Lung ischemia reperfusion injury (LIRI) is a pathologic process occurring when oxygen supply to the lung has been compromised followed by a period of reperfusion. The disruption of oxygen supply can occur either via limited blood flow or decreased ventilation termed anoxic ischemia and ventilated ischemia, respectively. When reperfusion occurs, blood flow and oxygen are reintroduced to the ischemic lung parenchyma, facilitating a toxic environment through the creation of reactive oxygen species, activation of the immune and coagulation systems, endothelial dysfunction, and apoptotic cell death. This review will focus on the mechanisms of LIRI, the current supportive treatments used, and the many therapies currently under research for prevention and treatment of LIRI.

Background The cellular mechanisms of neuropathic pain are inadequately understood. Previous investigations have revealed disrupted Ca2+ signaling in primary sensory neurons after injury. We therefore examined the effect of injury on intracellular Ca2+ stores of the endoplasmic reticulum, which critically regulate the Ca2+ signal and neuronal function. Methods Intracellular Ca2+ levels were measured with Fura-2 or mag-Fura-2 microfluorometry in axotomized fifth lumbar (L5) dorsal root ganglion neurons and adjacent L4 neurons isolated from hyperalgesic rats following L5 spinal nerve ligation, compared to neurons from control animals. Results Endoplasmic reticulum Ca2+ stores released by the ryanodine-receptor agonist caffeine decreased by 46% in axotomized small neurons. This effect persisted in Ca2+-free bath solution that removes the contribution of store-operated membrane Ca2+ channels, and after blockade of both the mitochondrial, sarco-endoplasmic Ca2+-ATPase, and the plasma membrane Ca2+ ATPase pathways. Ca2+ released by the sarco-endoplasmic Ca2+-ATPase blocker thapsigargin and by the Ca2+-ionophore ionomycin was also diminished by 25% and 41%, respectively. In contrast to control neurons, Ca2+ stores in axotomized neurons were not expanded by neuronal activation by K+ depolarization, and the proportionate rate of refilling by sarco-endoplasmic Ca2+-ATPase was normal. Luminal Ca2+ concentration was also reduced by 38% in axotomized neurons in permeabilized neurons. The adjacent neurons of the L4 dorsal root ganglia showed modest and inconsistent changes after L5 spinal nerve ligation. Conclusions Painful nerve injury leads to diminished releasable endoplasmic reticulum Ca2+ stores and a reduced luminal Ca2+ concentration. Depletion of Ca2+ stores may contribute to the pathogenesis of neuropathic pain.

Patients who incur unintentional dural punctures with large-gauge needles are surprisingly likely to continue to suffer chronic headaches. Treatment with an epidural blood patch does not enhance the risk of chronic back pain. The pathophysiology underlying these symptoms and the best treatment for this syndrome are not known.

Topics: Anesthetic ComplicationsU nintentional dural puncture during epidural anesthesia occurs in 0.4% to 6% of patients and can lead to acute severe positional headache in B70% to 80% of these parturients. The headaches are often self-limited or are treated with an epidural blood patch (EBP) or conservative therapy. Because long-term sequelae have not been investigated, this case-control study was performed to determine the incidence of and risk factors for chronic headache and chronic back pain in women who had an unintentional dural puncture compared with matched controls.Patients who were included had a known dural puncture with a 17-G Tuohy needle. Of 65 index cases, 40 patients met inclusion criteria and were matched to a control patient who had the same type of neuraxial anesthesia and delivery but no dural puncture, delivered within 1 week of the index patient, and was closest in height, age, and weight. At 12 to 24 months after the dural puncture, the patients and matched controls were contacted by telephone. Two validated questionnaires were used to assess headache and back pain symptoms. The questionnaire for evaluating headaches was derived from the Chronic Pain Grade Questionnaire, created to measure chronic pain for severity, persistence, and disability. The questionnaire for chronic back pain was derived from the Low Back Pain Rating Scale, which separately rates pain, disability, and physical impairment with pain scales.The average time between delivery and administration of the questionnaires was 18 ± 5.6 months and was similar in study patients and controls. Thirty-three patients (83%) who had an unintentional dural puncture reported an acute postdural puncture headache (PDPH) during hospitalization. Among the index cases, those with a higher body mass index and body weight were more likely to develop acute PDPH compared with patients with a lower body mass index and body weight (P = 0.023 and P = 0.022 for the comparisons, respectively). No other significant associations were found between demographic variables and the incidence of acute headache. EBP was used to treat acute PDPH in 24 of the 33 patients. The average time to resolution of the acute headache was 2.8 ± 2.8 days. At 18 months after delivery, 11 of 40 parturients (28%) who had dural puncture had chronic

Anesthesiologists face several perioperative challenges when patients need cytoreductive surgery and hyperthermic intraperitoneal chemoperfusion. To adequately care for these patients, anesthesiologists must understand the goals and objectives of the operation in addition to having a basic knowledge of the chemotherapeutic drugs that are frequently used. Optimal anesthetic management of patients treated with cytoreductive surgery and hyperthermic intraperitoneal chemoperfusion requires control of a complex interplay of physiologic mechanisms, including hyperthermia, abdominal hypertension, electrolyte abnormalities, coagulopathies, increased cardiac index, oxygen consumption, and decreased systemic vascular resistance. As this surgery continues to gain popularity among oncologic surgeons, further studies that clearly define the chemistry, pharmacokinetics, pharmacodynamics, and end points of efficacy need to be performed to elucidate optimal perioperative management.

Background Painful nerve injury leads to disrupted Ca2+ signaling in primary sensory neurons, including decreased endoplasmic reticulum (ER) Ca2+ storage. The present study examines potential causes and functional consequences of Ca2+ store limitation after injury. Methods Neurons were dissociated from axotomized fifth lumbar (L5) and the adjacent L4 dorsal root ganglia following L5 spinal nerve ligation that produced hyperalgesia, and were compared to neurons from control animals. Intracellular Ca2+ levels were measured with Fura-2 microfluorometry, and ER was labeled with probes or antibodies. Ultrastructural morphology was analyzed by electron microscopy of nondissociated dorsal root ganglia, and intracellular electrophysiological recordings were obtained from intact ganglia. Results Live neuron staining with BODIPY FL-X thapsigargin (Invitrogen, Carlsbad, CA) revealed a 40% decrease in sarco-endoplasmic reticulum Ca2+-ATPase binding in axotomized L5 neurons and a 34% decrease in L4 neurons. Immunocytochemical labeling for the ER Ca2+-binding protein calreticulin was unaffected by injury. Total length of ER profiles in electron micrographs was reduced by 53% in small axotomized L5 neurons, but increased in L4 neurons. Cisternal stacks of ER and aggregation of ribosomes occurred less frequently in axotomized neurons. Ca2+-induced Ca2+ release, examined by microfluorometry with dantrolene, was eliminated in axotomized neurons. Pharmacologic blockade of Ca2+-induced Ca2+ release with dantrolene produced hyperexcitability in control neurons, confirming its functional importance. Conclusions After axotomy, ER Ca2+ stores are reduced by anatomic loss and possibly diminished sarco-endoplasmic reticulum Ca2+-ATPase. The resulting disruption of Ca2+-induced Ca2+ release and protein synthesis may contribute to the generation of neuropathic pain.

Intra-aortic balloon pumps (IABPs) continue to be the most widely used cardiac support devices with an annual estimate of 200 000 IABPs placed worldwide. IABPs enhance myocardial function by maximizing oxygen supply and minimizing oxygen demand. The use of IABPs is not without risk, with major vascular injury, ischemia, and infection being the most common complications, especially in high-risk patients. While recent studies have questioned the use of IABPs in patients with cardiogenic shock secondary to myocardial infarction, these studies have limitations making it difficult to formulate definitive conclusions. This review will focus on the mechanisms of counterpulsation, the management of IABPs and the evidence supporting this ventricular support therapy.

We placed a superficial serratus anterior plane catheter in an elderly woman with dementia and elevated clotting times who presented with multiple rib fractures after a mechanical fall. She was not a surgical candidate, and treatment consisted of conservative management with physical therapy and pain control. She was not a candidate for a patient-controlled analgesia regimen because of her dementia. Given her elevated international normalized ratio, thoracic epidural and paravertebral analgesia was also contraindicated. We placed an ultrasound-guided serratus anterior plane catheter, allowing titratable continuous infusion in a trauma patient, resulting in excellent analgesia without adverse effects.