A 37-year-old primigravida presented at 8 weeks’ gestation with sudden abdominal pain, which lasted for one hour. An initial examination revealed a blood pressure (BP) of 89/54 mmHg with a pulse rate of 82/min. The uterus was of appropriately sized for gestational age without her abdominal muscular defence and the viable foetus was detectable by transvaginal ultrasonography. Her haemoglobin level was 11.2 g/dl. After two hours, her pain progressively worsened and abdominal guarding developed. The patient was pale and slightly delirious; her BP dropped to 60/47 mmHg and her pulse rate was 98/min. Suspicion of a surgical disease (e.g. lower gastrointestinal perforation), prompted a plain computed tomography (CT), despite it being a contraindication
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Surgical management continues to be the primary approach (e.g. nephrectomy, or repair of the RAA and reconstruction of the renal artery). However, the alternative approach of angiographic embolization has become, in recent years, better known (Prabulos AM et al. 1997). Majority of RAA ruptures usually occur in the third trimester and have left-sided predominance (Cohen et al. 1987; Hwang et al. 2011). This increased third-trimester risk is believed to be the result of: (1) expanded intravascular volume and increased BP, (2) increased intra-abdominal pressure, and (3) weakened structure of the major arteries following increased steroid production (Nakayama et al. 2013). Moreover, the physiological clockwise–rotation of the enlarged gravid uterus may compress the aorta and the right renal artery, thus increasing pressure on the left renal artery. To our knowledge, there are only two English papers describing cases of ruptured RAA in the first trimester of pregnancy (Whiteley et al. 1994; Meabed et al. 2002). RAA rupture in the first trimester of pregnancy remains unclear. Meabed et al. (2002) argued that repeated pregnancies produce irreversible vessel wall damage, which promotes a rapid increase in aneurysm size, subsequently causing rupture. Our case, however, was a primigravida at 8 weeks’ gestation. Davison et al. (1980) suggested that renal plasma flow and glomerular filtration rate of pregnant women in the first trimester rapidly increase to about 30-50% above the non-pregnant level; thus, increased blood flow to the kidneys may increase the pressure in the arteries, resulting in aneurysm expansion and rupture. For our case, possible factors may include: fibromuscular dysplasia, kinking, and increased renal plasma flow. RAA associated with fibromuscular dysplasia can be bilateral (7-39%) or multiple unilateral (7-13%) (Rijbroek 1994); we carefully looked for other aneurysms in the intracranial
Surgical management continues to be the primary approach (e.g. nephrectomy, or repair of the RAA and reconstruction of the renal artery). However, the alternative approach of angiographic embolization has become, in recent years, better known (Prabulos AM et al. 1997). Majority of RAA ruptures usually occur in the third trimester and have left-sided predominance (Cohen et al. 1987; Hwang et al. 2011). This increased third-trimester risk is believed to be the result of: (1) expanded intravascular volume and increased BP, (2) increased intra-abdominal pressure, and (3) weakened structure of the major arteries following increased steroid production (Nakayama et al. 2013). Moreover, the physiological clockwise–rotation of the enlarged gravid uterus may compress the aorta and the right renal artery, thus increasing pressure on the left renal artery. To our knowledge, there are only two English papers describing cases of ruptured RAA in the first trimester of pregnancy (Whiteley et al. 1994; Meabed et al. 2002). RAA rupture in the first trimester of pregnancy remains unclear. Meabed et al. (2002) argued that repeated pregnancies produce irreversible vessel wall damage, which promotes a rapid increase in aneurysm size, subsequently causing rupture. Our case, however, was a primigravida at 8 weeks’ gestation. Davison et al. (1980) suggested that renal plasma flow and glomerular filtration rate of pregnant women in the first trimester rapidly increase to about 30-50% above the non-pregnant level; thus, increased blood flow to the kidneys may increase the pressure in the arteries, resulting in aneurysm expansion and rupture. For our case, possible factors may include: fibromuscular dysplasia, kinking, and increased renal plasma flow. RAA associated with fibromuscular dysplasia can be bilateral (7-39%) or multiple unilateral (7-13%) (Rijbroek 1994); we carefully looked for other aneurysms in the intracranial