Over the last three decades since the introduction of the term ventilator-induced lung injury (VILI), we have recognized that positive pressure mechanical ventilation can injure the lungs. It is widely recognized that the cornerstone of lung protective ventilation requires control of tidal volume and transpulmonary pressure. On the other hand, there has been considerably less focus on the impact of respiratory rate and flow on VILI. Mechanical power unites the causes of ventilator-induced lung injury in a single variable that incorporates both the elastic and resistive load of the positive pressure breath.6 In other words, mechanical power quantifies the energy delivered to the lung during each positive pressure breath by assessing the relative contribution of pressure, volume, flow and respiratory rate.
Venous thromboembolism is considered one of the most preventable causes of in-hospital death. Venovenous extracorporeal membrane oxygenation (VV ECMO) utilization for severe respiratory failure has increased in the decade following the 2009 influenza A H1N1 pandemic and the publication of the CESAR trial.1 The interaction between a patient’s blood and the ECMO circuit produces an inflammatory response that can provoke both thrombotic and bleeding complications. In a systematic review of patients with H1N1 treated with VV ECMO published in 2013, the incidence of cannula-associated deep venous thrombosis (CaDVT) was estimated to be as low as 10 percent; however, more recent data suggests the incidence of venous thrombosis after decannulation is much higher. Additionally, a significant proportion of CaDVT are distal thrombi located in the vena cava, which would be missed with a traditional ultrasound diagnostic approach after decannulation from VV ECMO.
While most coronaviruses cause mild respiratory illness consistent with the common cold, two lethal coronaviruses have been previously identified, including the acute respiratory syndrome coronavirus (SARS-CoV) in 2002 demonstrating 10% mortality and the Middle East respiratory syndrome coronavirus (MERS-CoV) in 2012 producing 37% mortality. In December 2019, a novel coronavirus (2019-nCoV) was isolated from a cluster of patients with pneumonia in Wuhan, China. As reported in the Lancet last week, two thirds of the affected patients in a case series had a history of exposure to the Huanan seafood market.
You are assessing a 68 year old male who fell down three steps and struck his head on the ground. His history is significant for a drug eluting stent placed after a cardiac catheterization two months ago. As a result he is on dual antiplatelet therapy. You wonder what the impact of aspirin and clopidogrel is on the risk of intracranial hemorrhage (ICH).
Lung-protective mechanical ventilation with low tidal volume and restricted plateau pressure improves survival in ARDS. However, the optimal approach to PEEP titration to minimize VILI is still debated. Should oxygenation, lung compliance, driving pressure or transpulmonary pressure guide adjustment of PEEP in ARDS?
While your friends at home are shivering in the Camden, NJ winter, you are on an elective retrieval medicine rotation in New South Wales, Australia. A 32 year old patient arrives in a rural emergency department obtunded. His friends state he was out hiking and may have used some cocaine as well. His initial vital signs are notable for hypotension and a core temperature of 41.5C (106.7F). There are no fans available for evaporative cooling and no gel adhesive body temperature controlling devices (such as those used following cadiac arrest). The patient requires intubation which is done uneventfully, the staff asks what tools you might use to rapidly reduce the body temperature.
EMS brings in a 45 year old male with a PMHX of tobacco abuse who was rescued in a house fire. The report is that a cigarette dropped on the patient’s couch while he was sleeping and caused a smouldering fire. It resulted in a significant amount of smoke creation but very little fire damage in the house. The patient has no visible burns. On arrival, the patient’s pulse oximetry on room air is 84%. He is alert and oriented but notes a sense of persistent dyspnea. His workup is significant for a lactate of 2.2 but otherwise benign. Co-oximetry is normal without evidence of severe carbon monoxide poisoning. The patient does not display evidence of inhalational burns. The patient’s new hypoxia and dyspnea is worrisome so you planned admission to the hospital but wonder if you should give hydroxycobalamin empirically in case of occult cyanide toxicity.
As you scan the ED trackboard, you recognize the name of a 22 year old patient who you saw the week before after a house fire. At that time, the patient was treated for carbon monoxide (CO) poisoning and briefly admitted to the hospital. Today’s chief complaint is dyspnea and chest pain. You note that the patient is tachycardic, hypoxic, and complained of pleuritic chest pain at triage. You wonder if the prior exposure to carbon monoxide should raise your pre-test probability for certain diagnoses.
Patient-ventilator asynchrony is underrecognized yet associated with increased mortality, ICU length of stay and duration of mechanical ventilation in critical illness. How do you diagnose and treat it? Hint: the answer is rarely deep sedation or paralysis!