Use of Vasopressor Increases the Risk of Mortality in Traumatic Hemorrhagic Shock: A Nationwide Cohort Study in Japan

Objectives: To evaluate the possible association of vasopressor use with mortality in traumatic hemorrhagic shock patients. Design: Retrospective cohort study. Setting: Traumatic hemorrhagic shock patients at 260 emergency hospitals in Japan between 2004 and 2015. Patients: Three-thousand five-hundred fifty-one traumatic hemorrhagic shock patients who had systolic hypotension (

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ICU Management of Trauma Patients

Objectives: To describe the current state of the art regarding management of the critically ill trauma patient with an emphasis on initial management in the ICU. Data Sources and Study Selection: A PubMed literature review was performed for relevant articles in English related to the management of adult humans with severe trauma. Specific topics included airway management, hemorrhagic shock, resuscitation, and specific injuries to the chest, abdomen, brain, and spinal cord. Data Extraction and Data Synthesis: The basic principles of initial management of the critically ill trauma patients include rapid identification and management of life-threatening injuries with the goal of restoring tissue oxygenation and controlling hemorrhage as rapidly as possible. The initial assessment of the patient is often truncated for procedures to manage life-threatening injuries. Major, open surgical procedures have often been replaced by nonoperative or less-invasive approaches, even for critically ill patients. Consequently, much of the early management has been shifted to the ICU, where the goal is to continue resuscitation to restore homeostasis while completing the initial assessment of the patient and watching closely for failure of nonoperative management, complications of procedures, and missed injuries. Conclusions: The initial management of critically ill trauma patients is complex. Multiple, sometimes competing, priorities need to be considered. Close collaboration between the intensivist and the surgical teams is critical for optimizing patient outcomes. The authors have disclosed that they do not have any potential conflicts of interest. For information regarding this article, E-mail: stisherman@umm.edu Copyright © by 2018 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.

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A 3 adenosine receptor agonist attenuates neuropathic pain by suppressing activation of microglia and convergence of nociceptive inputs in the spinal dorsal horn

Abstract

Peripheral nerve injuries cause glial activation and neuronal hyperactivity in the spinal dorsal horn. These changes have been considered to be involved in the underlying mechanisms for the development and maintenance of neuropathic pain. Using double immunofluorescence labeling, we previously demonstrated that spinal microglial activation induced by nerve injury enhanced convergence of nociceptive inputs in the spinal dorsal horn from uninjured afferents. The adenosine A₃ receptor (A₃AR) agonists have been shown to have antinociceptive activities in several experimental neuropathic pain models. However, the mechanisms underlying these antinociceptive actions of the A₃AR agonist are still not fully explored. In this study, the effects of the A₃AR agonist (i.e., IB-MECA) on microglial activation, enhancement of convergent nociceptive inputs, and nocifensive behaviors were examined after tibial nerve injury. Injury to the tibial nerve initially caused hyposensitivity to touch stimulus at 3 days, and then resulted in tactile allodynia at 14-day post-injury. The daily systemic administration of IB-MECA (0.1 mg/kg/day) for 8 days in a row starting on the day of nerve injury or 7 days after nerve injury prevented the development of behaviorally assessed hypersensitivities, and spinal microglial activation induced by nerve injury. These treatments also suppressed anomalous convergence of nociceptive primary inputs in the spinal dorsal horn. The present findings indicate that the A₃AR agonist attenuates neuropathic pain states by suppressing enhanced microglial activation, and anomalous convergence of nociceptive inputs in the spinal dorsal horn from uninjured afferents after injury to the peripheral nerve.

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Fluid Management in Acute Brain Injury

Abstract

Purpose of the Review

The aims of fluid management in acute brain injury are to preserve or restore physiology and guarantee appropriate tissue perfusion, avoiding potential iatrogenic effects. We reviewed the literature, focusing on the clinical implications of the selected papers. Our purposes were to summarize the principles regulating the distribution of water between the intracellular, interstitial, and plasma compartments in the normal and the injured brain, and to clarify how these principles could guide fluid administration, with special reference to intracranial pressure control.

Recent Findings

Although a considerable amount of research has been published on this topic and in general on fluid management in acute illness, the quality of the evidence tends to vary. Intravascular volume management should aim for euvolemia. There is evidence of harm with aggressive administration of fluid aimed at achieving hypervolemia in cases of subarachnoid hemorrhage. Isotonic crystalloids should be the preferred agents for volume replacement, while colloids, glucose-containing hypotonic solutions, and other hypotonic solutions or albumin should be avoided. Osmotherapy seems to be effective in intracranial hypertension management; however, there is no clear evidence regarding the superiority of hypertonic saline over mannitol.

Summary

Fluid therapy plays an important role in the management of acute brain injury patients. However, fluids are a double-edged weapon because of the potential risk of hyper-hydration, hypo- or hyper-osmolar conditions, which may unfavorably affect the clinical course and the outcome.

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Gender differences in doxorubicin pharmacology for subjects with chemosensitive cancers of young adulthood

Abstract

Purpose

For many cancers, adolescents and young adults (AYA) have worse outcomes than for children and adults. Many factors may contribute to the AYA survival gap, including differences in biology, therapeutic intent, and adherence to therapy. It has been observed that male AYAs have poorer outcomes than females. The purpose of this work was to test the proposition that gender-related pharmacologic factors may account for a component of the AYA survival gap.

Patients and methods

A prospective, multi-institutional pharmacologic study of 79 patients in total with chemosensitive cancers (Ewing sarcoma, osteosarcoma and Hodgkin lymphoma) was conducted, with conventional doxorubicin treatment. Pharmacokinetic data of 13 children, 40 AYAs and 13 adults were valid for analysis. Population pharmacokinetics models were developed for doxorubicin and its metabolite doxorubicinol based on the data created in this study. Consequently, model-based analysis was conducted to investigate the relevant topics.

Results

The clearance of doxorubicinol (normalized to body surface area), the main active metabolite of doxorubicin, appears faster in male AYAs than female (p = 0.04, 95% CI 0.1–3.9 L/h). The exposure of doxorubicinol (normalized to dose) is lower in male AYA than female (p = 0.03, 95% CI − 0.005 to − 0.0002 h/L). These might be correlated to the observed difference on nadir neutrophil count between male AYA and female (p = 0.027, 95% CI 0.09–1.4).

Conclusion

Gender-related differences in doxorubicin pharmacology may account for worse outcomes for male AYAs with chemosensitive cancers compared to females. These findings may reduce the AYA survival gap compared to other age groups.

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Intracranial bleeding (ICB) as a catastrophic complication of Streptococcus gordonii infective endocarditis (IE) in an immunocompetent patient

We present an interesting case of late-onset intracranial bleeding (ICB) as a complication of Streptococcus gordonii causing infective endocarditis. A previously healthy young woman was diagnosed with infective endocarditis. While she was already on treatment for 2 weeks, she had developed seizures with a localising neurological sign. An urgent non-contrasted CT brain showed massive left frontoparietal intraparenchymal bleeding. Although CT angiogram showed no evidence of active bleeding or contrast blush, massive ICB secondary to vascular complication of infective endocarditis was very likely. An urgent decompressive craniectomy with clot evacuation was done immediately to release the mass effect. She completed total 6 weeks of antibiotics and had postoperative uneventful hospital stay despite having a permanent global aphasia as a sequel of the ICB.

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Rare cause of gastric outlet obstruction: xanthogranulomatous cholecystitis

Description 

A 62-year-old Indian female patient presented with right upper quadrant pain and multiple episodes of vomiting for 10 days. She denied history of fever, jaundice, past anorexia/weight loss and previous surgeries. She was dehydrated, tachycardia (120/min) was present, and there was tenderness in the right upper quadrant. Routine investigations revealed presence of anaemia (haemoglobin 9.1 g/dL), raised total leucocyte counts (17 x10^9/L) and hypokalaemia (2.8 mEq/L). All other blood tests (liver function/kidney function/blood sugar and coagulation profile) were normal. Patient was stabilised with intravenous fluids, antibiotics and other supportive management. Imaging with ultrasound (USG) was suboptimal due to the massive intestinal gas and uncooperative nature of the patient. A collapsed gallbladder (GB) and a mass with a smooth curvilinear surface and posterior acoustic shadowing in the distal part of the duodenum were the only distinguishable findings. Due to repeated episodes of vomiting, the patient underwent an upper gastrointestinal endoscopy, which was...

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