The growing impact of older patients in the emergency department: a 5-year retrospective analysis in Brazil.

BACKGROUND: The average age of the global population is rising at an increasing rate. There is a disproportional increase in Emergency Department (ED) visits by older people worldwide. In the Brazilian health system, complex and severely ill patients and those requiring specialized urgent procedures are referred to tertiary level care. As far as we know, no other study in Latin America has analyzed the impact of demographic changes in tertiary ED attendance. AIM: To describe the sociodemographic characteristics and outcomes of tertiary Brazilian ED users. METHODS: Design: Observational cross-sectional analytic study. SETTING: Emergency Department, tertiary university hospital, São Paulo, Brazil. PARTICIPANTS: patients aged 18 years or older attending a tertiary ED (2009-2013). The primary outcomes were hospitalization and mortality; the secondary outcome was ICU admission. Age was categorized as 'young adults' (18-39y), 'adults' (40-59y), 'young-older adults' (60-79y), and 'old-older adults' (80-109y). Other variables included sex, reason for attendance, time of ED visit, mode of presentation, type of hospitalization, main procedure, length of hospital stay (LOS) and length of ICU stay (ICU-LOS). We calculated descriptive statistics, built generalized linear mixed models for each outcome and estimated Odds Ratios (95% CI) for the independent categorical variables. The significance level was 5% with Bonferroni correction. RESULTS: Older age-groups represented 26.6% of 333,028 ED visits, 40.7% of admissions, 42.7% of ICU admissions and 58% of all deaths. Old-older patients accounted for 5.1% of ED visits, 9.5% of admissions and 10.1% of ICU admissions. Hospitalization, ICU admission and mortality rates increased with older age in both sexes. LOS and ICU-LOS were similar across age-groups. The proportions of visits and admissions attributed to young adults decreased annually, while those of people aged 60 or over increased. The ORs for hospitalization, ICU admission and mortality associated with the old-older group were 3.49 (95% CI = 3.15-3.87), 1.27 (1.15-1.39) and 5.93 (5.29-6.66) respectively, with young adults as the reference. CONCLUSIONS: In tertiary ED, age is an important risk factor for hospitalization and mortality, but not for ICU admission. Old-older people are at the greatest risk and demand further subgroup stratification.

Negative regulation of bacterial killing and inflammation by two novel CD16 ligands.

Sepsis, a leading cause of death worldwide, involves exacerbated proinflammatory responses and inefficient bacterial clearance. Phagocytic cells play a crucial part in the prevention of sepsis by clearing bacteria through host innate receptors. Here, we used a phage display library to identify two peptides in Escherichia coli that interact with host innate receptors. One of these peptides, encoded by the wzxE gene of E. coli K-12, was involved in the transbilayer movement of a trisaccharide-lipid intermediate in the assembly of enterobacterial common antigen. Peptide-receptor interactions induced CD16-mediated inhibitory immunoreceptor tyrosine-based activating motif signaling, blocking the production of ROS and bacterial killing. This CD16-mediated inhibitory signaling was abrogated in a WzxE(-/-) mutant of E. coli K-12, restoring the production of ROS and bacterial killing. Taken together, the two novel CD16 ligands identified negatively regulate bacterial killing and inflammation. Our findings may contribute toward the development of new immunotherapies for E. coli-mediated infectious diseases and inflammation.

Development of an algorithm to aid triage decisions for intensive care unit admission: a clinical vignette and retrospective cohort study.

BACKGROUND: Intensive care unit (ICU) admission triage is performed routinely and is often based solely on clinical judgment, which could mask biases. A computerized algorithm to aid ICU triage decisions was developed to classify patients into the Society of Critical Care Medicine's prioritization system. In this study, we sought to evaluate the reliability and validity of this algorithm. METHODS: Nine senior physicians evaluated forty clinical vignettes based on real patients. The reference standard was defined as the priorities ascribed by two investigators with full access to patients' records. Agreement of algorithm-based priorities with the reference standard and with intuitive priorities provided by the physicians were evaluated. Correlations between algorithm prioritization and physicians' judgment of the appropriateness of ICU admissions in scarcity and nonscarcity settings were also evaluated. Validity was further assessed by retrospectively applying this algorithm to 603 patients with requests for ICU admission for association with clinical outcomes. RESULTS: Agreement between algorithm-based priorities and the reference standard was substantial, with a median κ of 0.72 (interquartile range [IQR] 0.52-0.77). Algorithm-based priorities demonstrated higher interrater reliability (overall κ 0.61, 95% confidence interval [CI] 0.57-0.65; median percentage agreement 0.64, IQR 0.59-0.70) than physicians' intuitive prioritization (overall κ 0.51, 95% CI 0.47-0.55; median percentage agreement 0.49, IQR 0.44-0.56) (p = 0.001). Algorithm-based priorities were also associated with physicians' judgment of appropriateness of ICU admission (priorities 1, 2, 3, and 4 vignettes would be admitted to the last ICU bed in 83.7%, 61.2%, 45.2%, and 16.8% of the scenarios, respectively; p < 0.001) and with actual ICU admission, palliative care consultation, and hospital mortality in the retrospective cohort. CONCLUSIONS: This ICU admission triage algorithm demonstrated good reliability and validity. However, more studies are needed to evaluate a difference in benefit of ICU admission justifying the admission of one priority stratum over the others.

Septic shock in older people: a prospective cohort study.

BACKGROUND: Septic shock is the first cause of death in Intensive Care Units. Despite experimental data showing increased inflammatory response of aged animals following infection, the current accepted hypothesis claims that aged patients are immunocompromised, when compared to young individuals. RESULTS: Here, we describe a prospective cohort study designed to analyze the immune profile of this population. CONCLUSION: Older people are as immunocompetent as the young individual, regarding the cytokines, chemokines and growth factors response to devastating infection.

Leukocyte infiltration in lung, muscle, and liver after limb compression in rats.

Muscle crush injury is associated with systemic manifestations known as crush syndrome. A systemic inflammatory response syndrome may be triggered by isolated crush injury. Using myeloperoxidase (MPO) activity and plasma fatty acid composition, we investigated the inflammatory response in distant organs after isolated limb compression in rats. Male Wistar rats were submitted to 1h of hind limb compression by a latex ribbon. Myeloperoxidase activity was measured in muscle, liver, and lung at progressive times (1, 2 or 4h) after bandage release. Plasma fatty acid composition was evaluated as an indirect measure of oxidative stress. The liver and hind limb muscles showed a transient increase in MPO activity. Pulmonary MPO activity, otherwise, increased progressively throughout the study and reached statistically significant values at 4h when compared to all other groups (p<0.05). Plasma levels of unsaturated fatty acids decreased gradually after decompression (p<0.05 compared to controls after 4h). Blunt traumatic muscle compression was associated with rapid and transient muscle and liver inflammatory cell infiltration but otherwise, polymorphonuclear cells showed progressive aggregation in lungs. The plasmatic unsaturated index decreased throughout the 4h after muscle release. We demonstrated that limb compression was associated with oxidative stress and distant inflammatory responses. Progressive inflammatory cell infiltration in lungs could be related with the delayed systemic adverse responses found after crush injury.

Cerebral vasculitis caused by Aspergillus simulating ischemic stroke in an immunocompetent patient.

Although Aspergillus is widespread, clinically significant disease is rare in immunocompetent patients. We present a case of an otherwise healthy individual who developed cerebral vasculitis and stroke symptoms from Aspergillus, to raise awareness of this entity.

A decision-aid tool for ICU admission triage is associated with a reduction in potentially inappropriate intensive care unit admissions.

PURPOSE: Intensive care unit (ICU) admission triage occurs frequently and often involves highly subjective decisions that may lead to potentially inappropriate ICU admissions. In this study, we evaluated the effect of implementing a decision-aid tool for ICU triage on ICU admission decisions. METHODS: This was a prospective, before-after study. Urgent ICU referrals to ten ICUs in a tertiary hospital in Brazil were assessed before and after the implementation of the decision-aid tool. Our primary outcome was the proportion of potentially inappropriate ICU referrals (defined as priority 4B or 5 referrals, accordingly to the Society of Critical Care Medicine guidelines of 1999 and 2016, respectively) admitted to the ICU within 48 h. We conducted multivariate analyses to adjust for potential confounders and evaluated the interaction between phase and triage priority. RESULTS: Of the 2201 patients analyzed, 1184 (53.8%) patients were admitted to the ICU. After adjustment for confounders, implementation of the decision-aid tool was associated with a reduction in potentially inappropriate ICU admissions using either the 1999 [adjOR (95% CI) = 0.36 (0.13-0.97)] or 2016 [adjOR (95%CI) = 0.35 (0.13-0.96)] definitions. CONCLUSION: Implementation of a decision-aid tool for ICU triage was associated with a reduction in potentially inappropriate ICU admissions.

Comparison of the effects of volemic reposition with 7.5% NaCl or blood in an experimental model of muscular compression and hemorrhagic shock.

OBJECTIVE: Crush syndrome is characterized by traumatic muscular injuries with severe systemic clinical repercussions. The systemic inflammatory reaction characterized acutely by infiltration of neutrophils in the lungs has been studied as part of the spectrum of crush syndrome. Experimental research may demonstrate alternative treatments for crush syndrome. The authors studied the hypothesis that hypertonic saline solution (7.5% NaCl) could minimize the local and systemic effects in a model of muscular compression and hemorrhagic shock. METHODS: Rabbits were submitted to a new model of muscle compression associated with hemorrhagic shock. Compression was applied through an Esmarch bandage, used for 1 h on the entire right lower limb. Hemorrhagic shock was induced for 1 h by dissection and catheterization of the carotid artery. Blood replacement or hypertonic saline solution was used to treat the shock. Biochemical analysis of plasma, quantification of muscular edema, and infiltration of inflammatory cells in the lungs were carried out. RESULTS: Animals treated with hypertonic solution presented the same hemodynamic response as the blood treated patients, less water in the compressed muscles and less infiltration of inflammatory cells in the lungs. The blood group presented hypocalcemia, a facet of crush syndrome. CONCLUSIONS: The proposed model was effective for the study of crush syndrome associated with hemorrhagic shock. The treatment with hypertonic solution showed benefits when compared with blood volume replacement.

OBJETIVO: A síndrome de esmagamento é caracterizada por lesões musculares traumáticas com graves repercussões clínicas sistêmicas. A reação inflamatória sistêmica, caracterizada agudamente por infiltração de neutrófilos nos pulmões, tem sido estudada como parte do espectro da síndrome de esmagamento. A pesquisa experimental pode demonstrar opções de tratamento para a síndrome de esmagamento. Os autores estudaram a hipótese de que solução salina hipertônica (NaCl 7,5%) pudesse minimizar os efeitos locais e sistêmicos da síndrome de esmagamento em um modelo de compressão muscular e choque hemorrágico. MÉTODOS: Coelhos foram submetidos a um novo modelo de compressão muscular associado ao choque hemorrágico. A compressão foi feita por uma faixa de Esmarch aplicada por uma hora em todo membro inferior direito. O choque hemorrágico foi induzido durante uma hora por dissecção e cateterização da artéria carótida. O choque foi tratado com reposição de sangue ou solução salina hipertônica. Foram feitas análises bioquímicas do plasma, quantificação do edema muscular e infiltração de células inflamatórias nos pulmões. RESULTADOS: Os animais tratados com solução hipertônica apresentaram a mesma resposta hemodinâmica observada naqueles tratados com sangue, menor quantidade de água nos músculos comprimidos e menor infiltração de células inflamatórias nos pulmões. O grupo tratado com sangue apresentou hipocalcemia, característica da síndrome de esmagamento. CONCLUSÕES: O modelo proposto mostrou-se efetivo para o estudo da síndrome de esmagamento associada ao choque hemorrágico. O tratamento com solução hipertônica apresentou benefícios quando comparado com a reposição volêmica com sangue.

Hypertonic saline solution increases the expression of heat shock protein 70 and improves lung inflammation early after reperfusion in a rodent model of controlled hemorrhage.

Hypertonic saline solution (HS solution, NaCl 7.5%) has shown to restore hemodynamic parameters in hemorrhagic shock and to decrease the inflammation triggered by ischemia-reperfusion injury (I-R). Therefore, our objective was to investigate the effects of HS solution on the mechanisms involved in I-R, in an experimental model of controlled hemorrhagic shock. Wistar rats (280-350 g) were submitted to controlled bleeding, keeping the mean arterial pressure around 40 mmHg, for 1 h. After that, rats were randomized and treated with HS solution (4 mL/kg) or normal saline (34 mL/kg). There were no differences in hemodynamic parameters between both groups for at least 2 h after shock. No difference either was observed in reactive oxygen species generation (measured indirectly by malondialdehyde concentration) or cytokines (interleukins 6 and 10) production (measured by enzyme-linked immunosorbent assay). Quantitative analysis of lung tissue showed a smaller neutrophil infiltration in animals that received HS solution. Moreover, the animals in the HS group showed an increased expression of heat shock protein 70. Therefore, we concluded that treatment of hemorrhagic shock with HS solution can decrease pulmonary inflammation and increase cellular protection by up-regulating heat shock protein 70 expression.

The herbal drug Catuama reverts and prevents ventricular fibrillation in the isolated rabbit heart.

INTRODUCTION: Catuama, an herbal drug very popular in Brazil, was tested on the reversion and prevention of ventricular fibrillation (VF) in the isolated rabbit heart. MATERIALS AND METHODS: Catuama (a mixture of Trichilia catigua, Paullinia cupana, Ptychopetalum olacoides, and Zinziber officinalis) was perfused in the isolated perfused rabbit heart. Its effects on intraventricular conduction, heart rate, and monophasic action potential (MAP) duration were evaluated, and sustained VF was induced. The effects on reversion and reinduction of arrhythmia were observed, and new measures were taken in the hearts that reverted. RESULTS: Catuama and T catigua reverted VF in all hearts, prevented reinduction, and prolonged intraventricular conduction. Catuama prolonged MAP phase 2. On the other hand, P cupana reverted VF in 3 of 5 hearts, but depressed automatism, prolonged MAP phase 3, and did not prevent reinduction. DISCUSSION: Catuama reverted and prevented VF in this model. T catigua extract is probably the main agent responsible for the beneficial actions observed. Further studies are now in progress to clarify these actions.

B lymphocytes undergo apoptosis because of FcgammaRIIb stress response to infection: a novel mechanism of cell death in sepsis.

Sepsis is predominantly characterized by proinflammatory signs in its initial phase, but can be also associated with immune suppression that can be a consequence of apoptotic cell death. The role of Fc receptors (FcRs) is poorly understood in this disease, and it was recently shown that, in addition to the promotion of opposite inflammatory responses, they are implicated in apoptosis. Using a model of peritonitis in mice that do not express activating FcRs, we tested the hypothesis that FcgammaRIIb, the only known immunoglobulin G receptor capable of inducing apoptosis, would participate in the induction of this kind of cell death during serious infection. The blocking of this receptor by a monoclonal antibody significantly decreased the number of apoptotic splenic B cells, demonstrating its involvement in apoptosis. FcgammaRIIb-mediated apoptosis was neither the result of increased TNFalpha levels nor was it associated with IL-10 production. Finally, the decreased apoptosis after mice treatment with FcgammaRIIb-blocking antibody was not sufficient to increase its survival. Thus, we conclude that although apoptosis is a multifactorial phenomenon in sepsis, one of these factors is the inhibitory immunoglobulin G receptor FcgammaRIIb. FcgammaRIIb stress response to infection is a novel mechanism that contributes to the comprehension of apoptosis in sepsis.

Antimicrobial peptide LL-37 participates in the transcriptional regulation of melanoma cells.

Antimicrobial peptides are an ancient family of molecules that emerged millions of years ago and have been strongly conserved during the evolutionary process of living organisms. Recently, our group described that the human antimicrobial peptide LL-37 migrates to the nucleus, raising the possibility that LL-37 could directly modulate transcription under certain conditions. Here, we showed evidence that LL-37 binds to gene promoter regions, and LL-37 gene silencing changed the transcriptional program of melanoma A375 cells genes associated with histone, metabolism, cellular stress, ubiquitination and mitochondria.

Fc Gamma Receptor IIA (CD32A) R131 Polymorphism as a Marker of Genetic Susceptibility to Sepsis.

Sepsis is a devastating disease that can affect humans at any time between neonates and the elderly and is associated with mortality rates that range from 30 to 80%. Despite intensive efforts, its treatment has remained the same over the last few decades. Fc receptors regulate multiple immune responses and have been investigated in diverse complex diseases. FcγRIIA (CD32A) is an immunoreceptor, tyrosine-based activation motif-bearing receptor that binds immunoglobulin G and C-reactive protein, important opsonins in host defense. We conducted a study of 702 patients (184 healthy individuals, 171 non-infected critically ill patients, and 347 sepsis patients) to investigate if genetic polymorphisms in the CD32A coding region affect the risk of septic shock. All individuals were genotyped for a variant at position 131 of the FcγRIIA gene. We found that allele G, associated with the R131 genotype, was significantly more frequent in septic patients than in the other groups (p = 0.05). Our data indicate that FcγRIIA genotyping can be used as a marker of genetic susceptibility to sepsis.

Auditory brainstem response in gerbils submitted to ischemia and sepsis.

INTRODUCTION: An ischemic stroke is a clinical condition that affects thousands of people worldwide. As a result of this injury, neuronal death can be observed, and in the natural course of recovery, the individual may develop sepsis. Sepsis is a systemic inflammatory response that can lead the patient to death. To assess the clinical condition of a patient with this condition, the Auditory Brainstem Response (ABR) can be useful, since it is not an invasive procedure, it is a fast technique and it can be done at the bedside. PURPOSE: To assess auditory brainstem response (ABR) latency values in gerbils subjected to ischemia and sepsis. METHODS: ABR values were collected from 72 adult male gerbils, which were divided into six groups: control, sepsis, ischemia, sham, ischemia with sepsis, and sham with sepsis. For the induction of sepsis, lipopolysaccharide (LPS) was applied intraperitoneally in gerbils. The animals were anesthetized with a ketamine/xylazine combination before collection; their ABR were collected before any procedure (base collection), after ischemia, and 24 hours after the application of LPS. The absolute latency of wave IV was evaluated, and the values were compared between groups. RESULTS: There were significant differences in the groups submitted to sepsis in the latency value of wave IV in relation with the other groups. CONCLUSION: ABR was sensitive to sepsis with the increase in latency of wave IV during the development of the disease in the experimental model used.

Impact of Time on Fluid Resuscitation with Hypertonic Saline (NaCl 7.5%) in Rats with LPS-Induced Acute Lung Injury.

Acute lung injury (ALI) is a common complication associated with septic shock that directly influences the prognosis of sepsis patients. Currently, one of the main supportive treatment modalities for septic shock is fluid resuscitation. The use of hypertonic saline (HS: 7.5% NaCl) for fluid resuscitation has been described as a promising therapy in experimental models of sepsis-induced ALI, but it has failed to produce similar results in clinical practice. Thus, we compared experimental timing versus clinical timing effectiveness (i.e., early vs. late fluid resuscitation) after the inflammatory scenario was established in a rat model of bacterial lipopolysaccharide-induced ALI. We found that late fluid resuscitation with hypertonic saline (NaCl 7.5%) did not reduce the mortality rates of animals compared with the mortality late associated with early treatment. Late fluid resuscitation with both hypertonic and normal saline increased pulmonary inflammation, decreased pulmonary function, and induced pulmonary injury by elevating metalloproteinase-2 and metalloproteinase-9 activity and collagen deposition in the animals, unlike early treatment. The animals with lipopolysaccharide-induced ALI that received late resuscitation with any kind of fluids demonstrated aggravated pulmonary injury and respiratory function. Moreover, we showed that the therapeutic window for a beneficial effect of fluid resuscitation with hypertonic saline is very narrow.

Plasma cytokine expression after lower-limb compression in rats.

OBJECTIVES: Muscle injury due to crushing (muscle compression injury) is associated with systemic manifestations known as crush syndrome. A systemic inflammatory reaction may also be triggered by isolated muscle injury. The aim of this study was to investigate the plasma levels of interleukins (IL) 1, 6 and 10 and tumor necrosis factor alpha (TNF-α), which are markers for possible systemic inflammatory reactions, after isolated muscle injury resulting from lower-limb compression in rats. METHODS: Male Wistar rats were subjected to 1 h of compression of their lower limbs by means of a rubber band. The plasma levels of IL 1, 6 and 10 and TNF-α were measured 1, 2 and 4 h after the rats were released from compression. RESULTS: The plasma levels of IL 10 decreased in relation to those of the other groups, with a statistically significant difference (p < 0.05). The method used did not detect the presence of IL 1, IL 6 or TNF-α. CONCLUSION: Our results demonstrated that the changes in plasma levels of IL 10 that were found may have been a sign of the presence of circulating interleukins in this model of lower-limb compression in rats.

OBJETIVOS: A lesão muscular por esmagamento (lesão por compressão muscular) está associada a manifestações sistêmicas conhecidas como síndrome do esmagamento. A reação inflamatória sistêmica pode também ser desencadeada pela lesão muscular isolada. O objetivo deste estudo foi investigar os níveis plasmáticos de interleucinas (IL) 1, 6, 10 e TNF-α, marcadores de uma possível reação inflamatória sistêmica, após a lesão muscular isolada resultante da compressão de membros inferiores de ratos. MÉTODOS: Ratos Wistar machos foram submetidos a uma hora de compressão dos membros inferiores por uma faixa de borracha. Os níveis plasmáticos de IL 1, 6, 10 e TNF-α foram medidos uma, duas e quatro horas após a liberação da compressão. RESULTADOS: Os níveis plasmáticos de IL 10 diminuíram quando comparados com outros grupos com diferença estatisticamente significante (p < 0,05). Não houve detecção, pelo método, da presença de IL 1, 6 e TNF-α. CONCLUSÃO: Nossos resultados demonstraram que as alterações dos níveis plasmáticos de IL 10 encontradas podem ser um sinal da presença de interleucinas circulantes nesse modelo de compressão de membros inferiores de ratos.

Hypertonic Saline (NaCl 7.5%) Reduces LPS-Induced Acute Lung Injury in Rats.

Acute respiratory distress syndrome (ARDS) is the most severe lung inflammatory manifestation and has no effective therapy nowadays. Sepsis is one of the main illnesses among ARDS causes. The use of fluid resuscitation is an important treatment for sepsis, but positive fluid balance may induce pulmonary injury. As an alternative, fluid resuscitation with hypertonic saline ((HS) NaCl 7.5%) has been described as a promising therapeutical agent in sepsis-induced ARDS by the diminished amount of fluid necessary. Thus, we evaluated the effect of hypertonic saline in the treatment of LPS-induced ARDS. We found that hypertonic saline (NaCl 7.5%) treatment in rat model of LPS-induced ARDS avoided pulmonary function worsening and inhibited type I collagen deposition. In addition, hypertonic saline prevented pulmonary injury by decreasing metalloproteinase 9 (MMP-9) activity in tissue. Focal adhesion kinase (FAK) activation was reduced in HS group as well as neutrophil infiltration, NOS2 expression and NO content. Our study shows that fluid resuscitation with hypertonic saline decreases the progression of LPS-induced ARDS due to inhibition of pulmonary remodeling that is observed when regular saline is used.

Cardiovascular and respiratory interactions of hyperosmolar saline, scorpion toxin, and veratridine in rats.

This study evaluates the cardiovascular and respiratory effects evoked by hypertonic sodium chloride solution (HSS) and the possible interactions of these effects with scorpion toxin (TX) or veratridine (V). Groups 1 (1 mL/kg, rapid), 2 (4 mL/kg, rapid), and 3 (4 mL/kg, slow) were used for comparison of HSS administered by rapid or slow injection. HSS (4 mL/kg) was injected after bilateral vagotomy (group 4) or administration of atropine (group 5). In groups 6 (1 mL/kg in bolus), 7 (4 mL/kg in bolus), and 8 (4 mL/kg/60 s), HSS was injected 20 min after the administration of TX (250 microg/kg). In group 9, two doses of V (25 microg/kg, i.v.) were injected 10 min apart. Concomitantly with the second dose of V, HSS (4 mL/kg) was injected into the jugular vein. HSS administered by rapid injection (1 mL/kg) resulted in hypotension, hyperventilation, and a slight decrease in heart rate. However, when HSS was administered after TX, only bradypnea was observed. HSS (4 mL/kg, rapid) induced a rapid and marked fall in blood pressure, bradycardia, and apnea. However, when HSS was administered after TX, a more pronounced bradycardia and a smaller reduction in mean arterial pressure were observed. Slow injection of HSS (60 s) evoked hypotension, hyperventilation, and bradycardia. The same dose injected after TX resulted in bradypnea and a smaller reduction in blood pressure. The HSS-induced hypotension was attenuated by previous administration of atropine or by vagotomy, whereas bradycardia was prevented by previous injection of atropine, but not by bilateral vagotomy. Like vagotomy, atropinization prevented the apnea and bradypnea produced by HSS (4 mL/kg in bolus). V evoked a slight bradycardia, hypotension, and apnea. These effects were potentiated when V was injected concomitantly with HSS. The effects of HSS are dependent on both volume and speed of injection, and are affected by previous injection of TX or concomitant injection of V.

Neuroleptic-induced acute respiratory distress syndrome.

CONTEXT: A case of neuroleptic malignant syndrome and acute respiratory distress syndrome is presented and discussed with emphasis on the role of muscle relaxation, creatine kinase, and respiratory function tests. CASE REPORT: A 41-year-old man presented right otalgia and peripheral facial paralysis. A computed tomography scan of the skull showed a hyperdense area, 2 cm in diameter, in the pathway of the anterior intercommunicating cerebral artery. Preoperative examination revealed: pH 7.4, PaCO2 40 torr, PaO2 80 torr (room air), Hb 13.8 g/dl, blood urea nitrogen 3.2 mmol/l, and creatinine 90 mmol/l. The chest x-ray was normal. The patient had not eaten during the 12-hour period prior to anesthesia induction. Intravenous halothane, fentanyl 0.5 mg and droperidol 25 mg were used for anesthesia. After the first six hours, the PaO2 was 65 torr (normal PaCO2) with FiO2 50% (PaO2/FiO2 130), and remained at this level until the end of the operation 4 hours later, maintaining PaCO2 at 35 torr. A thrombosed aneurysm was detected and resected, and the ends of the artery were closed with clips. No vasospasm was present. This case illustrates that neuroleptic drugs can cause neuroleptic malignant syndrome associated with acute respiratory distress syndrome. Neuroleptic malignant syndrome is a disease that is difficult to diagnose. Acute respiratory distress syndrome is another manifestation of neuroleptic malignant syndrome that has not been recognized in previous reports: it may be produced by neuroleptic drugs independent of the manifestation of neuroleptic malignant syndrome. Some considerations regarding the cause and effect relationship between acute respiratory distress syndrome and neuroleptic drugs are discussed. Intensive care unit physicians should consider the possibility that patients receiving neuroleptic drugs could develop respiratory failure in the absence of other factors that might explain the syndrome.