AIM: This study described the basic characteristics of children aged 0-16 years who were treated in intensive care units (ICUs) and paediatric ICUs (PICUs), compared their outcomes and examined any causes of death.

METHODS: This was a retrospective cohort study of admissions to 74 ICUs and three PICUs in Sweden that were recorded in the Swedish Intensive Care Registry from January 1, 2008 to December 31, 2012.

RESULTS: We retrieved data on 12 756 children who were admitted 17 003 times. The case mix differed between the ICUs, which were mainly admissions for injuries, accidents and observation, and PICUs, which were mainly admissions for malformations, genetic abnormalities and respiratory problems (p < 0.001). The median stays in the ICUs and PICUs were 1.4 and 3.5 days (p < 0.001), respectively. The respective crude mortality rates were 1.1% and 2.0, and the Paediatric Index of Mortality version 2 standardised mortality ratios were 0.43 and 0.50. None of these differences were significant. Most deaths were within 24 hours: About 57% in the ICUs, mainly from brain anomalies, and 13% in the PICUs, mainly from circulatory problems.

CONCLUSION: Sweden had a low mortality rate in both ICUs and PICUs and the children admitted to these two types of unit differed.

INTRODUCTION. Most patients admitted to intensive care are discharged to a general ward in the same hospital, but some patients require transfer to another hospital. Indications for interhospital transfers (IHT) include referral for specialist treatment, lack of intensive care beds at the referring ICU and repatriation to ICU in home hospital [1].

OBJECTIVES. To review mortality of ICU-patients undergoing IHT and analyse whether different indications for transfer render different mortalities.

METHODS. Retrospective cohort register study using the Swedish Intensive Care Registry (SIR) during 2016-2018. The SIR collects data from 98.8% of Swedish ICUs including data on discharge from ICUs to other hospitals/ICUs. Transfers were divided into three categories: transfer due to medical reasons, lack of ICU beds or repatriation to ICU in home hospital. We analysed odds ratios (ORs) for dying within 30 days after discharge from ICU using risk adjusted (SAPS3 score) multi-level mixed effect logistic regression with ICUs as random effect.

RESULTS. We identified 12,356 patients who were discharged to another ICU and hospital, i.e. inter-hospital transfers. The unadjusted mortality 30 days after IHT was 17.2 % compared to 12.4 % if discharged to ward in the same hospital. Mortality after IHT varied with the cause of discharge (Figure).Main diagnoses for transfer due to specialist treatment were subarachnoid haemorrhage, head injury and multi-trauma whilst for lack of ICU beds post cardiac arrest, respiratory failure and pneumonia dominated. Risk adjusted analysis showed a significantly increased risk of dying after discharge due to lack of ICU-beds in comparison with other reasons for IHTs

CONCLUSION. The adjusted risk of dying within 30 days after interhospital transfer was greater among critically ill patients when the transfer was due to lack of beds in the referring ICU. The increased mortality lingered for at least 6 months underlining the importance to identify causes and intervene to avoid unnecessary loss of life.

INTRODUCTION. Most patients admitted to intensive care are discharged to a general ward in the same hospital, but some patients require transfer to another hospital. Indications for interhospital transfers (IHT) include referral for specialist treatment, lack of intensive care beds at the referring ICU and repatriation to ICU in home hospital [1].

OBJECTIVES. To review mortality of ICU-patients undergoing IHT and analyse whether different indications for transfer render different mortalities.

METHODS. Retrospective cohort register study using the Swedish Intensive Care Registry (SIR) during 2016-2018. The SIR collects data from 98.8% of Swedish ICUs including data on discharge from ICUs to other hospitals/ICUs. Transfers were divided into three categories: transfer due to medical reasons, lack of ICU beds or repatriation to ICU in home hospital. We analysed odds ratios (ORs) for dying within 30 days after discharge from ICU using risk adjusted (SAPS3 score) multi-level mixed effect logistic regression with ICUs as random effect.

RESULTS. We identified 12,356 patients who were discharged to another ICU and hospital, i.e. inter-hospital transfers. The unadjusted mortality 30 days after IHT was 17.2 % compared to 12.4 % if discharged to ward in the same hospital. Mortality after IHT varied with the cause of discharge (Figure).Main diagnoses for transfer due to specialist treatment were subarachnoid haemorrhage, head injury and multi-trauma whilst for lack of ICU beds post cardiac arrest, respiratory failure and pneumonia dominated. Risk adjusted analysis showed a significantly increased risk of dying after discharge due to lack of ICU-beds in comparison with other reasons for IHTs

CONCLUSION. The adjusted risk of dying within 30 days after interhospital transfer was greater among critically ill patients when the transfer was due to lack of beds in the referring ICU. The increased mortality lingered for at least 6 months underlining the importance to identify causes and intervene to avoid unnecessary loss of life.

BACKGROUND: Cardiac dysfunction is a well-known complication of sepsis, but its long-term consequences and implications for patients remain unclear. The aim of this study was to investigate cardiac outcome in sepsis by assessing causes of death up to 2 years after treatment in an Intensive Care Unit (ICU) in a nationwide register-based cohort collected from the Swedish Intensive Care Registry.

METHODS: A cohort of 13 669 sepsis and septic shock ICU patients from 2008 to 2014 was collected together with a non-septic control group, matched regarding age, sex and severity of illness (n = 6582), and all without preceding severe cardiac disease. For a large proportion of the severe sepsis and septic shock patients (n = 7087), no matches were found. Information on causes of death up to 2 years after ICU admission was sought in the Swedish National Board of Health and Welfare's Cause of Death Registry.

RESULTS: Intensive Care Unit mortality was nearly identical in a matched comparison of sepsis patients to controls (24% in both groups) but higher in more severely ill sepsis patients for whom no matches were found (33% vs 24%, P < 0.001). There was no association of sepsis to cardiac deaths in the first month (OR 1.03, 95%CI 0.87 to 1.20, P = 0.76) nor up to 2 years after ICU admission (OR 1.01, 95%CI 0.82 to 1.25, P = 0.94) in an adjusted between-group comparison.

CONCLUSIONS: There was no association with an increased risk of death related to cardiac disease in patients with severe sepsis or septic shock when compared to other ICU patients with similar severity of illness.

Background: Current knowledge about prognosis after intensive care for COPD exacerbation in patients with long-term oxygen therapy (LTOT) is limited.

Aims: To investigate survival after ICU admission for COPD exacerbation in patients with and without LTOT.

Material and methods: Nationwide observational cohort study including all first-time ICU admissions for COPD exacerbation in the Swedish Intensive Care Register 2008-2015. The National Quality Register for Respiratory Failure (Swedevox) provided data on LTOT. Mortality was traced through the Population Register.

Results: The cohort included 4828 patients (60% women) and 466 had LTOT before first ICU admission. LTOT patients were older (median 74 years (IQR 69-79) vs 72 years (IQR 66-78), p<0.001) and had higher simplified acute physiology score 3 (SAPS3) score; median 60 (IQR 54-68) vs 59 (IQR 52-66), p=0.008).

Mortality was higher for LTOT patients in the ICU (13.5% vs 7.5%; p<0.001) and at 30 days after ICU admission (37.8% vs 25.0%; p<0.001). In logistic regression adjusted for SAPS3 score and sex, LTOT was associated with increased 30-day mortality (OR 1.8; 95% CI 1.4-2.2).Median survival time from ICU admission was 3.2 months (IQR 0.2-17.7) for LTOT patients and 16.0 months (IQR 1.0-52.8) for patients without LTOT.

Background

Local formation of nitric oxide (NO) in the lung in proportion to ventilation, leading to vasodilation, is a putative mechanism behind ventilation- perfusion matching. We examined the role of local constitutive NO formation on regional distributions of ventilation (V) and perfusion (Q) and ventilation-perfusion matching (V/Q) in mechanically ventilated adult sheep with normal gas exchange.

Methods

V and Q were analyzed in lung regions (≈1.5 cm3) before and after inhibition of constitutive nitric oxide synthase (cNOS) with Nω-nitro-L-arginine methyl ester (L-NAME) (25 mg/kg) in seven prone sheep ventilated with PEEP. V and Q were measured using aerosolized fluorescent and infused radiolabeled microspheres, respectively. The animals were exsanguinated while deeply anaesthetized; lungs were excised, dried at total lung capacity and divided into cube units. The spatial location for each cube was tracked and fluorescence and radioactivity per unit weight determined.

Results

Pulmonary artery pressure increased significantly after L-NAME (from mean 16.6 to 23.6 mmHg, P<0.01) while there were no significant changes in PaO2, PaCO2 or SD log(V/Q). Distribution of V was not influenced by L-NAME but a small redistribution of Q from ventral to dorsal lung regions resulting in less heterogeneity in Q along the gravitational axis was seen (p<0.01). Perfusion to regions with the highest ventilation (5th quintile of the V distribution) remained unchanged with L-NAME.

Conclusions

There was minimal or no influence of cNOS inhibition by L-NAME on the distributions of V and Q, and V/Q in prone anesthetized and ventilated adult sheep with normal gas exchange.

Introduction: Cardiac dysfunction is a well-known complication of sepsis, but its long-term consequences remain unclear. The aim of this study was to investigate cardiac outcome after sepsis by assessing causes of death in a nationwide register-based cohort.

Methods: A cohort of 9,520 severe sepsis and septic shock intensive care (ICU) patients without preceding severe cardiac failure and discharged alive from the ICU was collected from the Swedish Intensive Care Registry (SIR) from 2008 to 2013, together with a nonseptic control group (n = 4,577). Patients were matched according to age, sex and severity of illness. Information on cause of death after ICU discharge was sought in the Swedish National Board of Health and Welfare’s Cause of Death Registry.

Results: After ICU discharge, 3,954 (42%) of severe sepsis or septic shock patients died. In 654 (16%) of these, cardiac failure was registered as the cause of death. The follow-up time was 17,693 person-years (median 583 days/person; maximum 5.7 years) and the median (IQR) time from ICU discharge to cardiac failure-related death 81 (17 - 379) days. With increasing severity of illness (quartiles of SAPS3), the hazard rate for cardiac failure-related death increased (hazard ratio (HR) 1.58 (95% CI 1.19 - 2.09, p <0.001) in the highest quartile compared to the lowest). In a matched comparison between severe sepsis or septic shock patients and controls, survival was similar, and the hazard rate for cardiac failurerelated death did not differ between groups (HR 0.97, 95% CI 0.88 – 1.10, p = 0.62).

Conclusions: The risk of death with cardiac failure as the cause of death after severe sepsis or septic shock increases with severity of illness on admission. Patients with severe sepsis or septic shock are not, however, at an increased risk of death with cardiac failure as the cause of death when compared to other ICU patients with similar severity of illness.