Lumbosacral plexopathy due to pelvic hematoma after extracorporeal membrane oxygenation: A case report.

RATIONALE: Peripheral nerve injury related to vascular complications associated with extracorporeal membrane oxygenation (ECMO) is perhaps underappreciated. Compared to the well-described central nervous system complications of ECMO, brachial plexopathy and lumbosacral plexopathy have rarely been reported. We report this case to heighten awareness of lumbosacral plexus injury due to pelvic hematoma formation after ECMO. PATIENT CONCERNS: A 53-year-old woman developed a large pelvic hematoma with significant mass effect on intrapelvic structures after receiving lifesaving venoarterial ECMO for cardiogenic shock following a cardiac arrest. During her hospital course, she developed bilateral foot drop that was attributed to critical illness. Her lack of neurological recovery after 6 months prompted referral to neuromuscular medicine for consultation. DIAGNOSIS: The patient was retrospectively diagnosed with bilateral lumbosacral plexopathy due to the large pelvic hematoma. INTERVENTION: Electromyography/nerve conduction study (EMG/NCS) obtained at the time of referral to neuromuscular medicine localized her neurological deficits to the bilateral lumbosacral plexus and demonstrated no volitional motor unit action potentials in her lower leg muscles. OUTCOMES: The patient had minimal recovery of strength at the level of the ankles but was ambulatory with solid ankle-foot orthoses due to spared proximal lower extremity strength. Unfortunately, the absence of any volitionally activated motor unit action potentials in her lower leg muscles on EMG performed 6 months after the initial injury was a poor prognostic indicator for successful reinnervation and future neurological recovery. LESSONS: Neurological deficits occurring during the course of administration of ECMO require accurate localization. Neurology consultation and/or EMG/NCS may be useful if localization is not clear. Lesions localizing to the lumbosacral plexus should prompt radiographic evaluation with computed tomography of the abdomen and pelvis. Hemostasis of a retroperitoneal hematoma may be achieved with embolization. However, if neurological deficits do not improve, surgical consultation for hematoma evacuation may be warranted.

Impact of hematopoietic cyclooxygenase-1 deficiency on obesity-linked adipose tissue inflammation and metabolic disorders in mice.

OBJECTIVE: Adipose tissue (AT)-specific inflammation is considered to mediate the pathological consequences of obesity and macrophages are known to activate inflammatory pathways in obese AT. Because cyclooxygenases play a central role in regulating the inflammatory processes, we sought to determine the role of hematopoietic cyclooxygenase-1 (COX-1) in modulating AT inflammation in obesity. MATERIALS/METHODS: Bone marrow transplantation was performed to delete COX-1 in hematopoietic cells. Briefly, female wild type (wt) mice were lethally irradiated and injected with bone marrow (BM) cells collected from wild type (COX-1+/+) or COX-1 knock-out (COX-1-/-) donor mice. The mice were fed a high fat diet for 16 weeks. RESULTS: The mice that received COX-1-/- bone marrow (BM-COX-1-/-) exhibited a significant increase in fasting glucose, total cholesterol and triglycerides in the circulation compared to control (BM-COX-1+/+) mice. Markers of AT-inflammation were increased and were associated with increased leptin and decreased adiponectin in plasma. Hepatic inflammation was reduced with a concomitant reduction in TXB2 levels. The hepatic mRNA expression of genes involved in lipogenesis and lipid transport was increased while expression of genes involved in regulating hepatic glucose output was reduced in BM-COX-1-/- mice. Finally, renal inflammation and markers of renal glucose release were increased in BM-COX-1-/- mice. CONCLUSION: Hematopoietic COX-1 deletion results in impairments in metabolic homeostasis which may be partly due to increased AT inflammation and dysregulated adipokine profile. An increase in renal glucose release and hepatic lipogenesis/lipid transport may also play a role, at least in part, in mediating hyperglycemia and dyslipidemia, respectively.