| JOURNAL HOME | CME HOME | THIS MONTH | PAST ISSUES | ETOC | COLLECTIONS |
| AUTHORS | REVIEWERS | EDITORIAL BOARD | FEEDBACK | RSS | HELP |
| ||||||||||||||
| ||||||||||||||
|
|
|
|
||||||||||||
|
||||||||||||||
Division of Anesthetics & Intensive Care, The University of the West Indies, St. Augustine, Trinidad
To the Editor:
I read with great interest the report by Borromeo et al. (1) on cortical blindness in a preeclamptic patient. I congratulate them on their attempt to clarify a rather complex and confusing condition. Because of its rarity, blindness associated with preeclampsia may pose significant problems and challenges to the obstetrician and anesthesiologist and can be very distressing to the patient and her relatives. It can also result in very expensive (sometimes unnecessary) investigations and therapies. I have encountered a similar case and shall describe it to highlight the similarities that should aid in diagnosis and management.
A 17-yr-old primigravid woman at 36-wk gestation without any prenatal care was brought to the obstetric emergency room having had a convulsive episode at home after complaints of nausea, vomiting, and epigastric pain. On examination, she was a woman of short stature (153 cm, 60 kg) with a slight tinge of scleral jaundice and mild pallor. She was afebrile and had bilateral pitting pedal edema up to knee level. Her arterial blood pressure (BP) was 170/130 mm Hg and heart rate 74 bpm. Urinary protein was 3+. She was diagnosed with eclampsia, and treatment was started with diazepam infusion and IV bolus doses of hydralazine 5–10 mg as required. Despite this, her BP control was unsatisfactory fluctuating between 150/100 and 170/120 mm Hg. Intrauterine fetal death was also noted. She was therefore transferred to the intensive care unit for further care. Laboratory investigations at this time indicated a hematocrit of 33%, white blood cell count of 19 x 109/L, with normal differentials and platelet count of 25 x 109/L. Prothrombin time, partial thromboplastin time, and bleeding time were all increased. Bilirubin was 20 mol/L (normal range, 0–18), alanine transaminase 170 IU/L (normal, 0–45) and aspartate transaminase 195 IU/L (normal, 0–40). A peripheral blood smear indicated microangiopathic hemolytic anemia with polychromasia, burr cells and unnucleated red blood cells. A diagnosis of HELLP syndrome in an eclamptic patient was made. Her BP was fairly well controlled, as was her sedation in the ICU. She was transfused with two units of cross-matched fresh whole blood. She suddenly went into spontaneous labor and delivered a female still birth. After this, her BP decreased from about 140/80 mm Hg to 120/70 mm Hg and remained stable at this level even after discontinuation of antihypertensive and sedative medications. She was transferred back to the maternity ward after 72 hr in the intensive care unit. She complained of total blindness in both eyes although she was now fully conscious, alert, and oriented. Ophthalmologic and neurologic consultations indicated cortical blindness likely resulting from vascular spasm and also bilateral edematous retinal detachments. The blindness lasted 2 days, after which there was gradual resolution over the next 3 days. By the time of her discharge 3 wks after her initial admission, her visual impairment was completely resolved and the platelet count, coagulation profile, and liver enzymes had all returned to within normal prepregnancy values.
The syndrome of HELLP, an acronym coined by Weinstein (2) for hemolysis, elevated liver enzymes and low platelets, is a consequence of severe preeclampsia/eclampsia. My patient was sicker than that of Borromeo et al. (1) but the evolution, resolution, and pathophysiologic basis of the condition are similar. Sudden severe visual impairment or total blindness is a frightening and terrifying experience in a previously healthy person. Fortunately, it almost always resolves spontaneously, as do the other laboratory and clinical indices of severe preeclampsia/eclampsia within days after removal of the fetus and placenta (3,4). The patient and relatives must be positively supported and reassured during this very trying period and most importantly, a thorough medical history and examination (including neurologic and ophthalmologic examinations) should be able to identify the condition and often avoid unnecessary tests and therapies.
References
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
