Anesthetic management of cesarean section in a patient with Takayasu’s arteritis: a case report

Background Takayasu’s arteritis (TA) is a chronic, progressive, inflammatory arteritis. We presented the case of cesarean section in a patient with TA. Case presentation A 31-year-old pregnant woman with TA underwent a planned cesarean section at 34 weeks of pregnancy. She had stenosis of the cerebral and coronary arteries and heart failure due to aortic regurgitation. Spinal anesthesia was performed. In addition to standard monitoring, arterial blood pressure in the dorsalis pedis artery and regional cerebral tissue oxygen saturation were monitored. Intraoperative arterial blood pressure was maintained using continuous infusion of noradrenaline with a careful intermittent bolus infusion of phenylephrine. All the procedures were successfully performed without significant complications. Conclusions In a pregnant woman with TA, severe stenosis of the cerebral and coronary arteries, and heart failure due to valvular heart disease, careful anesthetic management by selecting catecholamines and assessing the perfusion pressure for critical organs is important.

CLINICAL CASE OF ARTERIAL HYPERTENSION IN A NEWBORN

Aim. To use personal clinical experience in monitoring and treating a newborn with persistent arterial hypertension (AH) due to left renal artery stenosis to demonstrate the current state of this problem in the context of limited experience of work with such rare pathologies in children.Materials and methods. The research was based on the examination and treatment of a newborn with persistent AH due to left renal artery stenosis. The complex of diagnostic procedures included: clinical and laboratory examinations, X-ray examination methods (with the use of contrast agents), magnetic resonance imaging, ultrasound examination and Dopplerography, and histological examination of surgical material.Results. Conservative treatment of the patient's AH with the use of antihypertensive agents did not achieve desired results.Taking into account possible etiologic and pathogenetic factors of AH in newborns, Doppler examination was performed to exclude congenital heart defects (coarctation of the aorta). Pathology was excluded.Cortisol and 17-OH progesterone levels were determined to exclude suprarenal pathology and showed the following: cortisol level was 173.9% higher than the maximum permissible level; 17-OH progesterone level was 9.9% higher than the norm.Considering the presence of neurological symptoms, an MRI of the brain with angiography was performed. No pathology was detected.Due to the presence of persistent arterial hypertension, which did not respond to medication, a CT with contrast was ordered, during which were revealed CT-signs of critically small diameter of the left renal artery (probable dissection) with pronounced cystic and ischemic changes of the lateral half of the left kidney without excretory function at 15 min. The main treatment measures included the following: adequate preoperative preparation, anesthetic support and the selection of an adequate and effective operative method to eliminate the pathology. The only available method of surgical intervention was nephrectomy - removal of the left kidney.Analyzing the results of the investigation, it can be stated that nephrectomy is the pathogenetic method of treatment of this pathology. Steady stabilization of arterial blood pressure was achieved within 1 hour after the operation.Conclusions. 1. When persistent AH is detected in a newborn, the presence of organic pathology should be excluded. 2. If the patient has organic pathology that causes a persistent increase in arterial blood pressure, the root cause of the pathology should be eliminated if possible. 3. Conservative treatment of persistent AH in children caused by renovascular or renal factors does not provide significant results and is not appropriate. 4. Nephrectomy is the pathogenetic method of treating AHT in a newborn with renal artery stenosis.

The Impact of α-Adrenoceptors in the Regulation of the Hypotonicity-Induced Increase in Duodenal Mucosal Permeability In Vivo

The duodenal mucosa is regularly exposed to a low osmolality, and recent experiments suggest that hypotonicity increases mucosal permeability in an osmolality-dependent manner. The aim was to examine whether the sympathetic nervous system, via action on α-adrenoceptors, affects the hypotonicity-induced increase in duodenal mucosal permeability. The duodenum of anaesthetised rats was perfused in vivo with a 50 mM NaCl solution in the presence of adrenergic α-adrenoceptor drugs. Studied were the effects on mucosal permeability (blood-to-lumen clearance of 51Cr-EDTA), arterial blood pressure, luminal alkalinisation, transepithelial fluid flux, and motility. Hypotonicity induced a six-fold increase in mucosal permeability, a response that was reversible and repeatable. The α2-adrenoceptor agonist clonidine abolished the hypotonicity-induced increase in mucosal permeability, reduced arterial blood pressure, inhibited duodenal motility, and decreased luminal alkalinisation. The α2-adrenoceptor antagonists, yohimbine and idazoxan, prevented the inhibitory effect of clonidine on the hypotonicity-induced increase in mucosal permeability. The α1-agonist phenylephrine or the α1-antagonist prazosin elicited their predicted effect on blood pressure but did not affect the hypotonicity-induced increase in mucosal permeability. None of the α1- or α2-adrenoceptor drugs changed the hypotonicity-induced net fluid absorption. In conclusion, stimulation of the adrenergic α2-adrenoceptor prevents the hypotonicity-induced increase in mucosal permeability, suggesting that the sympathetic nervous system has the capability to regulate duodenal mucosal permeability.

Changes in peripheral arterial blood pressure after resuscitative endovascular balloon occlusion of the aorta (REBOA) in non-traumatic cardiac arrest patients

Background Resuscitative endovascular balloon occlusion of the aorta (REBOA) may be an adjunct treatment to cardiopulmonary resuscitation (CPR). Aortic occlusion may increase aortic pressure and increase the coronary perfusion pressure and the cerebral blood flow. Peripheral arterial blood pressure is often measured during or after CPR, however, changes in peripheral blood pressure after aortic occlusion is insufficiently described. This study aimed to assess changes in peripheral arterial blood pressure after REBOA in patients with out of hospital cardiac arrest. Methods A prospective observational study performed at the helicopter emergency medical service in Trondheim (Norway). Eligible patients received REBOA as adjunct treatment to advanced cardiac life support. Peripheral invasive arterial blood pressure and end-tidal CO2 (EtCO2) was measured before and after aortic occlusion. Differences in arterial blood pressures and EtCO2 before and after occlusion was analysed with Wilcoxon Signed Rank test. Results Five patients were included to the study. The median REBOA procedural time was 11 min and median time from dispatch to aortic occlusion was 50 min. Two patients achieved return of spontaneous circulation. EtCO2 increased significantly 60 s after occlusion, by a mean of 1.16 kPa (p = 0.043). Before occlusion the arterial pressure in the compression phase were 43.2 (range 12–112) mmHg, the mean pressure 18.6 (range 4–27) mmHg and pressure in the relaxation phase 7.8 (range − 7 – 22) mmHg. After aortic occlusion the corresponding pressures were 114.8 (range 23–241) mmHg, 44.6 (range 15–87) mmHg and 14.8 (range 0–29) mmHg. The arterial pressures were significant different in the compression phase and as mean pressure (p = 0.043 and p = 0.043, respectively) and not significant in the relaxation phase (p = 0.223). Conclusion This study is, to our knowledge, the first to assess the peripheral invasive arterial blood pressure response to aortic occlusion during CPR in the pre-hospital setting. REBOA application during CPR is associated with a significantly increase in peripheral artery pressures. This likely indicates improved central aortic blood pressure and warrants studies with simultaneous peripheral and central blood pressure measurement during aortic occlusion. Trial registration The study is registered in ClinicalTrials.gov (NCT03534011).

Activation of the Organum Vasculosum of the Lamina Terminalis Produces a Sympathetically Mediated Hypertension

Neurons in the organum vasculosum of the lamina terminalis (OVLT) sense extracellular NaCl and angiotensin II concentrations to regulate body fluid homeostasis and arterial blood pressure. Lesion of the anteroventral third ventricular region or OVLT attenuates multiple forms of neurogenic hypertension. However, the extent by which OVLT neurons directly regulate sympathetic nerve activity to produce hypertension is not known. Therefore, the present study tested this hypothesis by using a multi-faceted approach including optogenetics, single-unit and multifiber nerve recordings, and chemogenetics. First, optogenetic activation of OVLT neurons in conscious Sprague-Dawley rats (250–400 g) produced frequency-dependent increases in arterial blood pressure and heart rate. These responses were not altered by the vasopressin receptor antagonist (β-mercapto-β,β-cyclopentamethylenepropionyl1,O-me-Tyr2,Arg8)–vasopressin but eliminated by the ganglionic blocker chlorisondamine. Second, optogenetic activation of OVLT neurons significantly elevated renal, splanchnic, and lumbar sympathetic nerve activity. Third, single-unit recordings revealed optogenetic activation of the OVLT significantly increased the discharge of bulbospinal, sympathetic neurons in the rostral ventrolateral medulla. Lastly, chronic chemogenetic activation of OVLT neurons for 7 days significantly increased 24-hour fluid intake and mean arterial blood pressure. When the 24-hour fluid intake was clamped at baseline intakes, chemogenetic activation of OVLT neurons still produced a similar increase in arterial blood pressure. Neurogenic pressor activity assessed by the ganglionic blocker chlorisondamine was greater at 7 days of OVLT activation versus baseline. Collectively, these findings indicate that acute or chronic activation of OVLT neurons produces a sympathetically mediated hypertension.

Comparison of Non-Invasive Oscillometric and Intra-Arterial Blood Pressure Measurements in Children Admitted to the Pediatric Intensive Care Unit

Intra-arterial blood pressure (IABP) measurement, although considered the gold standard in critically ill children, is associated with certain risks and lacks widespread availability. This study was conducted to determine the differences and agreements between oscillometric non-invasive blood pressure (NIBP) and invasive IABP measurements in children. Inclusion criteria consisted of children (from 1 month to 18 years) admitted to the pediatric intensive care unit (PICU) of a teaching hospital who required arterial catheter insertion for blood pressure (BP) monitoring. The comparison between IABP and NIBP was studied using paired t-test, Bland–Altman analysis, and Pearson's correlation coefficient. In total, 4,447 pairs of simultaneously recorded hourly NIBP and IABP measurements were collected from 65 children. Mean differences between IABP and NIBP were −3.6 ± 12.85, −4.7 ± 9.3, and −3.12 ± 9.30 mm Hg for systolic, diastolic, and mean arterial BP, respectively (p < 0.001), with wide limits of agreement. NIBP significantly overestimated BP (p < 0.001) in all three BP states (hypotensive, normotensive, and hypertensive), except systolic blood pressure (SBP) during hypertension where IABP was significantly higher. The difference in SBP was most pronounced during hypotension. The difference in SBP was significant in children <10 years (p < 0.001), with the maximum difference being in infants. It was insignificant in adolescents (p = 0.28) and underweight children (p = 0.55). NIBP recorded significantly higher BP in all states of BP except SBP in the hypertensive state. SBP measured by NIBP tended to be the most reliable in adolescents and underweight children. NIBP was the most unreliable in infants, obese children, and during hypotension.

Efficacy and Safety of Dexmedetomidine Premedication in Balanced Anesthesia: A Systematic Review and Meta-Analysis in Dogs

Dexmedetomidine is commonly used in small animal anesthesia for its potent sedative and analgesic properties; however, concerns regarding its cardiovascular effects prevent its full adoption into veterinary clinical practice. This meta-analysis was to determine the effects of dexmedetomidine on sedation, analgesia, cardiovascular and adverse reactions in dogs compared to other premedications. Following the study protocol based on the Cochrane Review Methods, thirteen studies were included in this meta-analysis ultimately, involving a total of 576 dogs. Dexmedetomidine administration probably improved in sedation and analgesia in comparison to acepromazine, ketamine and lidocaine (MD: 1.96, 95% CI: [−0.08, 4.00], p = 0.06; MD: −0.95, 95% CI: [−1.52, −0.37] p = 0.001; respectively). Hemodynamic outcomes showed that dogs probably experienced lower heart rate and higher systolic arterial blood pressure and mean arterial blood pressure with dexmedetomidine at 30 min after premedication (MD: −13.25, 95% CI: [−19.67, −6.81], p < 0.0001; MD: 7.78, 95% CI: [1.83, 13.74], p = 0.01; MD: 8.32, 95% CI: [3.95, 12.70], p = 0.0002; respectively). The incidence of adverse effects was comparable between dexmedetomidine and other premedications (RR = 0.86, 95% CI [0.58, 1.29], p = 0.47). In summary, dexmedetomidine provides satisfactory sedative and analgesic effects, and its safety is proved despite its significant hemodynamic effects as part of balanced anesthesia of dogs.

Optimal Duration of the Apnea Test for Determining Brain Death: Benefit of the Short-Term Apnea Test

Background: The criteria for brain death determination have not been unified globally, and there is no global consensus on the apnea test, which is essential for determining brain death. Since the apnea test is associated with many complications, we aimed to determine an optimal duration of the apnea test.Methods: We analyzed the results of the apnea test performed for brain death determination between August 2013 and February 2021 at a single institution in South Korea. Elevations in the partial pressure of carbon dioxide and mean arterial blood pressure fluctuations over time in the apnea test were recorded.Results: In the 1st and 2nd tests, the mean partial pressure of carbon dioxide increased by more than 20 mmHg at 3 min after the apnea test compared to before the test (P < 0.05). At 4 min in the 1st test and 5 min in the 2nd test, the partial pressure of carbon dioxide exceeded 60 mmHg (P < 0.05). The fluctuation in the mean arterial blood pressure observed for 5 min during the apnea test was not significant. There was no significant fluctuation in the mean arterial blood pressure over time in the apnea test between patients with normal chest radiography findings and those with abnormal chest radiography findings (P = 0.888).Conclusion: Our study proposes that a short-term apnea test protocol is valid for the preservation of organs for donation.