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atation of cerebral and retinal arterioles in response to severe hypertension However, the observations of Byrom and of others indicate that overdistention of the arterioles (which have lost their adaptive capacity), rather than excessive constriction, may be responsible for the necrosis of the vessel wall (see reviews of Auer and of Chester et al) The brain edema is the result of active exocytosis of water rather than simply a passive leak from vessels subjected to high pressures A few eclamptic women will develop hemolysis, hepatic failure and thrombocytopenia hemolysis, elevated liver enzymes, low platelet count (HELLP syndrome) an illness that has similarities to disseminated intravascular coagulation (DIC) The interplay between eclampsia and HELLP in relation to cerebral lesions is complex and not fully understood (see further on) Treatment Lowering of the blood pressure with antihypertensive drugs may reverse the picture in a day or two In the past, when effective antihypertensive drugs were not available, the outcome was often fatal The BUN is only slightly elevated except in cases of renal failure, and the usual patient is not uremic The same can be accomplished by administering magnesium sulfate in the eclamptic woman Treatment consists of measures that promptly reduce arterial blood pressure, but antihypertensive drugs must be used cautiously; a safe target is a pressure of 150/100 mmHg One may use intravenous sodium nitroprusside, 05 to 08 mg/kg/min; a calcium channel blocker such as nifedipine, 10 to 20 mg sublingually; or intravenous beta-adrenergic blockers (labetalol, 20 to 40 mg intravenously followed by an infusion at 2 mg/min, or esmolol are favored) These must be followed by longer-acting antihypertensive agents such as ACE inhibitors or calcium channel blockers

or multiplying out the left-handside: : d1 785 00333333dr+ :-193 d2 0100000dr-- 00271300d2 d3 114 +

14:

Figure 34-30 MRI T2 signal changes in eclampsia Most of the vascular changes and edema are situated in the cortical watershed distributions between the middle and an anterior cerebral arteries These imaging ndings were transient, as was mild signal change in the occipital subcortical regions, the latter being typical of hypertensive encephalopathy, as in Fig 34-29

We cair solve the tirst equation for d, : 785, which can be substituted into the second equationto solve for d : : -193 * 00333333(785) -195617 :

} $SIG{__WARN__} = \&warn_handler;

If there is already evidence of brain edema and increased intracranial pressure, dexamethasone, 4 to 6 mg every 6 h, is usually added, but its effect, and the use of hyperosmolar therapy, have not been studied systematically; our clinical impression is that they have little effect

TUFACTORIZATION Bothd, andd, canbe substituted thethirdequation give into to : 700843 dt : 7 14- 01 (785) 002713(-19,5617) + Thus

We don t need to make any further modifications to the code (aside from adding the writelog function definition) From now on, all calls to warn will trigger this handler and force the output to be written to a file instead of STDERR Similar tricks allow us to report warnings through Tk:

and cocaine, but there are few well-studied cases These are discussed below, under Arteritis Symptomatic of Underlying Systemic Disease and Sympathomimetic Drug Reactions In all cases, including those noted above, the treatment is cessation of the offending drugs; nitroglycerin, nitroprusside, or beta-adrenergic infusions have been tried with uncertain effect

PROGRAMMING WITH PERL sub warn_handler { dialog(undef,"Warning", join(', ',@_), 'warning',1,"OK"); }

: {;r*y {,/}

.

Using $SIG{__DIE__}