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BACKGROUND: Orthotopic liver transplantation (OLT) is the definitive treatment for end-stage liver disease (ESLD). Patients with high acuity ESLD are frequently denied life-saving OLT by transplant centers due to reported inferior outcomes. We sought to analyze the impact of a specialized transplant critical care model (TCCM) on patient access to OLT and survival outcomes in high acuity patients. METHODS: From January 2009 to December 2016, 122 adults were wait-listed at our transplant center with laboratory Model for ESLD ≥35 or Status I. Outcomes in Era I (prior to TCCM) were compared to Era II (TCCM established October 1, 2012). RESULTS: Era II (TCCM) led to a significant increase in patients' access to OLT. Frequency and need to seek OLT at another center dropped 4-fold in Era II. Compared to Era I, the majority of patients in Era II required intensive care unit management (22% vs 83%, P < .01) and renal replacement therapy (11% vs 70%, P < .01) prior to OLT. Despite a higher acuity of illness in Era II, 1-year patient survival was comparable (89% Era I, 80% Era II, P = .35). CONCLUSION: Implementation of a specialized TCCM expanded OLT access to high acuity patients, reduced the need to seek higher level of care elsewhere, and achieved excellent short-term post-transplant survival outcomes.

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PURPOSE: Arachidonic acid is avidly metabolized to a potent vasoconstrictor, 20-hydroxyeicosatetraenoic acid (20-HETE), in the cerebral circulation. 20-HETE has been reported to contribute to the acute fall in cerebral blood flow following subarachnoid hemorrhage (SAH), but its role in the development of delayed vasospasm is unknown. The present study examined whether delayed vasospasm is associated with elevations in 20-HETE in CSF in the dual hemorrhage model of SAH in dogs and if blockade of the synthesis of 20-HETE with N-(3-chloro-4-morpholin-4-yl)phenyl-N'-hydroxyimido formamide (TS-011) can reverse delayed vasospasm in this model. MATERIALS AND METHODS: Delayed vasospasm was induced in 22 adult beagle dogs by dual injection of blood (0.5 mL/kg) into the cisterna magna on days 1 and 4. Sequential samples of CSF were collected before intracisternal injections of blood on days 1 and 4 and after the development of delayed vasospasm on day 7. Sequential angiograms were obtained before and after intracisternal injection of blood on days 1 and 4 and before and 1 hour after administration of TS-011 (1 mg/kg IV) on day 7. RESULTS: The dogs consistently developed delayed vasospasm, and the diameter of the basilar artery fell to 68 +/- 3% (n = 15), 3 days after the second intracisternal injection of blood. The levels of 20-HETE in CSF increased from 4 +/- 2 to 39 +/- 16 pg/mL. In 9 dogs with delayed vasospasm, acute blockade of the synthesis of 20-HETE with TS011 (1 mg/kg IV) significantly increased the diameter of the basilar artery by 39%. Chronic administration of TS-011 (1 mg/kg per day) attenuated the development of delayed vasospasm, and the diameter of the basilar artery fell by 17 +/- 1% versus the 33 +/- 3% decrease in diameter seen in control animals 3 days following the second injection of blood into the cisterna magna. CONCLUSIONS: These results indicate that the development of delayed vasospasm in dogs is associated with an increase in 20-HETE levels in CSF, and acute blockade of the synthesis of 20-HETE with TS-011 reverses delayed vasospasm in this model.

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Spontaneous, low frequency (4-12 cpm) fluctuations, independent of the cardiac and respiratory cycles, in human and animal brains were first recorded with the O2 polarographic technique in the late 1950s. They were seen in NADH and cytochrome oxidase and associated with spontaneous vasomotion pial and large cerebral arteries. Renewed interest in spontaneous fluctuations was generated by studies with laser-Doppler flowmetry (LDF), reflectance oximetry and functional MRI. Spontaneous fluctuations were consistently produced when cerebral perfusion was challenged by systemic or local manipulations; the fluctuation amplitude reached 30-40% of the mean. The most potent stimuli are hypotension, hyperventilation, cerebral artery occlusion and cerebral vasoconstriction elicited, for example, by a nitric oxide synthase inhibitor but not by indomethacin. The fluctuations are suspended by CO2 and halothane at concentrations that produce hyperemia. Recently, spontaneous fluctuations were recorded by LDF microprobes in areas as small as 130 microns and by video-microscopy in single capillaries. The fluctuations were absent in severe, focally ischemic brain territories. The dependence of spontaneous fluctuations on intravascular pressure argues for the importance of a myogenic mechanism, however, neuronal modulation may also play a role. Coherence of small vessel vasomotion may be required for the emergence of regional flow fluctuations. There is a need to elucidate the spatial and frequency domains in which fluctuations are present under normal physiological conditions and those in which they may reflect brain injury and pathologies of diagnostic or prognostic value.

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PURPOSE: This study aimed to examine the effects of sedative doses of morphine, fentanyl and sufentanil on intracranial pressure (ICP) in head-injured patients in whom changes in mean arterial pressure (MAP) were minimized. METHODS: Fifteen severely head-injured patients (GSC of < or = 8) were randomly assigned to receive either fentanyl, sufentanil or morphine, titrating the drug to a maximal 10% decrease in MAP. The patients were subsequently given an infusion of the same opioid. For four hours, ICP, MAP and heart rate were recorded. RESULTS: In all groups, there were no increases in ICP. There was a decrease in MAP in the sufentanil group at 10 min (P < 0.05) and 45 min after the initial opioid bolus. These decreases in MAP were not associated with increases in ICP. CONCLUSION: The study suggests that when opioids are titrated in head-injured patients, worsening intracranial pressure can be avoided.

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We describe the first case report of an epidural autologous blood patch used for the treatment of a durocutaneous fistula caused by a surgical dural tear. The epidural blood patch cured the patient's headache and was followed by a sequelae of back pain that responded to conservative therapy.

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The usual method of substantiating collateral circulation of the hand is with Allen's test. We used the pulse-detecting capability of the pulse oximeter to assess the presence of collateral circulation of the hand. Thirty-one patients undergoing radial artery cannulation for intraoperative monitoring were evaluated before cannulation with a modified Allen's test and by pulse oximetry. After the collateral circulation of the hand was tested by the modified Allen's test, a pulse oximeter probe was placed on the index finger. Both radial and ulnar arteries were occluded until no perfusion was detected by the pulse oximeter. The test was repeated twice on each hand, once for each artery. The time to reperfusion after arterial release was recorded. Reperfusion times greater than 15 seconds were considered abnormal. This sequence was repeated postoperatively after the radial artery cannulae were removed. A total of 68 tests were performed before cannulation; 3 showed an abnormal Allen's test, a finding confirmed by pulse oximetry evaluation. The Allen's test was indeterminate 13 times. In all of these cases, pulse oximetry demonstrated collateral blood flow. When collateral circulation was determined to be present by Allen's test, it was also found to be present with pulse oximetry. Three days after cannulation was discontinued, 8 patients had abnormal Allen's test results, a finding again confirmed by pulse oximetry evaluation. Of 15 patients with indeterminate Allen's test results, 12 had collateral blood flow determined by pulse oximetry and 3 had abnormal results. The ability of pulse oximetry to detect collateral circulation was significantly different (P less than 0.001) when compared with Allen's test both before and after radial artery cannulation.(ABSTRACT TRUNCATED AT 250 WORDS)

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