No abstract

The concentration H+ ([H+]) in intracellular fluid (ICF) must be maintained in a narrow range in all species for normal protein functions. Thus, mechanisms regulating ICF are of fundamental biological importance. Studies on the regulation of ICF [H+] have been hampered by use of pH notation,failure to consider the roles played by differences in the concentration of strong ions ( SID), the conservation of mass, the principle of electrical neutrality and that [H+] and [HCO3-] are dependent variables. This argument is based on the late Peter Stewart’s physical- chemical analysis of [H+] regulation reported in this journal nearly forty years ago. We start by outlining the principles of Stewart’s analysis and then provide a general understanding of its significance for regulation of ICF [H+]. The system may initially appear complex, but it becomes evident that changes in SID dominanate regulation of [H+]. The primary strong ions are Na+, K+ and Cl-, and a few organic strong anions. The second independent variable, PCO2, can easily be assessed. The third independent variable, the activity of intracellular weak acids ([Atot]), is much more complex but largely plays a modifying role. Attention to these principles potentially will provide new insights into ICF pH regulation.

Acute massive or submassive pulmonary embolism (PE) requires prompt diagnosis, risk-stratification and aggressive treatment. Mortality rates can rise up to 70% within the first hour of presentation and are strongly correlated with the degree of right ventricular (RV) dysfunction, cardiac arrest, and consequential congestive heart failure. While anticoagulation is universally employed, there are inadequate data to establish definitive guidelines for the management of massive PE despite the availability of multiple treatment modalities. Medical thrombolytic therapy has not been shown to significantly reduce mortality in patients with massive PE but is still widely employed, whereas surgical and catheter embolectomy are only reserved as last resort treatments for critically ill patients with hemodynamic instability, or for those who are either not candidates for or have failed thrombolysis. Following an extensive review of medical literature, we outline the treatment options for this clinical scenario while focusing on the role of surgical embolectomy. Although traditionally reserved as rescue therapy for cases of failed thrombolysis, surgical embolectomy is a safe procedure with low mortality when performed early and in a selected group of patients. Sufficient evidence exists to extend the criteria for surgical embolectomy from strictly rescue therapy to include hemodynamically stable patients with RV dysfunction. Multidisciplinary approach to this condition coupled with a meticulous surgical technique has significantly lowered the mortality associated with this surgical procedure over the last 10 years.

Haemophagocytic lymphohistiocytosis (HLH) causing multiorgan failure has been reported as an acute clinical presentation of COVID-19. However, the literature surrounding HLH in the context of a postacute COVID-19 syndrome is limited. This report presents a case of a life-threatening HLH occurring 6 weeks after a pauci-symptomatic COVID-19 infection in a previously healthy adult. A bone marrow aspirate confirmed the HLH and the patient was successfully treated with dexamethasone and etoposide. To our knowledge, this is the first case of HLH occurring as a postacute COVID-19 syndrome following a pauci-symptomatic initial infection.