Relationships Between Resting Energy Expenditure and Transcranial Doppler Measurements in Patients With and Without Brain Death.

Introduction Brain metabolism deteriorates during brain death, suggesting that cerebral metabolic measurements could serve as a prognostic factor. The application of transcranial Doppler can be useful in evaluating patients evolving to brain death. Resting energy expenditure is lower than expected in patients with brain death, and this is caused by the decrease in cerebral blood flow and consequently lower oxygen supply. The primary aim of this retrospective study is to investigate the early metabolic changes in patients with clinical criteria of brain death and examine if these changes are related to a gradual decrease in blood flow velocities in the middle cerebral artery. Methods All consecutive patients from 1st June 2018 to 30th April 2022, admitted to the ICU with brain injury and a GCS ≤ 8, were included retrospectively in the study. Patients were allocated into two groups: Group A, patients without clinical signs of brain death (n = 32), and Group B, patients with brain death (n = 34). In each group, three sets of metabolic measurements were performed concomitantly with cerebral blood flow velocities using transcranial Doppler (a) upon admission to the ICU, (b) once hemodynamic stabilization was obtained, and (c) 48 hours after their hemodynamic stabilization or when brain death was confirmed by clinical criteria. Resting energy expenditure (REE) measurements were performed using a metabolic computer. Cerebral blood flow velocities were measured after a period of 30 min using a 2-MHZ 2D ultrasound probe. Results Brain-dead patients had a significant decrease in their metabolic parameters as the cerebral blood flow velocities recorded with the transcranial Doppler deteriorated, (REE Group A = 1667.65 ± 597 vs Group B = 1376.12 ± 615, p = 0.05 and REE predicted Group A = 113.19 ± 44.9 vs Group B = 93.29 ± 41.5, p = 0.066 for measurement 1; REE Group A = 1844 ± 530.9 vs Group B = 1219.97 ± 489, p < 0.001 and REE predicted Group A = 124.38 ± 39 vs Group B = 81.35 ± 30.4, p < 0.001 for measurement 2; REE Group A = 1750.97 ± 414, p < 0.001 and REE predicted Group A = 116.38 ± 19.2 vs Group B = 56.09 ± 19.6, p < 0.001 for measurement 3). Multiple stepwise regression analysis revealed a strong relationship between age, the worsening of the blood flow velocities pattern, and the decrease in REE (multiple R = 0.264, F = 5.55, p = 0.009). Furthermore, a statistically significant correlation was found between temperature and REE (correlation coefficient = 0.500, 0.674, 0.784 for measurements 1, 2, and 3, respectively, and p < 0.001 for all measures). Conclusions In brain-dead patients, the gradual decrease in cerebral blood flow leads to a decrease in REE as well as thermogenetic control. These changes can be detected early after the patient's admission to the ICU.

Unexpected Tension Pneumothorax-Hemothorax during Induction of General Anaesthesia.

Tension pneumothorax during general anaesthesia is a rare but possibly deleterious event, especially where predisposing factors are absent or unknown, making diagnosis even challenging. We describe a case of a healthy middle-aged woman, who was planned to receive general anaesthesia for total thyroidectomy. After intubation, the patient experienced marked hypoxemia (SpO2=75%), hypotension, and tachycardia. Manual positive pressure ventilation seemed to worsen hypoxemia and tachycardia, while apnoeic oxygenation through circle system with valve open slightly improved cardiorespiratory collapse. The effect of positive ventilation, along with the absence of breath sounds in the right hemithorax and cardiorespiratory collapse, established the diagnosis of tension pneumothorax, managed immediately with emergency thoracentesis and placement of a thoracostomy tube. The patient was improved and pneumothorax was confirmed with chest X-ray and CT. The latter also confirmed the presence of bilateral multiple bullae. The operation was postponed and the patient was extubated a few hours later, in good condition. After thorough evaluation for any systemic disease, which was negative, the patient underwent two-stage thoracotomy for bullectomy.

Inadvertent injection of succinylcholine as an epidural test dose / Injeção inadvertida de succinilcolina como uma dose teste epidural

Abstract Background and objectives: Epidural action of neuromuscular blocking agents could be explained under the light of their physicochemical characteristics and epidural space properties. In the literature there are few cases of accidental neuromuscular agent's epidural administration, manifesting mainly with neuromuscular blockade institution or fasciculations. Case report: We report a case of accidental succinylcholine administration as an epidural test dose, in a female patient undergoing scheduled laparotomy, under combined general and epidural anesthesia. Approximately 2 min after the succinylcholine injection the patient complained for shortness of breath, while mild fasciculations appeared in her trunk and face, managed by immediate general anesthesia institution. With the exception of a relatively longer duration of neuromuscular blockade compared with intravenous administration, no neurological or cardiovascular sequelae or other symptoms of local or systemic toxicity were observed. Conclusions: Oral administration of diazepam seems to lessen the adverse effects from accidental epidural administration of succinylcholine. The meticulous and discriminative labeling of syringes, as well as keeping persistent cautions during all anesthesia procedures remains of crucial importance.

Resumo Justificativa e objetivos: A ação epidural de agentes bloqueadores neuromusculares pode ser explicada à luz de suas características físico-químicas e propriedades do espaço epidural. Na literatura existem poucos casos sobre a administração acidental em espaço epidural de agente neuromuscular que se manifesta principalmente com a instituição de bloqueio neuromuscular ou fasciculações. Relato de caso: Relatamos um caso de administração acidental de succinilcolina como uma dose teste epidural em uma paciente submetida à laparotomia programada, sob anestesia combinada geral e peridural. Aproximadamente dois minutos após a injeção de succinilcolina, a paciente queixou-se de falta de ar, enquanto fasciculações leves apareceram em seu tronco e rosto, tratadas com a instituição imediata de anestesia geral. Exceto pela duração relativamente longa do bloqueio neuromuscular em comparação com a administração intravenosa, sequelas neurológicas ou cardiovasculares ou outros sintomas de toxicidade local ou sistêmica não foram observados. Conclusões: A administração oral de diazepam parece diminuir os efeitos adversos da administração epidural acidental de succinilcolina. A meticulosidade e discriminação dos rótulos das seringas, bem como os cuidados persistentes mantidos durante todos os procedimentos de anestesia, continuam a ser de importância crucial.

[Inadvertent injection of succinylcholine as an epidural test dose]. / Injeção inadvertida de succinilcolina como uma dose teste epidural.

BACKGROUND AND OBJECTIVES: Epidural action of neuromuscular blocking agents could be explained under the light of their physicochemical characteristics and epidural space properties. In the literature there are few cases of accidental neuromuscular agent's epidural administration, manifesting mainly with neuromuscular blockade institution or fasciculations. CASE REPORT: We report a case of accidental succinylcholine administration as an epidural test dose, in a female patient undergoing scheduled laparotomy, under combined general and epidural anesthesia. Approximately 2min after the succinylcholine injection the patient complained for shortness of breath, while mild fasciculations appeared in her trunk and face, managed by immediate general anesthesia institution. With the exception of a relatively longer duration of neuromuscular blockade compared with intravenous administration, no neurological or cardiovascular sequelae or other symptoms of local or systemic toxicity were observed. CONCLUSIONS: Oral administration of diazepam seems to lessen the adverse effects from accidental epidural administration of succinylcholine. The meticulous and discriminative labeling of syringes, as well as keeping persistent cautions during all anesthesia procedures remains of crucial importance.

Efficacy and safety of prophylactic levetiracetam in supratentorial brain tumour surgery: a systematic review and meta-analysis.

AIMS: The aim of this study was to perform an up-to-date systematic review and meta-analysis on the efficacy and safety of prophylactic administration of levetiracetam in brain tumour patients. METHOD: A systematic review of studies published until April 2015 was conducted using Scopus/Elsevier, EMBASE and MEDLINE. The search was limited to articles reporting results from adult patients, suffering from brain tumour, undergoing supratentorial craniotomy for tumour resection or biopsy and administered levetiracetam in the perioperative period for seizure prophylaxis. Outcomes included the efficacy and safety of levetiracetam, as well as the tolerability of the specific regimen, defined by the discontinuation of the treatment due to side effects. RESULTS: The systematic review included 1148 patients from 12 studies comparing levetiracetam with no treatment, phenytoin and valproate, while only 243 patients from three studies, comparing levetiracetam vs phenytoin efficacy and safety, were included in the meta-analysis. The combined results from the meta-analysis showed that levetiracetam administration was followed by significantly fewer seizures than treatment with phenytoin (OR = 0.12 [0.03-0.42]: χ(2) = 1.76: I(2) = 0%). Analysis also showed significantly fewer side effects in patients receiving levetiracetam, compared to other groups (P < 0.05). The combined results showed fewer side effects in the levetiracetam group compared to the phenytoin group (OR = 0.65 [0.14-2.99]: χ(2) = 8.79: I(2) = 77%). CONCLUSIONS: The efficacy of prophylaxis with levetiracetam seems to be superior to that with phenytoin and valproate administration. Moreover, levetiracetam use demonstrates fewer side effects in brain tumour patients. Nevertheless, high risk of bias and moderate methodological quality must be taken into account when considering these results.

Cerebral oxygenation impairment and S-100ß protein release during off-pump coronary artery revascularization.

OBJECTIVE: To elucidate the magnitude of global cerebral oxygenation impairment, using cerebral oxygenation indices and S-100ß protein as potential markers, during off-pump coronary artery bypass grafting (OPCAB). DESIGN: Prospective cohort study. SETTING: Tertiary cardiac center. PARTICIPANTS: Thirty-five patients undergoing OPCAB. INTERVENTIONS: Jugular bulb and arterial blood samples for cerebral oxygenation indices (arterial oxygen and carbon dioxide partial pressures, jugular bulb oxygen saturation, arterial-jugular bulb oxygen content, arterial-jugular carbon dioxide partial pressure, brain oxygen extraction ratio, and estimated respiratory quotient) and S-100ß protein determination were collected at anesthesia induction; anterior, inferior, and posterior wall anastomoses; after sternal closure; and 6 hours postoperatively. Concomitant hemodynamic data were obtained. The S-100ß determination was extended to 12 and 24 hours postoperatively. MEASUREMENTS AND MAIN RESULTS: Heart positioning for the target vessel exposure induced significant hemodynamic deterioration (p < 0.001). Although cerebral oxygenation indices were influenced adversely by a low-cardiac-output state mainly during vertical heart dislocation (p < 0.001), they remained within normal limits. Hemodynamic and cerebral oxygenation statuses reverted to baseline within 6 hours postoperatively. Similarly, S-100ß jugular bulb and arterial protein levels presented a gradual increase, which peaked by the end of surgery (means, 0.54 and 0.62 µg/L, respectively; p < 0.001) and then decreased by the first postoperative day. Jugular bulb-arterial S-100ß levels were maximized during posterior wall anastomosis (0.098 µg/L; p < 0.01). CONCLUSION: Although exposure of the 3 main coronary arteries during OPCAB promotes derangement of the cerebral oxygen indices and S-100ß release, this seems to be transient, remains within the near-normal range, and is reversible almost completely 6 hours postoperatively.

Correlation of central venous-arterial and mixed venous-arterial carbon dioxide tension gradient with cardiac output during neurosurgical procedures in the sitting position.

BACKGROUND AND OBJECTIVE: The study was conducted to evaluate the correlation of central venous-arterial and mixed venous-arterial pCO(2) gradient with cardiac output in patients being operated in the sitting position. METHODS: Fifty-one patients, aged 41-69 years, classified as American Society of Anesthesiologists physical status II and III, scheduled to undergo elective neurosurgical procedures in the sitting position, were enrolled in this prospective cohort study. Simultaneous blood gas samples from arterial, central venous and pulmonary artery catheters were collected at four different time points during supine and sitting position. Cardiac index (CI) determination was accomplished simultaneously, with continuous cardiac output technique. The mixed venous-arterial pCO(2) and central venous-arterial pCO(2) gradients were calculated and related to CI at the specific time points, thus a total of 204 points of comparison were obtained. RESULTS: Changing from the supine to the sitting position induced a significant deterioration of CI, right atrial pressure, mean pulmonary arterial pressure and pulmonary wedge pressure. The mean delta pCO(2) difference (bias) in the four time points ranged between -0.07 and -0.27. The upper (1.59-1.71 mmHg) and lower limits of agreement (-2.16 to -1.82 mmHg) were quite narrow, suggesting an acceptable overall agreement between the mixed and central venous pCO(2) differences. The coefficient of determination (R(2)) between the venous-arterial pCO(2) and CI for mixed and central venous circulations was 0.830 and 0.760 (P < 0.001 for both), respectively. In contrast, R(2) values between mixed and central venous oxygen saturation values and CI were 0.324 and 0.286, respectively (P < 0.001 for both), illustrating a rather weak relationship. CONCLUSION: It seems that venous-arterial pCO(2) values obtained from mixed and central venous circulations can be reliably interchanged in estimating CI in patients undergoing neurosurgical procedures in the sitting position. Thus, central venous-arterial pCO(2) gradient could serve as a useful and simple method for estimating cardiac performance, in which further invasive monitoring is not strongly indicated.

Baroreceptors discharge due to bilateral aortic denervation evokes acute neuronal damage in rat brain.

Deep hypothermic circulatory arrest in cardiothoracic surgery evokes severe brain damages. On the other hand, blood pressure stimuli discontinuation to the brain has been found to induce alterations in neurotransmitter release, including glutamate, in numerous brain regions. Furthermore, it is well established that excessive glutamate release can induce neuronal injury, a process called excitotoxicity. Aim of the present study was the evaluation of possible acute neuronal damage after bilateral aortic denervation (bAD), imitating the baroreceptors discharge during circulatory arrest. Male, Wistar rats underwent either bAD or Sham operation under continuous hemodynamic monitoring. Two hours after completion of the procedure, rats were sacrificed and the brains were dissected and cut in specific levels corresponding to selective brain regions, based on either their participation in neuronal circuits, regulating blood pressure, or their vulnerability, after deep hypothermic circulatory arrest. Slices were stained and examined under light microscope using morphometric techniques. Increased number of necrotic neurons were found among bAD rats in amygdaloid complex (p=0.005), motor cortex (p=0.001), CA1 and CA3 (p=0.02 and 0.015) but not in posterior hypothalamic nucleus and Purkinje cell. Higher ratios of necrotic neurons were found in amygdaloid complex (p=0.002), motor layer (p=0.003 and p=0.000) and the hippocampal CA1 region (p=0.027) of bAD rats. The present study shows that baroreceptors discharge due to bAD may induce acute neuronal loss in brain regions involved in blood pressure regulation. Neuronal loss might be attributed to excitotoxic phenomena and it is following the same topographic distribution seen in deep hypothermic circulatory arrest, revealing a concurrent to hypoxia/ischemia mechanism of brain damage.

Efficacy of pregabalin and gabapentin for neuropathic pain in spinal-cord injury: an evidence-based evaluation of the literature.

BACKGROUND: Spinal-cord injury (SCI) is a leading cause of neuropathic pain (NP). Current pharmaceutical treatments for NP in SCI patients are not effective. Two promising options are gabapentin (GP) and pregabalin (PB). Their predominant mechanism of action is believed to be the inhibition of calcium currents, leading in turn to reduced neurotransmitter release and attenuation of postsynaptic excitability. This could explain much of their efficacy in the treatment of both seizure disorders and pain syndromes. However, evidence for their efficacy in attenuating NP of SCI is still controversial. OBJECTIVE: To efficiently integrate valid information and provide a basis for rational decision making, through determining PB and GP efficacy in treating NP in SCI. METHODS: Literature was systematically reviewed. Medline, Embase, CINAHL and Cochrane Database were searched using search terms 'gabapentin', 'pregabalin', 'neurontin', 'lyrica', 'neuropathic pain' and 'spinal-cord injury'. Studies were assessed independently by two authors. RESULTS: Five studies were eligible for inclusion. Two of them studied PB and three GP. Both GP and PB appear to be efficacious for NP in SCI. A clear comparison between the two drugs could not be performed. The literature data suggest that PB is more efficacious than GP in many important variables for NP in SCI, although PB use is followed by more side effects than GP. PB reduced Visual Analogue Score (VAS) in both studies (P < 0.001 and P = 0.016). On the other hand, for GP a maximum dosage of 3,600 mg/day reduced VAS score (P = 0.000), whereas a maximum dosage of 1,200 mg/day failed to do so. CONCLUSION: There is a lack of studies comparing GP and PB in treating NP in SCI. This systematic review indicates the possible efficacy of PB and GP in NP of SCI. Recommendations for future research to inform clinical practice should include cost-effectiveness studies and dose-response analysis in order to determine the schema employed and the duration of treatment.

Unexpected complication of massive intraoperative pulmonary embolism following elective sigmoidectomy in the supine position.

We describe a case of massive intraoperative pulmonary thromboembolism during elective sigmoidectomy in the supine position. During recovery from anesthesia, the patient developed hemodynamic compromise and severe hypoxemia. Intravenous inotropes and mechanical ventilation were instituted. The abrupt onset of symptoms and the pulmonary artery catheter, chest radiograph, and transesophageal echocardiography findings suggested massive pulmonary thromboembolism as a possible cause of the hemodynamic compromise and hypoxemia. Emergent angiography could not be carried out due to the patient's poor clinical status. Lack of experience in performing embolectomy, along with contraindication for thrombolysis, imposed the use of intravenous heparin and hemodynamic support as the only appropriate therapeutic modality. After 2 days' aggressive hemodynamic and ventilatory support, the patient had an uneventful course, and was discharged from the intensive care unit (ICU) 14 days later.

Deferoxamine decreases the excitatory amino acid levels and improves the histological outcome in the hippocampus of neonatal rats after hypoxia-ischemia.

Hypoxic-ischemic encephalopathy is a severe complication of perinatal asphyxia and causes lifelong deficits in infants and children. Multiple mechanisms acting in serial or parallel fashion are likely to be involved in this procedure. The neuronal injury is strongly related to iron-catalysed oxygen radical production and subsequent peroxidative damage to lipids and protein. Excessive release of excitatory amino acids (EAA) glutamate and aspartate, with consequent overstimulation of glutamate receptors, is also thought to be an important mechanism in this brain injury. Deferoxamine (DFO), a chelator of non-protein-bound iron, has been shown to inhibit lipid peroxidation and hydroxyl radical production via the Fenton reaction and to decrease hypoxic-ischemic and reperfusion associated brain injury. However, the exact mechanism of neuroprotection of DFO and its possible effect on the neurotransmitters' release is currently being investigated. In the present study, a well-established model of perinatal asphyxia was used to investigate the effect of DFO on hypoxic-ischemic-induced damage to different hippocampal brain structures. DFO was administrated subcutaneously immediately after the asphyctic insult. Histological examination of the hippocampus was conducted and the tissue levels of glutamate and aspartate in the same area were determined. A remarkable reduction of hypoxia-ischemia-evoked neurons in the CA1 hippocampal region and a decrease in the asphyxia-induced hippocampal tissue levels of glutamate and aspartate was noted after DFO treatment. These findings suggest a complex action of DFO, which could be neuroprotective when administrated in the immature brain immediately after hypoxia-ischemia.