Apnoeic oxygenation using transnasal humidified rapid-insufflation ventilatory exchange during rigid bronchoscopy: a report of four cases

General anaesthesia with a muscle relaxant is usually performed for rigid bronchoscopy (RB), but ventilation is challenging due to large amounts of leakage. Optiflow™ supplies 100% humidified, warmed oxygen at a rate of up to 70 l/min and this high flow rate may overcome the leakage problem. This case report describes four patients that were scheduled for RB. The lung lesions were all located below the carina, so a bronchial tube was inserted under general anaesthesia. Once a large amount of leakage was confirmed by manual ventilation, Optiflow™ was connected to the bronchial tube (flow rate, 70 l/min). All of the ports of the bronchoscopy were left open to prevent the risk of outlet obstruction. Oxygenation was well maintained with stable vital signs throughout the procedures, which took up to 34 min without airway intervention. There were no occurrences of cardiac arrhythmia or changes in the electrocardiograms. Respiratory acidosis recovered after emergence, which was confirmed by arterial blood gas analysis in all cases. Apnoeic oxygenation using Optiflow™ was applied successfully during RB. Applying Optiflow™ could make cases of difficult ventilation during RB much easier for the anaesthetist. Larger studies need to demonstrate the efficacy and safety of this technique.

Comparative study between ketamine-S-dexmedetomidine and ketamine-S-midazolam-methadone in the anesthesia of capuchin monkeys (Sapajus apella)

ABSTRACT: Anesthetic protocols have been developed to obtain the most effective and safe association in wildlife. This study compared the anesthetic effects and cardiorespiratory parameters of ketamine-S (+) (10 mg/kg)/dexmedetomidine (0.020 mg/kg) (KD ) and ketamine-S (+) (10 mg/kg)/midazolam (0.5 mg/kg)/methadone (1.0 mg/kg) (KMM ) in capuchin monkeys (Sapajus apella). Eight capuchin monkeys were randomly assigned to KD (n = 4) or KMM (n = 4) to evaluate induction, immobilization, and recovery scores, heart and respiratory rate parameters, besides systolic, mean, diastolic arterial pressure and arterial blood gas. There was no difference (P = 0.56) in the quality of induction, immobilization, and anesthetic recovery between the protocols. The time for anesthetic induction was 4 ± 1 min in the KD group and 5 ± 1 min in the KMM group, and these values were statistically equal (P = 0.28). The mean immobilization time in the KD and KMM groups were 35 ± 13 and 33 ± 15 min, respectively. Heart rate was lower in animals in the KD group (P < 0.001), while respiratory rate (P = 0.03), and mean blood pressure (P = 0.046) were higher than that of the animals in the KMM group. Respiratory acidosis occurred in the KMM group, with lower pH (7.25±0.047; P = 0.0055) and higher pCO2 (51 ± 6;mmHg; P = 0.008). Both protocols exhibited good induction quality, immobilization, and anesthetic recovery, despite cardiorespiratory and blood gas alterations observed, which warrants monitoring of cardiorespiratory variables during KD or KMM chemical restraint.

Exacerbation of COPD Treatment Combination Therapy NIV with Thermal Helium- Oxygen Plus Nitric Oxide: A Case Report

Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality worldwide despite increased health care efforts, financial costs, and research concerning its early diagnosis and proper management [1]. The most relevant event affecting COPD mortality is the acute exacerbation of COPD (AECOPD), a catastrophic event during the clinical course of the disease [2]. In cases of acute respiratory acidosis, noninvasive mechanical ventilation (NIV) is considered. Nevertheless, in 30% of patients with severe exacerbation of COPD, NIV does not lead to the desired results [3]. However, there have been cases of NIV failure in patients with severe respiratory acidosis, and associated pulmonary arterial hypertension. Many studies have shown that thermal helium-oxygen and nitric oxide gas heat treatment has many effects. Here we are reporting a case of severe exacerbation COPD, 67 years old male patient, who came to us with shortness of breath, fever, wheezing and a cough with yellow phlegm. He had a history of smoking 30 pack-year smoker many years. He was given NIV treatment with a combination of helium and nitric oxide heat. And we have had very good results.

Trans-cerebral HCO3− and PCO2 exchange during acute respiratory acidosis and exercise-induced metabolic acidosis in humans

This study investigated trans-cerebral internal jugular venous-arterial bicarbonate ([HCO3−]) and carbon dioxide tension (PCO2) exchange utilizing two separate interventions to induce acidosis: 1) acute respiratory acidosis via elevations in arterial PCO2 (PaCO2) (n = 39); and 2) metabolic acidosis via incremental cycling exercise to exhaustion (n = 24). During respiratory acidosis, arterial [HCO3−] increased by 0.15 ± 0.05 mmol ⋅ l−1 per mmHg elevation in PaCO2 across a wide physiological range (35 to 60 mmHg PaCO2; P < 0.001). The narrowing of the venous-arterial [HCO3−] and PCO2 differences with respiratory acidosis were both related to the hypercapnia-induced elevations in cerebral blood flow (CBF) (both P < 0.001; subset n = 27); thus, trans-cerebral [HCO3−] exchange (CBF × venous-arterial [HCO3−] difference) was reduced indicating a shift from net release toward net uptake of [HCO3−] (P = 0.004). Arterial [HCO3−] was reduced by −0.48 ± 0.15 mmol ⋅ l−1 per nmol ⋅ l−1 increase in arterial [H+] with exercise-induced acidosis (P < 0.001). There was no relationship between the venous-arterial [HCO3−] difference and arterial [H+] with exercise-induced acidosis or CBF; therefore, trans-cerebral [HCO3−] exchange was unaltered throughout exercise when indexed against arterial [H+] or pH (P = 0.933 and P = 0.896, respectively). These results indicate that increases and decreases in systemic [HCO3−] – during acute respiratory/exercise-induced metabolic acidosis, respectively – differentially affect cerebrovascular acid-base balance (via trans-cerebral [HCO3−] exchange).

Clinical features of respiratory syncytial virus bronchiolitis in an infant: rapid and fatal brain involvement

Background Respiratory Syncytial Virus (RSV) infection is a significant cause of bronchiolitis and pneumonia, mostly responsible for hospitalization and infant death worldwide. However, in recent years the importance of extrapulmonary RSV manifestations, especially at neurological level, have become evident. Seizures, lethargy, ataxia and status epilepticus are suggestive of brain involvement, but also in their absence a direct neurological damage RSV-related need to be evaluated. Case presentation A 40-day old male infant was admitted to the Emergency Department with severe bronchiolitis and dyspnea. The patient was reported to be coughing for a week with a vomiting episode in the previous two days. The nasopharyngeal swab confirmed the diagnosis of RSV infection and blood gas test showed hypoxemia and respiratory acidosis. For these reasons, the patient was provided with oxygen therapy. A few hours later, after an initial improvement in clinical parameters, a worsening of respiratory dynamics occurred and the patient was prepared for endotracheal intubation, but in the meantime death occurred. During all the observation period in the Emergency Room, no signs of neuropathological damage were evident. Post mortem examination showed lungs congestion with alveolar atelectasis and white matter degradation with severe edema at brain level. Microbiological analysis performed on autoptic samples confirmed the presence of RSV genome in tracheobronchial aspirate, meningeal swabs, pericardic and abdominal fluids, lung and brain biopsies. Conclusions RSV is usually associated with respiratory diseases, however, as reported by an increasingly number of studies, the systemic dissemination of virus during severe disease can lead to a sudden infant death. The clinical picture herein reported showed a severe bronchiolitis resulting in a fatal and underestimated cerebral involvement due to RSV neurotropic behaviour and underline the need for clinicians to pay more attention to neurological involvement of RSV infection, even in absence of cerebral damage evidence.

Case report: “an unexpected origin of coma in a young adult”

We report a peculiar case of acute non-traumatic coma due to neuromuscular hypoventilation syndrome caused by a non-traumatic spinal cord injury (NTSCI). A 21-year-old patient presented to the emergency room complaining of sudden onset weakness in his lower limbs and shortness of breath. While in the ER, he briefly became comatose and labs revealed an acute respiratory acidosis. Detailed neurologic examination ultimately revealed upper motor neuron signs and quadriplegia. He was ultimately diagnosed with a non-traumatic spinal cord injury, in particular, a cervical transverse myelitis which had caused acute diaphragmatic weakness. Although a very rare cause of coma, emergency medicine physicians need to be aware of transverse myelitis, a disorder that may result in rapidly progressive neurologic decline and is treated with immunomodulation.

Cardiogenic shock with highly complicated course after influenza A virus infection treated with vva-ECMO and Impella CP (ECMELLA): a case report

Background The value of mechanical circulatory support (MCS) in cardiogenic shock, especially the combination of the ECMELLA approach (Impella combined with ECMO), remains controversial. Case presentation A previously healthy 33-year-old female patient was submitted to a local emergency department with a flu-like infection and febrile temperatures up to 39 °C. The patient was tested positive for type-A influenza, however negative for SARS-CoV-2. Despite escalated invasive ventilation, refractory hypercapnia (paCO2: 22 kPa) with severe respiratory acidosis (pH: 6.9) and a rising norepinephrine rate occurred within a few hours. Due to a Horovitz-Index < 100, out-of-centre veno-venous extracorporeal membrane oxygenation (vv-ECMO)-implantation was performed. A CT-scan done because of anisocoria revealed an extended dissection of the right vertebral artery. While the initial left ventricular function was normal, echocardiography revealed severe global hypokinesia. After angiographic exclusion of coronary artery stenoses, we geared up LV unloading by additional implantation of an Impella CP and expanded the vv-ECMO to a veno-venous-arterial ECMO (vva-ECMO). Clinically relevant bleeding from the punctured femoral arteries resulted in massive transfusion and was treated by vascular surgery later on. Under continued MCS, LVEF increased to approximately 40% 2 days after the initiation of ECMELLA. After weaning, the Impella CP was explanted at day 5 and the vva-ECMO was removed on day 9, respectively. The patient was discharged in an unaffected neurological condition to rehabilitation 25 days after the initial admission. Conclusions This exceptional case exemplifies the importance of aggressive MCS in severe cardiogenic shock, which may be especially promising in younger patients with non-ischaemic cardiomyopathy and potentially reversible causes of cardiogenic shock. This case impressively demonstrates that especially young patients may achieve complete neurological restoration, even though the initial prognosis may appear unfavourable.

Intracardiac Thrombosis in A Neonate: A Case Report

Background: Life-threatening intracardiac thrombosis is rare. Intracardiac thrombosis may affect neonates from the first months of life. Because of the potential risk of serious bleeding, the use of recombinant plasminogen activator (rt-PA) in neonates along with heparin is controversial. Case Report: We reported a 37- day- old term infant presented with fever, restlessness, malaise, and respiratory acidosis. Right atrial thrombose was identified by ECHO, results of laboratory tests, and examination. She was successfully treated with rt-PA and rivaroxaban. Conclusion: Early echocardiographic detection before the clot grows large and organized, allows complete, safe, and rapid thrombolysis with rt-PA and rivaroxaban.

Treatment of Acute Severe Asthma Exacerbation with Extracorporeal Membrane Oxygenation and Inhaled Volatile Anesthetic

Severe asthma affects approximately 1-2% of all asthmatic patients. Acute exacerbations are associated with high mortality in this population. There are many treatment options for asthma exacerbation; however, if these treatments fail, patients can develop progressive hypoxia, hypercarbia, respiratory acidosis, and hemodynamic instability. Extracorporeal membrane oxygenation (ECMO) and inhaled anesthetic both have a role in the management of acute severe refractory asthma exacerbation, though there is limited information about the use of both together. We present the case of a patient with severe asthma who suffered a refractory asthma exacerbation and was successfully managed with veno-venous ECMO and inhaled anesthetic. ECMO and inhaled volatile anesthetic both have a role in the management of severe refractory asthma exacerbations. It is safe and beneficial to use these therapies together and more benefit is noted if initiated early in the course of the patient’s illness.