complications in patients treated with total parenteral nutrition (TPN) may be caused by altered immune responses. Neutrophils and monocytes are the first line of defence against bacterial and fungal infection through superoxide anion production during the respiratory burst. To characterize the impact of three different types of lipid solutions that are applied as part of TPN formulations, we investigated the unstimulated respiratory burst activation of neutrophils and monocytes in whole blood. METHODS: Whole blood samples were incubated with LCT (Intralipid(R)), LCT/MCT (Lipofundin(R)) and LCT-MUFA (ClinOleic(R)) in three concentrations (0.06, 0.3 and 0.6 mg ml-1) for time periods up to one hour. Hydrogen peroxide production during the respiratory burst of neutrophils and monocytes was measured by flow cytometry. RESULTS: LCT and LCT-MUFA induced a hydrogen peroxide production in neutrophils and monocytes without presence of a physiological stimulus in contrast to LCT/MCT. CONCLUSION: We concluded that parenteral nutrition containing unsaturated oleic (C18:1) and linoleic (C18:2) acid can induce respiratory burst of neutrophils and monocytes, resulting in an elevated risk of tissue damage by the uncontrolled production of reactive oxygen species. Contradictory observations reported in previous studies may in part be the result of different methods used to determine hydrogen peroxide production.

Ethanol-induced malfunction of neutrophils respiratory burst on patients suffering from alcohol dependence.

BACKGROUND: Polymorphonuclear, neutrophil granulocytes (PMN) play a major role in the control of infections, and people who abuse alcohol are susceptible to infections. Resistance against infections ensues intracellularly following initial phagocytosis of microorganisms with the oxygen-dependent respiratory burst, the key enzyme of which is the respiratory burst oxidase, whereby oxygen radicals are produced for microbial destruction. To date there is insufficient information available in connection with the process of impaired defence against infection in patients suffering from alcohol dependence. Therefore, our investigation was carried out to determine the influence of alcohol exposition on the formation of oxygen radicals and the respiratory burst. METHODS: 4.5 ml of whole blood was taken from 10 healthy adults and 10 patients suffering from alcohol dependence. An additional 3.5 ml of whole blood was taken from the alcoholic patients for determination of the blood alcohol concentration. The respiratory burst of PMN was tested using the Four-Colour-Continuous Flow Cytometer. Each experimental procedure consisted of 4 test samples [negative controls, Escherichia coli, FMLP-supplement (N-formyl-l-methionyl-l-leucyl-l-phenylalanin), PMA-supplement (phorbol-12-myristate-13-acetate)]. Differing concentrations of ethanol were also introduced to each of the tests performed (0.20 to 4.00 g/l). RESULTS: Ethanol revealed a marked decrease of burst activity in those patients suffering from alcoholism with increased alcohol concentration. A dependence between the burst activity and the ethanol concentration was seen to be statistically significant. This effect was only evident after stimulation with E. coli and FMLP in those patients with alcohol dependence. CONCLUSION: The results presented in this study show an impairment in the function of PMN in those patients addicted to alcohol due to the decrease in burst activity. In view of the results of the different stimuli, the second-messenger effects were not evident. A clarification of this phenomenon could well be assumed as an allosteric receptor effect on the burst oxidase, namely, a direct effect on the phagocytosis interaction between circulating granulocytes and causative organisms.