İlkin Çankayalı

Neuromuscular deterioration in the early stage of sepsis in rats

IntroductionCritical 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.MethodsWe 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.ResultsCMAP 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).ConclusionThe 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.

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.

The effects of dexmedetomidine on spontaneous contractions of isolated gravid rat myometrium.

The direct effects of dexmedetomidine on isolated gravid rat myometrium were investigated in this in vitro study; such effects may have clinical repercussions in the administration of anesthesia to obstetric patients. Samples of myometrium were taken from 12 gravid rats. Myometrial strips were dissected microscopically and mounted on the myograph at a resting tension of 1 gin bath that contained Krebs solution. After spontaneous contractions of the myometrium had been steadily established, increasing concentrations of dexmedetomidine were added to baths via micropipette, and the effects of these additions were recorded via myograph. Dexmedetomidine in vitro caused a significant increase in the amplitude, frequency, and area under the curve of myometrial contractions in a dose-dependent manner. Results of this study demonstrate that dexmedetomidine increases spontaneous contractions in rat myometrium; however, further investigation is needed to clarify the usefulness of dexmedetomidine in the administration of obstetric anesthesia.

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 10mg/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 QTc 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 QTc 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 QTc interval. Further research about the toxic effects of organophosphate compounds on myocardial cells is warranted.

Ventilator-associated pneumonia in critically ill patients with intensive antibiotic usage.

Objective: Ventilator-associated pneumonia (VAP) is an infection with high mortality and morbidity that prolongs the length of stay in the intensive care unit (ICU) and hospitalisation. VAP is one of the most common infections in critically ill patients. This study aimed to prospectively determine the VAP rate and associated factors in critically ill patients with intensive antibiotic usage during a one-year period. Methods: In total, 125 out of 360 patients admitted to the intensive care unit during the one-year study period (September 2010-2011) were included for follow-up for VAP diagnosis. Demographic data, APACHE II scores, diagnoses on admission, clinical pulmonary infection scores (CPIS), CRP, procalcitonin, risk factors for infection, time to VAP diagnosis, and bacteriological culture results were recorded. All data were assessed in terms of ICU, hospital and 28-day mortality. Results: In total, 56 (45%) out of 125 patients were diagnosed with VAP. In addition, 91% of patients diagnosed with VAP were administered antibiotics before diagnosis. In the VAP patients, the mortality rates were 48, 68 and 71% for 28-day, ICU and hospital mortality, respectively. Conclusion: The coexistence of clinical and microbiological parameters should not be sought when diagnosing VAP in patients who use antibiotics intensively. VAP can be diagnosed when CPIS≤6 in cases with sufficient microbiological evidence. This strategy may decrease mortality by preventing a delay in therapy.

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.

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.

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 patients 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.