Helmet continuous positive airway pressure vs. high flow nasal cannula oxygen in acute cardiogenic pulmonary oedema: a randomized controlled trial.

AIMS: Non-invasive ventilation represents an established treatment for acute cardiogenic pulmonary oedema (ACPO) although no data regarding the best ventilatory strategy are available. We aimed to compare the effectiveness of helmet CPAP (hCPAP) and high flow nasal cannula (HFNC) in the early treatment of ACPO. METHODS AND RESULTS: Single-centre randomized controlled trial of patients admitted to the emergency department due to ACPO with hypoxemia and dyspnoea on face mask oxygen therapy. Patients were randomly assigned with a 1:1 ratio to receive hCPAP or HFNC and FiO2 set to achieve an arterial oxygen saturation >94%. The primary outcome was a reduction in respiratory rate; secondary outcomes included changes in heart rate, PaO2/FiO2 ratio, Heart rate, Acidosis, Consciousness, Oxygenation, and Respiratory rate (HACOR) score, Dyspnoea Scale, and intubation rate. Data were collected before hCPAP/HFNC placement and after 1 h of treatment. Amongst 188 patients randomized, hCPAP was more effective than HFNC in reducing respiratory rate [-12 (95% CI; 11-13) vs. -9 (95% CI; 8-10), P < 0.001] and was associated with greater heart rate reduction [-20 (95% CI; 17-23) vs. -15 (95% CI; 12-18), P = 0.042], P/F ratio improvement [+149 (95% CI; 135-163) vs. +120 (95% CI; 107-132), P = 0.003] as well as in HACOR scores [6 (0-12) vs. 4 (2-9), P < 0.001] and Dyspnoea Scale [4 (1-7) vs. 3.5 (1-6), P = 0.003]. No differences in intubation rate were noted (P = 0.321). CONCLUSION: Amongst patients with ACPO, hCPAP resulted in a greater short-term improvement in respiratory and hemodynamic parameters as compared with HFNC. TRIAL REGISTRATION: Clinical trial submission: NMRR-17-1839-36966 (IIR). Registry name: Medical Research and Ethics Committee of Malaysia Ministry of Health. Clinicaltrials.gov identifier: NCT04005092. URL registry: https://clinicaltrials.gov/ct2/show/NCT04005092.

Pericardial decompression syndrome: A complication of pericardiocentesis.

Pericardial Decompression Syndrome (PDS) is an uncommon but life-threatening complication following pericardiocentesis for cardiac tamponade. We report PDS after pericardiocentesis in two patients that presented to the emergency department with cardiac tamponade. In both cases, pericardiocentesis was performed under ultrasound guidance using the left parasternal approach and approximately 1200-1500 mL of pericardial fluid was removed. Immediately after pericardiocentesis, the haemodynamic status of the patients improved. However, 2-3 h post decompression, both patients developed hypotension and pulmonary edema with reduced left ventricular function, suggestive of PDS. PDS is a condition that is described as paradoxical worsening of vital signs after successful decompression of the pericardium in the setting of acute tamponade. Three possible mechanisms explaining PDS are ischaemic, hemodynamic and autonomic processes. If PDS is unrecognized and untreated, it is associated with a high mortality rate secondary to pulmonary edema and cardiogenic shock. If managed urgently, the cardiopulmonary dysfunction in PDS is usually transient and largely reversible with supportive care.

Fat embolism in right internal jugular vein: incidental ultrasound finding during internal jugular vein cannulation.

BACKGROUND: We report a case study of fat embolism seen on ultrasound at right internal jugular vein during central venous cannulation in a patient diagnosed with fat embolism syndrome. This case demonstrates the importance of ultrasound for evaluation of trauma cases with suspicion of fat embolism. CASE PRESENTATION: A 23-year-old trauma patient with closed fracture of left femoral shaft and left humerus presented to our emergency department (ED). 11 h after admission to ED, patient became confused, hypoxic and hypotensive. He was then intubated for respiratory failure and mechanically ventilated. Transesophageal ultrasound revealed hyperdynamic heart, dilated right ventricle with no regional wall abnormalities and no major aorta injuries. Whole-body computed tomography was normal. During central venous cannulation of right internal jugular vein (IJV), we found free floating mobile hyperechoic spots, located at the anterior part of the vein. A diagnosis of fat embolism syndrome later was made based on the clinical presentation of long bone fractures and fat globulin in the blood. Despite aggressive fluid resuscitation, patient was a non-responder and needed vasopressor infusion for persistent shock. Blood aspirated during cannulation from the IJV revealed a fat globule. Patient underwent uneventful orthopedic procedures and was discharged well on day 5 of admission. CONCLUSIONS: Point-of-care ultrasound findings of fat embolism in central vein can facilitate and increase the suspicion of fat embolism syndrome.