Case report: serial serum HCG measurements in a patient with an ectopic pregnancy: a case for caution. (57/1078)

Improvements in the use of ultrasound in early pregnancy have resulted in improved diagnosis of miscarriage and ectopic pregnancy. There are still, however, a significant number of women with a suspected abnormal pregnancy, where transvaginal ultrasound is unable to locate the pregnancy. The concern is the possibility of ectopic pregnancy. An alternative diagnostic tool is required and it has been suggested that it is possible to monitor serum beta human chorionic gonadotrophin. The present case highlights the potential dangers of this management.  (+info)

Primary peritoneal pregnancy implanted on the uterosacral ligament: a case report. (58/1078)

Peritoneal pregnancies are classified as primary and secondary. Primary implantation on the peritoneum is extremely rare in extrauterine pregnancy and is a potentially life-threatening variation of ectopic pregnancy within the peritoneal cavity, representing a grave risk to maternal health. Secondary abdominal pregnancies are by far the most common and result from tubal abortion or rupture, or less often, after uterine rupture with subsequent implantation within abdomen. Early diagnosis and appropriate surgical management, regardless of stage of gestation, appear to be important in achieving good results. We report a case of primary peritoneal pregnancy in a 28-year-old woman, who had severe lower abdominal pain one day before laparotomy for a preoperative diagnosis of ectopic pregnancy. The conceptus was implanted on the left uterosacral ligament. A fresh embryo of approximately 8 weeks' gestation was found in the conceptus.  (+info)

Can induction of systemic hypotension help prevent nidus rupture complicating arteriovenous malformation embolization?: analysis of underlying mechanism achieved using a theoretical model. (59/1078)

BACKGROUND AND PURPOSE: Nidus rupture is a serious complication of intracranial arteriovenous malformation (AVM) embolotherapy, but its pathogenetic mechanisms are not well described. An AVM model based on electrical network analysis was used to investigate theoretically the potential role of hemodynamic perturbations for elevating the risk of nidus vessel rupture (Rrupt) after simulated AVM embolotherapy, and to assess the potential benefit of systemic hypotension for preventing rupture. METHODS: Five separate hypothetical mechanisms for nidus hemorrhage were studied: 1) intranidal rerouting of blood pressure; 2) extranidal rerouting of blood pressure; 3) occlusion of draining veins with glue; 4) delayed thrombosis of draining veins; and 5) excessively high injection pressures proximal to the nidus. Simulated occlusion of vessels or elevated injection pressures were implemented into the AVM model, and electrical circuit analysis revealed the consequent changes in intranidal flow, pressure, and Rrupt for the nidus vessels. An expression for Rrupt was derived based on the functional distribution of the critical radii of component vessels. If AVM rupture was observed (Rrupt > or = 100%) at systemic normotension (mean pressure [P] = 74 mm Hg), the theoretical embolization was repeated under systemic hypotension (minor P = 70 mm Hg, moderate P = 50 mm Hg, or profound P = 25 mm Hg) to assess the potential benefit of this maneuver in reducing hemorrhage rates. RESULTS: All five pathogenetic mechanisms under investigation were able to produce rupture of AVMs during or after embolotherapy. These different mechanisms had in common the capability of generating surges in intranidal hemodynamic parameters resulting in nidus vessel rupture. The theoretical induction of systemic hypotension during and after treatment was shown to be of significant benefit in attenuating these surges and reducing Rrupt to safer levels below 100%. CONCLUSION: The induction of systemic hypotension during and after AVM embolization would appear theoretically to be of potential use in preventing iatrogenic nidus hemorrhage. The described AVM model should serve as a useful research tool for further theoretical investigations of AVM embolotherapy and its hemodynamic sequelae.  (+info)

Dorsal perforation of prepuce: a common end point of severe ulcerative genital diseases? (60/1078)

Severe ulcerative genital diseases can cause destruction of the prepuce, glans, or sometimes of the whole penis (phagedena). We observed a characteristic pattern of partial destruction of the prepuce as a result of a wide variety of ulcerative genital diseases. Five patients, two with severe genital herpes, one with hidradenitis suppurativa, and two with donovanosis presented with perforation on the dorsal surface of the prepuce. In four of them, the glans protruded through the defect and in one, the defect was not large enough to allow protrusion of the glans. In two patients, the preputial sac was obliterated. The relatively decreased blood supply of the prepuce is the probable explanation for perforation at this selective site.  (+info)

Spontaneous rupture of renal angiomyolipoma presenting as acute abdomen. (61/1078)

Five cases of renal angiomyolipoma which underwent spontaneous rupture are described. These patients presented as an "acute abdomen" for which the diagnosis was not initially apparent. A high index of suspicion is required to make the diagnosis even with modern imaging techniques. The treatment of these tumours is discussed.  (+info)

Pneumatic colonic rupture accompanied by tension pneumoperitoneum. (62/1078)

Rupture of the colon caused by high pressure compressed air is a rare, unique and traumatic intra-abdominal injury. As the use of compressed air in industrial work has increased, so has the risk of associated pneumatic injuries from its improper use. Recently we experienced a case of pneumatic rupture of the sigmoid colon accompanied by tension pneumoperitoneum, which caused respiratory distress. The patient's respiration was very rapid with the rate of 44 breaths per minute. On arterial blood gas analysis, pH was 7.40, pO2 68 mmHg, pCO2 44 mmHg, and SaO2 90%. Chest X-ray film showed marked pneumoperitoneum and an elevated diaphragm. The respiratory distress was severe and required immediate relief by emergency decompression peritoneocentesis before surgical intervention consisting of the serosal tear repair, colonic rupture colostomy and abdominal cavity irrigation. A follow up operation 2 months later for colostomy repair completed the patient's recovery.  (+info)

Ruptured internal carotid aneurysm resulting from neurofibromatosis: treatment with intraluminal stent graft. (63/1078)

PURPOSE: This report shows a method of treatment for life-threatening hemorrhage due to rupture of an aneurysm in the cervical internal carotid artery caused by neurofibromatosis. METHODS: Ten days after delivery of healthy twins, a 28-year-old woman with known neurofibromatosis had sudden massive swelling in the left neck. After initial tracheostomy, angiography confirmed rupture of the mid cervical internal carotid artery as well as contribution to the resultant pseudoaneurysm from external carotid branches. Treatment began with coil embolization of the external carotid branches. The internal carotid lesion, a defect approximately 1 cm in length, was then closed through use of two stent grafts, each made from Palmaz stents and 3-mm polytetrafluorethylene grafts predilated to 6 mm. The neck hematoma was then evacuated surgically. RESULTS: Completion angiography and computed tomographic scanning confirmed control of the hemorrhage. The patient survived neurologically intact with the exception of cranial nerve deficits caused by the hemorrhage. The tracheostomy tube was removed 3 weeks postoperatively. Follow-up computed tomographic scanning showed a gradual decrease in the size of the cervical soft tissue and no recurrent aneurysm. CONCLUSION: Neurofibromatosis is a rare cause of aneurysmal degeneration of blood vessels. Repair of a ruptured cervical internal carotid artery aneurysm, though feasible, is difficult with stent grafts; however, this is a better option than surgical intervention in inaccessible vessels.  (+info)

Experimental radiosurgery simulations using a theoretical model of cerebral arteriovenous malformations. (64/1078)

BACKGROUND AND PURPOSE: A novel biomathematical arteriovenous malformation (AVM) model based on electric network analysis was used to investigate theoretically the potential role of intranidal hemodynamic perturbations in elevating the risk of rupture after simulated brain AVM radiosurgery. METHODS: The effects of radiation on 28 interconnected plexiform and fistulous AVM nidus vessels were simulated by predefined random or stepwise occlusion. Electric circuit analysis revealed the changes in intranidal flow, pressure, and risk of rupture at intervals of 3 months during a 3-year latency period after simulated partial/complete irradiation of the nidus using doses <25 and >/=25 Gy. An expression for risk of rupture was derived on the basis of the functional distribution of the critical radii of component vessels. The theoretical effects of radiation were also tested on AVM nidus vessels with progressively increasing elastic modulus (E:) and wall thickness during the latency period, simulating their eventual fibrosis. RESULTS: In an AVM with E=5. 0x10(4) dyne/cm(2), 4 (14.3%) of a total 28 sets of AVM radiosurgery simulations revealed theoretical nidus rupture (risk of rupture >/=100%). Three of these were associated with partial nidus coverage and 1 with complete treatment. All ruptures occurred after random occlusion of nidus vessels in AVMs receiving low-dose radiosurgery. Intranidal hemodynamic perturbations were observed in all cases of AVM rupture; the occlusion of a fistulous component resulted in intranidal rerouting of flow and escalation of the intravascular pressure in adjacent plexiform components. Risk of rupture was found to correlate with nidus vessel wall strength: a low E: of 1.9x10(4) dyne/cm(2) resulted in a 92.8% incidence of AVM rupture, whereas a higher E: of 7.0x10(4) dyne/cm(2) resulted in only a 3.6% incidence of AVM rupture. A dramatic reduction in rupture incidence was observed when increasing fibrosis of the nidus was modeled during the latency period. CONCLUSIONS: It was found that the theoretical occurrence of AVM hemorrhage after radiosurgery was low, particularly when radiation-induced fibrosis of nidus vessels was considered. When rupture does occur, it would appear from a theoretical standpoint that the occlusion of intranidal fistulas or larger-caliber plexiform vessels could be a significant culprit in the generation of critical intranidal hemodynamic surges resulting in nidus rupture. The described AVM model should serve as a useful research tool for further theoretical investigations of cerebral AVM radiosurgery and its hemodynamic sequelae.  (+info)