Sengstaken-Blakemore tube in critical upper gastrointestinal bleeding: Implications for aeromedical retrieval.

Sengstaken-Blakemore tubes (SBTs) are rarely used in Australia, because of improved access to endoscopy and interventional radiology, as well as overall lower rate of variceal haemorrhage from improvements in primary prophylaxis. SBT's use is associated with significant rate of serious complications, such as oesophageal perforation, mucosal necrosis, aspiration pneumonia and respiratory compromise secondary to external compression of the trachea. As such, SBT is currently only recommended for use in life-threatening variceal haemorrhage, where endoscopic, embolization and pharmacologic therapy have been unsuccessful or are unavailable. No data exist for its use in Australasia but one area that it could be indicated is for hemodynamically unstable patients in remote setting, where long transfer times often means delayed access to endoscopy. We present a case of SBT insertion in retrieval medicine and discuss placement in the management of an unstable upper gastrointestinal bleed, complicating factors such as lack of radiology to confirm balloon position, the impact of flight altitude on balloon pressures, the maintenance of traction in flight and logistics of long flight times across the state of Queensland. This is the first case report of SBT use in the Australian aeromedical environment. It is also the first one where SBT has been used for duodenal bleeding, although the source of bleeding was unknown prior to insertion.

A national survey of intensive care follow-up clinics in Australia.

BACKGROUND: Intensive care follow-up clinics (ICFCs) have been implemented internationally with the aim to address the growing number of patients living with sequalae of critical illness and intensive care. However, data on Australian intensive care follow-up practice are rare. OBJECTIVES: The primary objective was to determine the proportion of Australian intensive care units (ICUs) that offer a dedicated ICFC to ICU survivors, with the intention of improving long-term outcomes of critical illness. Secondary objectives were to identify models of ICU follow-up and barriers to the implementation of ICFCs. METHODS: A custom-designed, pilot-tested 12-question online survey was sent to the nurse unit managers and medical directors of all 167 Australian ICUs listed in the database of the Australian and New Zealand Intensive Care Society. Outcome measures included proportion of ICUs offering ICFCs, details on types of follow-up services with staffing, funding source, and reasons for not providing ICU follow-up. RESULTS: One hundred seven of the 167 ICUs contacted responded to the survey. Of these, two (2%) operated a dedicated ICFC. Both ICFCs were nursing-led, with one receiving dedicated funding and the other being unfunded. Three units (3%) conducted routine outpatient follow-up by telephone; one of these services was doctor-led, and two were nurse-led. Four units (4%) were performing outpatient follow-up as part of research studies only. Among the units not operating an ICFC, the main reason given for not doing so were financial constraints (58%), followed by lack of clinical need (19%) and perceived lack of evidence (11%). CONCLUSION: In Australia, only two ICUs operated an ICFC. Only one outpatient follow-up service received dedicated funding, and financial constraints were the main reason given for units not offering outpatient follow-up services.

Inhalation of the ETA receptor antagonist LU-135252 selectively attenuates hypoxic pulmonary vasoconstriction.

Endogenous endothelin (ET)-1 modulates hypoxic pulmonary vasoconstriction (HPV). Accordingly, intravenously applied ET(A) receptor antagonists reduce HPV, but this is accompanied by systemic vasodilation. We hypothesized that inhalation of an ET(A) receptor antagonist might act selectively on the pulmonary vasculature and investigated the effects of aerosolized LU-135252 in an experimental model of HPV. Sixteen piglets (weight: 25 +/- 1 kg) were anesthetized and mechanically ventilated at an inspiratory oxygen fraction (Fi(O(2))) of 0.3. After 1 h of hypoxia at Fi(O(2)) 0.15, animals were randomly assigned either to receive aerosolized LU-135252 as bolus (0.3 mg/kg for 20 min; n = 8, LU group), or to receive aerosolized saline (n = 8, controls). In all animals, hypoxia significantly increased mean pulmonary arterial pressure (32 +/- 1 vs. 23 +/- 1 mmHg; P < 0.01; means +/- SE) and increased arterial plasma ET-1 (0.52 +/- 0.04 vs. 0.37 +/- 0.05 fmol/ml; P < 0.01) compared with mild hyperoxia at Fi(O(2)) 0.3. Inhalation of LU-135252 induced a significant and sustained decrease in mean pulmonary arterial pressure compared with controls (LU group: 27 +/- 1 mmHg; controls: 32 +/- 1 mmHg; values at 4 h of hypoxia; P < 0.01). In parallel, mean systemic arterial pressure and cardiac output remained stable and were not significantly different from control values. Consequently, in our experimental model of HPV, the inhaled ET(A) receptor antagonist LU-135252 induced selective pulmonary vasodilation without adverse systemic hemodynamic effects.