Neuromuscular Dysfunction in Experimental Sepsis and Glutamine.

BACKGROUND: Electrophysiological studies show that critical illness polyneuromyopathy appears in the early stage of sepsis before the manifestation of clinical findings. The metabolic response observed during sepsis causes glutamine to become a relative essential amino acid. AIMS: We aimed to assess the changes in neuromuscular transmission in the early stage of sepsis after glutamine supplementation. STUDY DESIGN: Animal experimentation. METHODS: Twenty male Sprague-Dawley rats were randomized into two groups. Rats in both groups were given normal feeding for one week. In the study group, 1 g/kg/day glutamine was added to normal feeding by feeding tube for one week. Cecal ligation and perforation (CLP) surgery was performed at the end of one week. Before and 24 hours after CLP, compound muscle action potentials were recorded from the gastrocnemius muscle. RESULTS: Latency measurements before and 24 hours after CLP were 0.68±0.05 ms and 0.80±0.09 ms in the control group and 0.69±0.07 ms and 0.73±0.07 ms in the study group (p<0.05). CONCLUSION: Since enteral glutamine prevented compound muscle action potentials (CMAP) latency prolongation in the early phase of sepsis, it was concluded that enteral glutamine replacement might be promising in the prevention of neuromuscular dysfunction in sepsis; however, further studies are required.

Predictive Value of Brain Arrest Neurological Outcome Scale (BrANOS) on Mortality and Morbidity After Cardiac Arrest.

OBJECTIVE: There are several prediction scales and parameters for prognosis after a cardiac arrest. One of these scales is the brain arrest neurological outcome scale (BrANOS), which consists of duration of cardiac arrest, Glasgow Coma Scale score and Hounsfield unit measured on cranial computed tomography (CT) scan. The objective of this study is to investigate the effectiveness of BrANOS on predicting the mortality and disability after a cardiac arrest. METHODS: We retrospectively investigated cardiac arrest patients who were hospitalized in our intensive care unit (ICU) within a 3-year period. Inclusion criteria were age over 18 years old, survival of more than 24 hours after cardiac arrest and availability of cranial CT. We recorded the age, sex, diagnosis, duration of cardiac arrest and hospital stay, mortality, Glasgow Outcome Score (GOS) and BrANOS score. The primary endpoint of the study was to establish the relationship between mortality and BrANOS score in patients who survived for more than 24 hours after a cardiac arrest. The secondary endpoint of the study was to determine the 2-year life expectancy and GOS after cardiac arrest. RESULTS: The mean age of the patients was 57±17 years (33 females, 67 males). ICU mortality rate was 57%. The BrANOS mean score was 10.3±3.2. There was a significant difference between survivors and non-survivors in terms of the BrANOS score (8.8±3.2 vs. 11.6±2.7; p<0.001). BrANOS reliably predicted the survival with a ROC area under the curve of 0.733. The scale of >14 predicted death with 100% accuracy. All the patients without disability had a BrANOS score of <10. The BrANOS score also correlated well with GOS (p<0.001). The 2-year life expectancy rate was 31% in patients who survived more than 24 hours after a cardiac arrest. CONCLUSION: In this study, we demonstrated that BrANOS provided reliable data for prognostic evaluation after a cardiac arrest.

Neuromuscular Functions on Experimental Acute Methanol Intoxication.

OBJECTIVE: The incidence of accidental or suicidal ingestion of methyl alcohol is high and methyl alcohol intoxication has high mortality. Methyl alcohol intoxication causes severe neurological sequelae and appears to be a significant problem. Methyl alcohol causes acute metabolic acidosis, optic neuropathy leading to permanent blindness, respiratory failure, circulatory failure and death. It is metabolised in the liver, and its metabolite formic acid has direct toxic effects, causing oxidative stress, mitochondrial damage and increased lipid peroxidation associated with the mechanism of neurotoxicity. Methanol is known to cause acute toxicity of the central nervous system; however, the effects on peripheral neuromuscular transmission are unknown. In our study, we aimed to investigate the electrophysiological effects of experimentally induced acute methanol intoxication on neuromuscular transmission in the early period (first 24 h). METHODS: After approval by the Animal Experiment Ethics Committee of Ege University, the study was carried out on 10 Wistar rats, each weighing about 200 g. During electrophysiological recordings and orogastric tube insertion, the rats were anaesthetised using intra-peritoneal (IP) injection of ketamine 100 mg kg(-1) and IP injection of xylazine 10 mg kg(-1). The rats were given 3 g kg(-1) methyl alcohol by the orogastric tube. Electrophysiological measurements from the gastrocnemius muscle were compared with baseline. RESULTS: Latency measurements before and 24 h after methanol injection were 0.81±0.11 ms and 0.76±0.12 ms, respectively. CMAP amplitude measurements before and 24 h after methanol injection were 9.85±0.98 mV and 9.99±0.40 mV, respectively. CMAP duration measurements before and 24 h after methanol injection were 9.86±0.03 ms and 9.86±0.045 ms, respectively. CONCLUSION: It was concluded that experimental methanol intoxication in the acute phase (first 24 h) did not affect neuromuscular function.

Recurrent Spontaneous Pneumothorax during the Recovery Phase of ARDS Due to H1N1 Infection.

The pregnant patients are prone to influenza A (H1N1) virus infection, which may rapidly progress to lower respiratory tract infection and subsequent respiratory failure and acute respiratory distress syndrome (ARDS). Pneumothorax might develop in ARDS under mechanical ventilation. But post-ARDS pneumothorax in spontaneously breathing patient has not been reported in the literature. We report a 31-year old pregnant woman infected with influenza A (H1N1) virus and progressed to ARDS. Mechanical ventilation with high PEEP improved patient's gas exchange parameters within 3 weeks. However spontaneous pneumothorax was developed one week after she weaned off the ventilator. After successful drainage therapy, the patient was discharged. However she re-admitted to the hospital because of a recurrent pneumothorax one week later. She was discharged in good health after being treated with negative continuous pleural aspiration for 10 days. Influenza might cause severe pulmonary infection and death. In addition to diffuse alveolar damage, sub-pleural and intrapulmonary air cysts might occur in influenza-related ARDS and may lead to spontaneous pneumothorax. This complication should always be considered during the recovery period of ARDS and a long-term close follow-up is necessary.

Effects of IgM-enriched immunoglobulin and fluid replacement on nerve conduction velocity in experimental sepsis.

BACKGROUND: Neuromuscular abnormalities in sepsis, termed critical illness polyneuropathy (CIP), have been suggested to be induced by inflammatory mechanisms and/or relative hypovolemia. CIP is characterized by early electrophysiological findings before the clinical symptoms. This study aimed to investigate the effect of intravenous immunoglobulin (IVIG) and volume replacement therapies on the possible nerve conduction velocity (NCV) alterations in the early phase of experimental sepsis. METHODS: Forty-six Sprague-Dawley rats were randomly assigned to four groups. Cecal ligation/perforation was performed to induce experimental sepsis. NCV was assessed in the tail nerve. RESULTS: There was no statistically significant difference in NCV levels within and among the Sham-operated, colloid- and IVIG-treated groups. In the sepsis without treatment group, there was a statistically significant decrease in NCV levels. CONCLUSION: NCV is decreased in the early stage of experimental sepsis and it may be accepted as an early electrophysiological sign in CIP. Treatment with either IgM-enriched IVIG or early volume replacement appears to prevent the decrease in NCV in the early phase of experimental sepsis. Results were statistically indistinguishable between the IVIG- and colloid-treated groups. No statistical difference between these groups is noteworthy. There is a need to clarify the mechanisms of action with further randomized, clinical and experimental trials.

Nutritional risk of hospitalized patients in Turkey.

BACKGROUND & AIMS: We conducted a multicentre study to assess nutritional risk at hospital admission, hospital-associated iatrogenic malnutrition and the status of nutritional support in Turkish hospitals. METHODS: A database which allowed for online submission of hospital and patient data was developed. A nutritional risk screening system (NRS-2002) was applied to all patients and repeated weekly in patients with hospital stays greater than one week and no invasive procedures. Patient-specific nutritional support was recorded during the study period. RESULTS: Thirty-four hospitals from 19 cities contributed data from 29,139 patients. On admission, 15% of patients had nutritional risk. Nutritional risk was common (52%) in intensive care unit patients and lowest (3.9%) in otorhinolaryngology patients. Only 51.8% of patients with nutritional risk received nutritional support. Nutritional risk was present in 6.25% of patients at the end of the first week and 5.2% at the end of the second week, independent of nutritional support. In patients with nutritional risk on admission who were hospitalized for two weeks and received nutritional support, the NRS-2002 score remained > or =3 in 83% of cases. CONCLUSIONS: Nutritional risk is common in hospitalized Turkish patients. While patients at nutritional risk often do not receive nutritional support when hospitalized, nutritional risk occurs independent of nutritional support.

Thermogenic and metabolic response to amino acid solution in brain-dead patients.

BACKGROUND: There is a strong correlation between amino acid infusion and increase in energy expenditure and thermogenesis. In this study, the effects of amino acid solutions on thermogenesis and energy expenditure were investigated in intensive care patients who were diagnosed as brain death. METHODS: Twenty-six brain-dead patients were included in the study. The patients received a 4 h infusion of standard amino acid solution. Energy expenditure was measured by indirect calorimetric method. ANOVA and Bonferroni tests were used for statistical analysis. RESULTS: The predicted energy expenditure (PEE) values were higher than the resting energy expenditure (REE) values in 24 patients. The mean REE/PEE value in all patients indicated that there was a 29% decrease in REE when compared to PEE. Body temperature and energy expenditure values were not increased during the parenteral infusion of amino acid solutions. There was no statistically significant difference between mean metabolic measurements and basal values at any time interval during the study period. CONCLUSION: We conclude that the stimulatory effect of amino acid solution on energy expenditure and thermogenesis is abolished in brain-dead patients. This result may indicate a possible central pathway responsible for the increase in energy expenditure and thermogenesis.

Neuromuscular deterioration in the early stage of sepsis in rats.

INTRODUCTION: Critical illness polyneuropathy (CIP) is a clinical condition frequently seen in patients being treated in critical care units in the final stage of sepsis. The etiopathology of CIP is still unclear, and the onset time of appearance of the electrophysiological findings has not been elucidated. The very little research that has been carried out on this topic is limited to clinical electrophysiological and histopathological studies. In this study, electrophysiological alterations in the early stage of experimentally induced sepsis were investigated in septic rats. METHODS: We conducted a prospective, randomized, controlled experimental study in an animal basic science laboratory with 30 male Sprague-Dawley rats, weighing 200 to 250 g. All of the rats were randomly assigned to one of two groups. In the sepsis group (n = 20), cecal ligation and puncture (CLP) was performed to induce experimental sepsis. In the sham-operated group (n = 10), laparotomy without CLP was performed. Before and 24 hours after CLP and laparotomy, the right sciatic nerve was stimulated from the sciatic notch and compound muscle action potentials (CMAPs) were recorded from the gastrocnemius muscle. Recordings of latency, amplitude, and duration of the CMAP were evaluated. RESULTS: CMAP durations before and 24 hours after surgery were 0.45 +/- 0.05 ms and 0.48 +/- 0.05 ms, respectively, in the sham-operated group and 0.46 +/- 0.05 ms and 0.55 +/- 0.01 ms, respectively, in the sepsis group. Latency measurements in the sham-operated group were 0.078 +/- 0.010 ms and 0.080 +/- 0.015 ms, respectively, whereas measurements were found to be prolonged in the sepsis group: 0.094 +/- 0.015 ms and 0.149 +/- 0.054 ms before and 24 hours after surgery, respectively (p < 0.05). CMAP amplitudes in the sham-operated group before and 24 hours after surgery were 8.41 +/- 0.79 mV and 8.28 +/- 1.92 mV, respectively, whereas in the sepsis group the amplitude measurements decreased to 7.60 +/- 1.75 mV and 4.87 +/- 3.44 mV, respectively (p < 0.05). CONCLUSION: The results of the study indicate that electrophysiological alterations appear in the first 24 hours after experimental sepsis and are characterized by an increase in latency and a decrease in CMAP amplitude. The results also suggest that electrophysiological findings seen in patients with CIP might appear before clinical signs of CIP.

An interesting thinner intoxication case: intrathoracic injection.

Thinners, including aromatic hydrocarbons such as toluene, xylene, and N-hexane, are widely used in industry for the production of plastics, varnish, paint, and glue. Use of these toxic agents frequently leads to chronic intoxication caused by abuse or misuse of solvents, which are usually taken in through inhalation. Thinners may have neurotoxic, myotoxic, hepatotoxic, nephrotoxic, and cardiotoxic systemic effects. The patient described in this report attempted to commit suicide by injecting 10 cc thinner into the left hemithorax. Acute chemical empyema developed at the left hemithorax. No bacterial growth was noted in empyema liquid and blood samples. Empyema was treated with tube thoracostomy, and full remission was observed after 33 d. No systemic toxic signs were noted, other than a low level of hepatotoxicity. Although pleural effusion, atelectasis, and pleural thickening were observed at the acute phase on computed tomography (CT) of the thorax, only pleural thickening persisted on CT of the thorax after 1 y. Investigators could not find a documented case of parenteral use of thinners in the medical literature.

The comparison of therapeutic effects of atropine and pralidoxime on cardiac signs in rats with experimental organophosphate poisoning.

Organophosphate poisoning causes disturbances in cardiac conduction and potentially fatal severe cardiac rhythm abnormalities. This study investigated the cardiac effects of atropine and pralidoxime in the treatment of organophosphate poisoning in rats. Three groups of 10 adult male Wistar rats were anesthetized with an intraperitoneal injection of ketamine 100 mg/kg and xylazine 10 mg/kg and connected to a computerized electrocardiographic monitor. Each rat was then injected intraperitoneally with the pesticide dichlorvos 70 mg/kg. Sixty seconds after the injection, 10 rats were injected with saline, 10 with pralidoxime mesylate 20 mg/kg, and 10 with atropine 10 mg/kg. During the computerized electrocardiographic monitoring, each rat's heart rate and QT(c) intervals were recorded and analyzed as the injections were administered. The heart rates in all 3 groups did not differ before the dichlorvos was administered, nor at 60 seconds afterward, but in the atropine group, the time elapsed before the first decline in heart rate was significantly longer than that in the control group (P<.05). In addition, the interval before death was significantly longer in the atropine group than in either the control group or the pralidoxime group (P<.05 for both). The QT(c) was almost identical in each of the groups. Atropine has beneficial effects on the heart rate, prolongs the time before the heart rate declines, and delays death but has no effect on the QT(c) interval. Further research about the toxic effects of organophosphate compounds on myocardial cells is warranted.

The effects of N-acetylcysteine on oxidative stress in organophosphate poisoning model.

Organophosphate compounds act by irreversible inhibition of cholinesterase. In addition to their muscarinic, nicotinic, and central nervous system effects, some organophosphate insecticides cause oxidative stress by increasing lipid peroxidation in erythrocytes and by increasing levels of the enzymes superoxide dismutase and catalase. In this study, the effects of an antioxidant, N-acetylcysteine (NAC), in organophosphate poisoning were investigated. After obtaining Animal Ethics Committee approval, 16 male Wistar rats were divided into 2 groups. Following anesthesia, rats were tracheostomized and mechanically ventilated. Invasive hemodynamic monitoring was begun and all rats were injected with 70 mg/kg of dichlorvos (DDVP) intraperitoneally. The rats in group 1 received placebo intravenous 0.9% NaCl and the rats in group 2 received 150 mg/kg intravenous NAC. Blood samples were obtained before injection of DDVP and 60 minutes after injection to determine levels of malondialdehyde, superoxide dismutase, and catalase. Hemodynamic data and biochemistry test results were compared by analysis of variance and Wilcoxon test. P<.05 was regarded as statistically significant. Superoxide dismutase and malondialdehyde levels were significantly increased in group 1 while no difference was observed in group 2. It was concluded that organophosphate compounds might cause oxidative stress by interfering with antioxidant defense mechanisms in erythrocytes and that NAC might prevent increased lipid peroxidation. In addition to classic treatments, drugs with antioxidant effects might therefore be promising in the treatment of organophosphate poisoning.

The effects of standard and branched chain amino acid enriched solutions on thermogenesis and energy expenditure in unconscious intensive care patients.

BACKGROUND & AIMS: This study aims to compare the effects of standard and branched chain amino acid enriched solutions on thermogenesis and energy expenditure in unconscious and mechanically ventilated intensive care patients. DESIGNS: The study was carried out at multidisciplinary intensive care unit. Twenty unconscious and mechanically ventilated patients (18-65 years of age) were included in the study. Patients were hemodynamically stable and all received continuous enteral nutrition. Energy expenditure was calculated using the Harris-Benedict Equation for all of the patients. Patients were randomly assigned to receive a 4h infusion of 0.4 g/kg protein as amino acid solution. Group I (n = 10) received standard amino acid solution and group II (n = 10) received branched chain amino acid enriched solution. Energy expenditure, oxygen consumption and carbon dioxide production were measured by indirect calorimetric method every 30 min during the 4h infusion period and 3h thereafter. Rectal temperature was recorded concomitantly with the metabolic measurements throughout the study. RESULTS: There was a statistically significant increase in body temperature during the infusion of amino acid solution between 30 and 210 min in group I and between 30 and 120 min in group II (P <0.05). We observed a significant increase in energy expenditure at 30, 150, 180 and 210 min in group I and at 30-240 min in group II (P <0.05). There were no differences between the two groups in terms of thermogenesis or energy expenditure values during the study (P >0.05). CONCLUSION: Thermogenesis and energy expenditure values were increased during the parenteral infusion of both standard amino acid and branched chain amino acid enriched solutions in unconscious intensive care patients without any significance in between.