July 30, 2020

What is it HLH? Hemophagocytic Lymphohistiocytosis (HLH) is a rare and often fatal syndrome of uncontrolled and ineffective inflammatory response to a certain trigger. It is characterized by excessive proliferation of lymphocytes and macrophages (histiocytes), hence the name “lymphohistiocytosis”. This results in the overproduction of cytokines, responsible for many of the clinical features present in this syndrome. Familial, or genetic, HLH occurs as a result of a genetic mutation leading to impaired cytotoxic function. There have been several genetic mutations indicated in the development of HLH, including an association with congenital immunodeficiency syndromes, such as Chediak-Higashi, Griscelli and X-Linked Lymphoproliferative Syndromes. This form most often occurs within the first year of life (median age 8 months), with the majority of pediatric cases occurring <2 years of age, but can range from infancy to adulthood. Acquired HLH occurs in the setting of an underlying condition, such as immunodeficiency, malignancy, or autoimmune disease. When HLH is secondary to a predisposing autoimmune disease, it is referred to as macrophage activating syndrome (MAS).  Acquired HLH is the most common cause of this syndrome in adults, but this form can be seen in all ages. Overall, the syndrome is most often triggered by an infectious agent in an otherwise healthy person.

July 16, 2020

Background: The cornerstones of sepsis management continues to include early identification, early appropriate empiric antibiotics, definitive source control, and vasopressors to support end organ perfusion. There have been multiple studies looking at the co-administration of hydrocortisone, ascorbic acid, and thiamine (known as HAT therapy or the metabolic cocktail) to help reduce mortality and reverse shock. Despite the original Marik study showing an association between HAT therapy and a 31.9% overall decrease in mortality and a 3-fold decrease in time to vasopressor discontinuation in patients presenting with severe sepsis and septic shock, the mortality benefit has not been reproduced in subsequent randomized clinical trials.  Studies focused specifically on the use of corticosteroids have demonstrated reduced time on vasopressors in patients in septic shock.  The bigger question is does vitamin C and thiamine add anything additional to help improve mortality (The ORANGES Trial)?

June 29, 2020

Background: In patients with acute respiratory distress syndrome (ARDS) the National Heart, Lung, and Blood Institute ARDS clinical trials network recommends a target partial pressure of arterial oxygen (Pao2) between 55 and 80 mmHg. Goals of arterial oxygenation are not based on robust experimental data and prior evidence has shown the feasibility of targeting a lower partial pressure of arterial oxygen in patients with ARDS. The authors of this trial, aptly named the study, LOCO2 (Liberal Oxygenation vs Conservative Oxygenation). They sought to determine whether a lower oxygen strategy was safe in patients with ARDS.

June 11, 2020

Background: In end-stage renal disease (ESRD) patients on hemodialysis (HD), infection is the second most common cause of mortality after cardiovascular disease (Sarnik 2000). Because of the systemic inflammation and increased capillary permeability, septic patients are at significant risk for fluid imbalances and frequently require large volumes of crystalloids. The Surviving Sepsis Campaign guidelines provide a strong recommendation with low quality of evidence for administering a 30mL/kg fluid bolus within 3 hours of recognition of sepsis-induced hypoperfusion (Rhodes 2016). Further fluid administration should be guided by hemodynamic assessment (bedside echocardiography, passive leg-raise, etc.). In the general population, this early administration of fluids to patients with hypotension or sepsis-induced hypoperfusion has been associated with improved outcomes. However, there is significant confusion regarding the effects of a large 30mL/kg bolus on ESRD patients due to a lack of studies. While these patients may appear, volume overloaded on physical exam, they may be intravascularly volume deplete. Physicians may be hesitant to administer a large fluid bolus in ESRD patients because of the risk of precipitating cardiogenic shock, pulmonary edema, and respiratory failure. In fact, multiple studies show that patients who have ESRD are less likely to receive the full 30mL/kg fluid bolus compared to non-ESRD patients (Lowe 2018, Truong 2019, Dagher 2015). Furthermore, some studies show equivalent outcomes between ESRD patients who receive the full bolus and those who do not. We will review two studies that examined this topic.

June 4, 2020

Traditionally, vasopressor infusions have been done through central venous catheters (CVCs) due to the hypothetical risk of extravasation injury to extremities when given through peripheral IVs.  The documented risk of extravasation from peripheral pressors is 3 – 6% [1][3][4][5]. Hypothetically, the extravasation rate can be further reduced.  At Essentials of EM 2020 I gave a short 10-minute talk on 6 pearls I have implemented.  This post will serve as a summary of that talk.