Biomedical subjects
Publications and source records attributed to L C Brown.
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You are the chief executive officer of Friendly Neighbor Medical Center, an acute care hospital. On your desk is a letter from your counterpart at The Behemoth Clinic, a large local medical group that not only is very active in managed care contracting in your service area, but also has an important relationship with your hospital. Behemoth has requested extensive access to Friendly Neighbor's peer review files and patient records in order to investigate the care provided by one of Behemoth's physicians. You happen to be aware that the physician has been the subject lately of peer review scrutiny at your hospital, and you would like to cooperate with Behemoth. Can you do so without jeopardizing the legal confidentiality protections available to your hospital's peer review records, not to mention the peer review process generally?
EMTALA has always been an especially worrisome law for providers because its requirements are both sweeping and vague, with potentially drastic penalties for violations. The new regulations remove only some of the law's vagueness. As with previous EMTALA amendments, all United States hospitals, as well as emergency department physicians and other doctors who see patients in the emergency department, should carefully review their internal policies regarding patient ++ transfers in light of the new regulations. For example, hospitals must have an internal policy for following up on suspicious transfers, as failure to detect an inappropriate transfer can now potentially result in a Medicare decertification action. Also, hospitals with specialized services (e.g., burn units or shock-trauma units) should review their policies on receiving transfer patients in light of the greater specificity of the new regulations. Finally, because of the confusing new requirements regarding ambulance services, all hospitals should review their relationships with and policies regarding, ambulance services and ambulance diversion.
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Forty-two patients who had attempted suicide by burning were admitted to the North West Thames Regional Burns Unit over a 5-year period. Over three-quarters of these patients had previous psychiatric illness and a quarter had previously attempted suicide. In no case was political or religious protest a motive. The number of non-Caucasians was higher than expected from population statistics and fatal burns were more common in this group. The mean age was 36 years and the overall mortality rate was 48 per cent. The mortality was not significantly higher than for accidental burns of comparable severity.
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Hepatic blood volume decreases in response to a rapid hemorrhage (15.3 mL/min) were measured in cats anesthetized with pentobarbital or ketamine-chloralose, by use of in vivo plethysmography alone or in combination with various surgical procedures and vascular circuits. The hepatic blood volume contracts during hemorrhage to compensate for a constant proportion (26 +/- 6%) of the blood loss regardless of the extent of the actual blood loss. Following denervation of the liver and alpha adrenoreceptor blockade (3 mg phentolamine, intraportal) the liver compensation was unaltered. After denervation, nephrectomy, hypophysectomy, and adrenalectomy the liver was still able to compensate for 20 +/- 7.4% of the hemorrhage. Decreases in liver volume were linearly related to decreases in total hepatic blood flow that ensued whether the decreased blood flow was induced by hemorrhage or by clamping of the arteries supplying the splanchnic organs (superior mesenteric artery, celiac artery). The hepatic volume response to hemorrhage could be predicted accurately (97 +/- 6.6%) simply from the linear passive relationship between flow and volume for a particular animal. However when hepatic venous pressure was experimentally elevated, the volume response to passive flow decrease was markedly reduced whereas the response to hemorrhage and noradrenaline infusion was unimpaired suggesting that active control factors were required to produce normal hepatic volume responses to hemorrhage at raised venous pressure. Phentolamine reduced the response at raised venous pressure but was without effect at normal venous pressure in the same animal, indicating that the hepatic nerves and (or) adrenal catecholamines are of paramount importance in control of the response at raised venous pressure when the passive flow influence is much reduced.
The effects of intravenous and intraportal infusions of hypertonic NaCl and glucose solutions on the resistance and capacitance vessels of the intact feline liver were studied. All doses infused produced vasodilation of the hepatic artery. A rough estimate would suggest that the tonicity changes equal to those seen after hemorrhage might produce an increase of arterial conductance to no less than 110% and no greater than 140% of control conductance. In response to intravenous infusions, portal flow increased to the same extent as did arterial flows. The resistance vessels were equally affected by equal osmolal loads of glucose or NaCl but the hepatic volume changes were quite different depending on the substances infused. In marked contrast with the resistance vessel response to hypertonic NaCl, the hepatic capacitance vessels did not dilate. Liver volume decreased but whether due to mild capacitance stimulation or water egress from hepatocytes is not known. Cessation of the infusion resulted in increases of hepatic volume to above control levels. Glucose produced consistent steady increases in volume that may have been associated with fluid uptake by the hepatocytes in conjunction with glucose uptake.