This month’s case is by David R Bell PhD, co-author of Medical Physiology: Principles for Clinical Medicine, 3e (ISBN: 9781451110395) For more information, or to purchase your copy, visit: http://tiny.cc/Rhoades4e, with 15% off using the discount code: MEDUCATION. The case below is followed by a quiz question, allowing you a choice of diagnoses. Select the one letter section that best describes the patient’s condition. The Case A 28-year old woman has an unremarkable pregnancy through her first 28 weeks of gestation, with normal weight gain and no serious complications. She has no previous history of diabetes, hypertension of other systemic disease before or during her current pregnancy. During her 30-week checkup, her blood pressure measures 128/85, and she complains about feeling slightly more “bloated” than usual with swelling in her legs that seems to get more uncomfortable as the day goes on. Her obsterician recommends that she get more bed rest, stay off her feet as much as possible and return for evaluation in one week. At the one-week follow-up, the patient presents with noticable”puffiness” in her face, and a blood pressure of 145/95. She complains she has been developing headaches, sporadic blurred vision, right-sided discomfort and some shortness of breath. She has gained more than 10 lb (4.5kg) in the past week. A urinalysis on the patient revelas no glucose but a 3+ reading for protein. Her obstetrician decides to admit her immediately to a local tertiary care hospital for further evaluation. Over the next 24 hours, the patient’s urine output is recorded as 500mL and contains 6.8 grams of protein. Her plasma albumin level is 3.1 g/dl, hemacrit 48%, indirect bilirubin 1.5mg/dl and blood platelets=77000/uL, respectively. Her blood pressure is now 190/100. It is decided to try to deliver the foetus. The expelled placenta is small and shows signs of widespread ischmic damage. Within a week of delivery, the mother’s blood pressure returns to normal, and her oedema subsides. One month later, the mother shows no ill effects of thos later-term syndrome. Question What is the clinical diagnosis of this patient’s condition and its underlying pathophysiology? A. Gestational Hypertension B. Preeclampsia C. Gestational Diabetes D. Compression of the Inferior Vena Cava Answer The correct answer is "B. Preeclampsia". The patient’s symptoms and laboratory findings are consistent with a diagnosis of Preeclampsia, which is a condition occurring in some pregnancies that causes life-threatening organ and whole body regulatory malfunctions. The patient’s negative urine glucose is inconsistent with gestational diabetes. Gestational hypertension or vena caval compression cannot explain all of the patient findings. The patient has three major abnormal findings- generalised oedema, hypertension and proteinuria which are all common in preeclampsia. Although sequalae of a normal pregnancy can include water and salt retention, bloating, modest hypertension and leg swelling (secondary to capillary fluid loss from increased lower limb capillary hydrostatic pressure due to compression of the inferior vena cava by the growing foetus/uterus), oedema in the head and upper extremities, a rapid 10 pound weight gain and shortness of breath suggests a generalized and serious oedematous state. The patient did not have hypertension before or within 20 weeks gestation (primary hypertension) and did not develop hypertension after the 20th week of pregnancy with no other abnormal findings (gestational hypertension). Hypertension with proteinuria occurring beyond the 20th week of pregnancy however is a hallmark of preeclampsia. In addition, the patient has hemolysis (elevated bilirubin and LDH levels), elevated liver enzyme levels and thrombocytopenia. This is called the HELLP syndrome (HELLP = Hemolysis, Elevated Liver enzymes and Low Platelets.), and is considered evidence of serious patient deterioration in preeclampsia. A urine output of 500 ml in 24 hours is 1/2 to 1/4 of normal output in a hydrated female and indicates renal insufficiency. Protein should never be found in the urine and indicates loss of capillaries integrity in glomeruli which normally are not permeable to proteins. The patient has substantial 24 urine protein loss and hypoalbuminemia. However, generally plasma albumin levels must drop below 2.5 gm/dl to decrease plasma oncotic pressure enough to cause general oedema. The patient’s total urinary protein loss was insufficient in this regard. Capillary hyperpermeability occurs with preeclampsia and, along with hypertension, could facilitate capillary water efflux and generalized oedema. However myogenic constriction of pre-capillary arterioles could reduce the effect of high blood pressure on capillary water efflux. An early increase in hematocrit in this patient suggests hemoconcentration which could be caused by capillary fluid loss but the patient’s value of 48 is unremarkable and of little diagnostic value because increased hematocrit occurs in both preeclampsia and normal pregnancy. PGI2, PGE2 and NO, produced during normal pregnancy, cause vasorelaxation and luminal expansion of uterine arteries, which supports placental blood flow and development. Current theory suggests that over production of endothelin, thromboxane and oxygen radicals in preeclampsia antagonize vasorelaxation while stimulating platelet aggregation, microthrombi formation and endothelial destruction. These could cause oedema, hypertension, renal/hepatic deterioration and placental ischemia with release of vasotoxic factors. The patient’s right-sided pain is consistent with liver pathology (secondary to hepatic DIC or oedematous distention). Severe hypertension in preeclampsia can lead to maternal end organ damage, stroke, and death. Oedematous distension of the liver can cause hepatic rupture and internal hemorrhagic shock. Having this patient carry the baby to term markedly risks the life of the mother and is not considered current acceptable clinical practice. Delivery of the foetus and termination of the pregnancy is the only certain way to end preeclampsia. Read more This case is by David R Bell PhD, co-author of Medical Physiology: Principles for Clinical Medicine, 3e (ISBN: 9781451110395) For more information, or to purchase your copy, visit: http://tiny.cc/Rhoades4e. Save 15% (and get free P&P) on this, and a whole host of other LWW titles at (lww.co.uk)[http://lww.co.uk] when you use the code MEDUCATION when you check out! 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