Long-term outcomes and quality of life in critically ill patients with hematological or solid malignancies: a single center study.

PURPOSE: Data concerning long-term outcomes and quality of life (QOL) in critically ill cancer patients are scarce. The aims of this study were to assess long-term outcomes and QOL in critically ill patients with hematological (HM) or solid malignancies (SM) 3 months and 1 year after intensive care unit (ICU) discharge, to compare these with QOL before ICU admission, and to identify prognostic indicators of long-term QOL. METHODS: During a 1 year prospective observational cohort analysis, consecutive patients with HM or SM admitted to the medical or surgical ICU of a university hospital were screened for inclusion. Cancer data, demographics, co-morbidity, severity of illness, organ failures, and outcomes were collected. The QOL before ICU admission, 3 months, and 1 year after ICU discharge was assessed using standardized questionnaires (EuroQoL-5D, Medical Outcomes Study 36-item Short Form Health Survey). Statistical significance was attained at P < 0.05. RESULTS: There were 483 patients (85 HM, 398 SM) (64% men) with a median age of 62 years included. Mortality rates of HM compared to SM were, respectively: hospital (34 vs. 13%), 3 months (42 vs. 17%), and 1 year (66 vs. 36%) (P < 0.001). QOL declined at 3 months, but improved at 1 year although it remained under baseline QOL, particularly in HM. Older age (P = 0.007), severe comorbidity (P = 0.035), and HM (P = 0.041) were independently associated with poorer QOL at 1 year. CONCLUSIONS: Long-term outcomes and QOL were poor, particularly in HM. Long-term expectations should play a larger role during multidisciplinary triage decisions upon referral to the ICU.

Early recognition of malignant lactic acidosis in clinical practice: report on 6 patients with haematological malignancies.

BACKGROUND: Malignant lactic acidosis is a potentially overlooked but life-threatening complication in patients with haematological malignancies. The aim of this study is to describe the features of six patients with malignant lactic acidosis and to discuss how its initial presentation can be differentiated from that of severe sepsis. METHODS: We prospectively collected data of all consecutive patients with haematological malignancies, admitted to the Ghent University Hospital Intensive Care Unit (ICU) between 2000 and 2007. RESULTS: Of 372 patients with haematological malignancies admitted to the ICU for life- threatening complications, 58 presented with lactic acid levels > or = 5 mmol/L. Six were diagnosed with malignant lactic acidosis. All patients with malignant lactic acidosis had high-grade lymphoblastic malignancies and were referred with a tentative diagnosis of severe sepsis or septic shock; lactic acid levels exceeded 9.45 mmol/L and lactate dehydrogenase (LDH) levels were at least 1785 U/L. Two patients had hypoglycaemia. All had a pronounced polypnea. In all patients hepatic malignant involvement was suspected. Two of the six patients survived their episode thanks to the early recognition of malignant lactic acidosis and the prompt administration of chemotherapy. One patient was still alive 6 months after initiating chemotherapy. CONCLUSION: Malignant lactic acidosis is a rare and often rapidly fatal metabolic complication if not promptly recognized and treated. An elevated lactic acid concentration, in disproportion with the level of tissue hypoxia, together with high serum LDH are cornerstones in the diagnosis. In contrast to septic shock patients, pronounced polypnea (Kussmaul's breathing pattern) rather than the haemodynamic instability is prominent.

Aspiration pneumonia: an underestimated cause of severe respiratory failure in patients with haematological malignancies and severe oral mucositis?

Aspiration pneumonia is rarely considered in the differential diagnosis of respiratory failure in patients suffering from haematologic malignancies in daily practice. We describe four patients who were admitted with severe respiratory failure in the ICU over a one-year-period prospective survey (a total of 72 patients with haematological malignancies of which 34 presented with respiratory failure). All of these patients had chemotherapy-induced severe oral mucositis (WHO grade ILL-IV) for which three of them received opioids. All had a history of cough after oral rinsing and two of them experienced sudden brief desaturation in the days before ICU referral. Two of these patients, both in allogeneic bone marrow transplant setting, died. With this data, we want to draw the attention to the diagnosis of aspiration pneumonia in this group of patients.

Effect of ozone exposure on allergic sensitization and airway inflammation induced by dendritic cells.

BACKGROUND: Epidemiological studies suggest that ozone exposure is related to increased asthma symptoms. Dendritic cells (DCs) are the principal antigen-presenting cells in the airways. OBJECTIVE: We have examined whether ambient doses of ozone (100 ppb for 2 h) enhance allergic sensitization and/or airway inflammation in a mouse model. METHODS: C57BL/6 mice were sensitized to inhaled ovalbumin (OVA) by intratracheal instillation of OVA-pulsed DCs on day 0. Daily exposure to OVA aerosol on days 14-20 resulted in an eosinophilic airway inflammation, as reflected in bronchoalveolar lavage fluid and lung histology. In a first experiment, mice were exposed to ozone or room air immediately prior to and following sensitization. Subsequently, we tested the effect of ozone exposure during antigen challenge in DC-sensitized mice. RESULTS: Exposure to ozone during sensitization did not influence airway inflammation after subsequent allergen challenge. In contrast, in sensitized mice, challenge with OVA together with ozone (days 14-20) resulted in enhanced airway eosinophilia and lymphocytosis, as compared with mice exposed to OVA and room air (1.91 x 106 +/- 0.46 x 106 vs. 0.16 x 106 +/- 0.06 x 106 eosinophils/mL lavage fluid; P = 0.015; 0.49 x 106 +/- 0.11 x 106 vs. 0.08 x 106 +/- 0.03 x 106 lymphocytes/mL lavage fluid; P = 0.004). Ozone exposure without subsequent OVA exposure did not cause airway inflammation. CONCLUSION: Ozone exposure does not increase allergic sensitization but enhances antigen-induced airway inflammation in mice that are sensitized via the airways.