Risk of Injury to Retroperitoneal Structures in Prone and Lateral Decubitus Transpsoas Approaches to Lumbar Interbody Fusion: A Pilot Cadaveric Anatomical Study.

Introduction The retroperitoneal approach for lateral lumbar interbody fusion (LLIF) originally described an initial posterolateral fascial incision enabling finger dissection from behind the peritoneum and guidance of instruments through a second direct-lateral fascial incision. It has since become common for single direct-lateral incisional access to the retroperitoneum. This study attempted to quantify the distance of the peritoneum from posterior landmarks in the space, assess the risk of peritoneal violation in each access trajectory (i.e., posterolateral versus direct lateral retroperitoneal dissection), and determine whether there are differences based on patient position (prone versus lateral decubitus). Methods In three prone cadaveric torsos, Steinman pins were percutaneously placed mid-disc at each level L2-5 bilaterally (for a total of 18 prone approaches). Open dissections exposed the retroperitoneum including the quadratus lumborum and psoas muscles, maintaining the natural reflection of the peritoneum. Visual assessment qualified whether any pin violated any retroperitoneal structure. Distance from the anterior border of the quadratus lumborum to the posterior-most reflection of the peritoneum was measured. For comparison, three additional torsos were positioned in lateral decubitus, and the above steps were repeated, only unilaterally (for a total of nine lateral decubitus approaches). Results In prone, no pin violated the peritoneum; three (3/18 total approaches) violated the kidney, all at L2-3 (3/6 approaches at L2-3). In lateral decubitus, all three L2-3 pins violated the kidney (3/3 approaches at L2-3); five of the six remaining pins from L3-5 violated the peritoneum (totaling eight violations in the nine total approaches). The incidence of any violation was significantly greater in lateral decubitus vs. prone (8/9 vs. 3/18, p=0.0006). The structure at risk (kidney vs. peritoneum) was significantly associated with disc level (p=0.0041): all kidney violations occurred at L2-3 and all peritoneal violations occurred at L3-4 or L4-5. Distance from the quadratus lumborum to the posterior-most reflection of the peritoneum averaged 8.7 cm (range: 6-10) in prone, and 2.9 cm (range: 2.5-3.2) in lateral decubitus (p=0.0129). Conclusion A cadaveric study of retroperitoneal anatomy demonstrates that there is an increased distance from the quadratus lumborum to the peritoneum in prone versus lateral decubitus and that the trajectory of approach to the lumbar discs risks violation of the peritoneum more frequently when accessing directly laterally versus posterolaterally. In either approach, care should be taken to identify and release the peritoneal reflection to create a safe passage to the lumbar discs.

Developmental programming of mitochondrial substrate metabolism in skeletal muscle of adult sheep by cortisol exposure before birth.

Prenatal glucocorticoid overexposure causes adult metabolic dysfunction in several species but its effects on adult mitochondrial function remain largely unknown. Using respirometry, this study examined mitochondrial substrate metabolism of fetal and adult ovine biceps femoris (BF) and semitendinosus (ST) muscles after cortisol infusion before birth. Physiological increases in fetal cortisol concentrations pre-term induced muscle- and substrate-specific changes in mitochondrial oxidative phosphorylation capacity in adulthood. These changes were accompanied by muscle-specific alterations in protein content, fibre composition and abundance of the mitochondrial electron transfer system (ETS) complexes. In adult ST, respiration using palmitoyl-carnitine and malate was increased after fetal cortisol treatment but not with other substrate combinations. There were also significant increases in protein content and reductions in the abundance of all four ETS complexes, but not ATP synthase, in the ST of adults receiving cortisol prenatally. In adult BF, intrauterine cortisol treatment had no effect on protein content, respiratory rates, ETS complex abundances or ATP synthase. Activity of citrate synthase, a marker of mitochondrial content, was unaffected by intrauterine treatment in both adult muscles. In the ST but not BF, respiratory rates using all substrate combinations were significantly lower in the adults than fetuses, predominantly in the saline-infused controls. The ontogenic and cortisol-induced changes in mitochondrial function were, therefore, more pronounced in the ST than BF muscle. Collectively, the results show that fetal cortisol overexposure programmes mitochondrial substrate metabolism in specific adult muscles with potential consequences for adult metabolism and energetics.

Abnormal patterns of sleep and EEG power distribution during non-rapid eye movement sleep in the sheep model of Huntington's disease.

Sleep disruption is a common invisible symptom of neurological dysfunction in Huntington's disease (HD) that takes an insidious toll on well-being of patients. Here we used electroencephalography (EEG) to examine sleep in 6 year old OVT73 transgenic sheep (Ovis aries) that we used as a presymptomatic model of HD. We hypothesized that despite the lack of overt symptoms of HD at this age, early alterations of the sleep-wake pattern and EEG powers may already be present. We recorded EEG from female transgenic and normal sheep (5/group) during two undisturbed 'baseline' nights with different lighting conditions. We then recorded continuously through a night of sleep disruption and the following 24 h (recovery day and night). On baseline nights, regardless of whether the lights were on or off, transgenic sheep spent more time awake than normal sheep particularly at the beginning of the night. Furthermore, there were significant differences between transgenic and normal sheep in both EEG power and its pattern of distribution during non-rapid eye movement (NREM) sleep. In particular, there was a significant decrease in delta (0.5-4 Hz) power across the night in transgenic compared to normal sheep, and the distributions of delta, theta and alpha oscillations that typically dominate the EEG in the first half of the night of normal sheep were skewed so they were predominant in the second, rather than the first half of the night in transgenic sheep. Interestingly, the effect of sleep disruption on normal sheep was also to skew the pattern of distribution of EEG powers so they looked more like that of transgenic sheep under baseline conditions. Thus it is possible that transgenic sheep exist in a state that resemble a chronic state of physiological sleep deprivation. During the sleep recovery period, normal sheep showed a significant 'rebound' increase in delta power with frontal dominance. A similar rebound was not seen in transgenic sheep, suggesting that their homeostatic response to sleep deprivation is abnormal. Although sleep abnormalities in early stage HD patients are subtle, with patients often unaware of their existence, they may contribute to impairment of neurological function that herald the onset of disease. A better understanding of the mechanisms underlying EEG abnormalities in early stage HD would give insight into how, and when, they progress into the sleep disorder. The transgenic sheep model is ideally positioned for studies of the earliest phase of disease when sleep abnormalities first emerge.