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Transpulmonary thermodilution devices have been widely shown to be accurate in septic shock patients in assessing fluid responsiveness. We conducted a systematic review to assess the relationship between fluid therapy protocols guided by transpulmonary thermodilution devices on fluid balance and the amount of intravenous fluid used in septic shock. We searched MEDLINE, Embase and The Cochrane Library. Studies were eligible for inclusion if they were prospective, parallel trials that were conducted in an intensive care setting in patients with septic shock. The comparator group was either central venous pressure, early goal-directed therapy or pulmonary artery occlusion pressure. Studies assessing only the accuracy of fluid responsiveness prediction by transpulmonary thermodilution devices were excluded. Two reviewers independently performed the search, extracted data and assessed the bias of each study. In total 27 full-text articles were identified for eligibility; of these, nine studies were identified for inclusion in the systematic review. Three of these trials used dynamic parameters derived from transpulmonary thermodilution devices and six used primarily static parameters to guide fluid therapy. There was evidence for a significant reduction in positive fluid balance in four out of the nine studies. From the available studies, the results suggest the benefit of transpulmonary thermodilution monitoring in the septic shock population with regard to reducing positive fluid balance is seen when the devices are utilised for at least 72 hours. Both dynamic and static parameters derived from transpulmonary thermodilution devices appear to lead to a reduction in positive fluid balance in septic shock patients compared to measurements of central venous pressure and early goal-directed therapy.

In patients with septic shock, a correlation between positive fluid balance and worsened outcomes has been reported in multiple observational studies worldwide. No published data exists in an Australasian cohort. We set out to explore this association in our institution. We conducted a retrospective audit of patient records from August 2012 to May 2015 in a single-centre, 24-bed surgical and medical intensive care unit (ICU) in Sydney, Australia. All patients with septic shock were included. Exclusion criteria included length of stay less than 24 hours or vasopressors needed for less than six hours. Data was gathered on fluid balance for the first seven days of ICU admission, biochemical data and other clinical indices. The primary outcome measure was survival to hospital discharge. One hundred and eighty-six patients with septic shock were included, with an overall hospital mortality of 23.7%. Seventy-five percent of patients required mechanical ventilation, and 27.4% required haemodialysis. The mean daily fluid balance on the first day of admission was positive 1,424 ml and 1,394 ml for ICU and hospital survivors, respectively. On average, the daily fluid balance for non-survivors was higher than the survivors: ICU non-survivors were 602 (95% confidence intervals 230, 974) ml (P=0.0015) and hospital non-survivors were 530 [95% confidence intervals 197, 863] ml (P=0.0017) higher than the survivors. In line with other recently published data, after adjustment for confounders (severity of illness based on the Acute Physiology and Chronic Health Evaluation score) we found a correlation between positive fluid balance and worsened hospital mortality in critically ill patients with sepsis and septic shock. Further research investigating rational use of fluids in this patient group is needed.

Diabetic ketoacidosis (DKA) is a life-threatening complication of type 1 diabetes (T1D), which without treatment leads to death. Fulminant type 1 diabetes (FT1D) is a subtype characterised by a markedly rapid and almost complete destruction of pancreatic β-cells, with acute onset leading to severe metabolic derangement and commonly ICU admission. We present a case of an 18-year-old male presenting with FT1D with two rare complications of pneumomediastinum and stress-induced cardiomyopathy (SIC) with significant myocardial necrosis. We also discuss the aetiology of the pneumomediastinum; the latest thoughts on SIC: moving beyond the simple description of ‘Takotsubo cardiomyopathy’; the role of troponins in critical illness; and genetic predisposition for DKA due to FT1D.