Hellp

Principio del formulario
Controversies With the Diagnosis and Management of HELLP Syndrome
[New Developments in Preeclampsia]
O'Brien, John M MD; Barton, John R MD
Perinatal Diagnostic Center, Central Baptist Hospital, Lexington, Kentucky
Correspondence: John M. O'Brien, MD, Director, Perinatal Diagnostic Center, Central Baptist Hospital, 1740 Nicholasville Road, Lexington, KY 40503. E-mail:jobrien@bhsi.com
Introduction[pic]
The spectrum of disease resulting from the pathophysiology of preeclampsia continues to challenge the diagnostic acumen of clinicians. One of preeclampsia's various manifestations includes the specific entity of HELLP syndrome. Recently, investigators have provided evidence some cases of HELLP syndrome represent a vasculopathy mediated by an abnormalconcentration of vascular growth factors.1 However, until the underlying etiology for preeclampsia is better defined and testing for such factors is commonplace, controversies in the diagnosis and management of HELLP syndrome will persist as its numerous clinical findings will lead to varied inpressions of severity and to varied thresholds for intervention.
Controversies in Diagnosis[pic]
Thepreeclamptic patient with the constellation of hemolysis, hepatic dysfunction, and low platelets has been described in the literature for decades with early accurate descriptions by Prichard et al and Chesley.2,3 It was not until 1982, however, when Weinstein coined the acronym HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets) that clinicians could more easily recognize and discuss thisgroup of patients with remarkable hepatic involvement by severe preeclampsia.4
Investigations into the pathophysiology of preeclampsia, and specifically HELLP syndrome, have revealed a disorder characterized by hepatic endothelial disruption followed by platelet activation, aggregation, and consumption ultimately resulting in distal ischemia and hepatocyte death.5,6 This vasculopathy can belimited to a hepatic segment or occur diffusely throughout the liver. Most commonly, HELLP syndrome involves smaller terminal arterioles yielding a process with characteristic histologic features. The classic hepatic lesion associated with HELLP syndrome is periportal or focal parenchymal necrosis in which hyaline deposits of fibrin-like material can be seen in the sinusoids.7-9 Alternatively and lessfrequently, larger-vessel disease can impact wider vascular distributions in the liver with more catastrophic outcomes such as hepatic infarction or subcapsular hematoma. This rare large-vessel disease is more readily visible by imaging studies such as magnetic resonance imaging (MRI) or computed tomography (CT) scanning and is associated with worse laboratory values indicating more dramatichepatic dysfunction.10
The greatest controversy involving HELLP syndrome is in the diagnosis of the condition. The syndrome outlined by Weinstein in the early 1980s provided a description of the disease process and gave clinicians an easier framework to understand the pathophysiology. Namely, his group of 29 patients with severe preeclampsia/eclampsia manifested more pronounced hepatic involvementrather than primarily cerebral or renal disease. Later, Sibai et al established laboratory criteria for the diagnosis and provided standards for subsequent discussions in the literature (see Table 1).11 In his classification, Sibai defined laboratory abnormalities sufficient for the diagnosis of each element of the syndrome: hemolysis by an abnormal peripheral smear, elevated bilirubin >1.2 mg/dL, orelevated lactate dehydrogenase (LDH) >600 U/L; elevated liver enzymes by an aspartate aminotransferase (AST) >70 IU/L (which was greater than 2 standard deviations of normal) and lactate dehydrogenase (LDH) >600 U/L; and low platelets defined as 100,000/mm3, as this value was standard in other fields of medicine.

[pic]
|[pic] |TABLE 1. Classifications of HELLP...