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Query: UMLS:C0000737 (
abdominal pain
)
31,184
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Spontaneous hemoperitoneum secondary to intraabdominal variceal rupture, is an uncommon and highly lethal complication of cirrhosis. We report a case of a 68 years old male submitted because of
abdominal pain
and fainting. The clinical and laboratory work up concluded that the patient had cirrhosis and hemoperitoneum. He was operated on and the exploration showed a massive hemoperitoneum caused by bleeding gastrosplenic
varices
. The patient died in the immediate postoperative period.
...
PMID:[Spontaneous hemoperitoneum caused by intraabdominal variceal rupture in a patient with liver cirrhosis. Clinical case]. 1209 Jan 10
The Indian Contraceptive Testing Unit started making field trials with oral contraceptives in 1964. By June 1968, 958 women were taking oral contraceptives. Combination tablets used contained a minimum amount of progestogen (.5-3 mg) and a suitable amount of estrogen. The 21-tablet pack was found mot suitable. It was found that if a woman missed taking the tablets in the latter half of the cycle usually no harm resulted, but if she missed them at the beginning of the cycle pregnancy might follow as ovulation would not be inhibited. Main contraindications are liver damage, toxic hyperthyroidism, thromboembolic disease, and cancer of the genital tract or breast. Caution is advised for persons with chronic nephritis, a history of eclampsia, hypertension,
varicose veins
, ophthalmological disorders, or psychic depressive states. Side effects have been less with the smaller doses. The most serious side effect is thromboembolism. Those reported have been leg pain, giddiness, headache, breakthrough bleeding, nausea, vomiting, amenorrhea,
abdominal pain
, weakness, increased blood pressure, and skin rashes. Others have reported ocular disease and cranial nerve palsy. Sequential therapy has been reported to have a lower incidence of side effects but a higher rate of pregnancy. Low-dose progestogen therapy, the "minipill," does not inhibit ovulation but is effective by causing changes in the endometrium and in the mucus. The chlormadinone in the minipill does not affect lactation. However, the incidence of pregnancy is similar to that with an IUD (Lippes loop) which is 2.6/100 cases. Laboratory tests have been normal, except an increase in the thymol turbidity test. Vaginal cytology has revealed no case of malignancy. Results show that oral contraceptives are suitable for use on a mass scale as a method of population control.
...
PMID:Experience with oral contraceptives. 1225 72
This study indicates the relationship between tubal sterilization and pelvic venous stasis syndrome. Exploratory laparatomy was performed in 24 patients with symptoms of lower
abdominal pain
and intercourse pain after tubal ligation who had failed to respond to medical treatment for a long time. During the operation the author found that the venous vessels within the mesosalpinx had enlarged with hyperemia and
varicosities
in 17 cases. All of them got satisfactory effects after operative therapy. The etiology, prevention, and treatment of this syndrome following tubal sterilization are discussed and emphasis is laid on how to take precautions against pelvic venous stasis during tubal ligation.
...
PMID:[Tubal sterilization and pelvic venous stasis syndrome]. 1226 31
Portal cavernoma is a network of veins whose caliber, initially millimetric or microscopic, is increased and which contain hepatopedal portal blood. It results from occlusion, thrombotic and always chronic, of the extra-hepatic portal system. Diagnosis is mainly done by imaging. Clinical signs of portal cavernoma are usually related to extra-hepatic portal hypertension (hematemesis due to rupture of oeso-gastric
varices
, splenomegaly, rectal bleeding from ano-rectal
varices
, growth retardation in children) and sometimes to the cause of portal hypertension (
abdominal pain
, venous bowel infarction). Occurrence of portal thrombosis is often the conjunction of a local cause and a prothrombotic disorder which must be systematically detected. Biliary consequences of cavernoma are related to compression of common bile duct and are usually asymptomatic. In case of jaundice or cholangitis, portal decompression by portosystemic shunt can be performed to treat both biliary symptoms and portal hypertension.
...
PMID:[Portal cavenorma: diagnosis, aetiologies and consequences]. 1253 94
DIAGNOSTIC CIRCUMSTANCES: Portal vein thrombosis is the second cause of portal hypertension after cirrhosis in Western countries. Diagnosis can be either made at the acute stage in the context of
abdominal pain
or after appearance of a porto-portal collateral venous circulation leading to the formation of a portal cavernoma, the diagnosis being made in the circumstance of rupture of oesophageal
varicose veins
or manifestations of hypersplenism. AETIOLOGICAL SURVEY: In the absence of hepatocellular carcinoma, causes that need to be investigated are cirrhosis, local factors (intra-abdominal sepsis, abdominal surgery, splenectomy or pancreatitis), and one or several prothrombotic affections (acquired or inherited prothrombotic states are present in 70% of cases, with myeloproliferative disease ranking first). REGARDING TREATMENT: Anticoagulant therapy generally allows recanalisation of the thombosed veins in recently constituted thrombosis. Some patients at the portal cavernoma stage can also benefit from anticoagulant therapy: patients with a prothrombotic state without large oesophageal-gastric
varicose veins
. In the case of large oesophageal-gastric
varicose veins
that have never bled, treatment to prevent haemorrhages due to portal hypertension according to the same modalities as in cirrhosis must be associated with the prescription of an anticoagulant. In the absence of prothrombotic affection or in patients having already suffered from haemorrhages due to portal hypertension, the benefit of anticoagulant therapy is less clearly established.
...
PMID:[Portal vein thrombosis]. 1453 80
In three women, aged 34, 52 and 30 years, respectively, who suffered from chronic pelvic symptoms such as a heavy feeling and
abdominal pain
, atypical
varicose veins
were observed on the medial side of the upper thighs together with
varicose veins
of the vulva; these are indicators of insufficiency of the pelvic veins. The symptoms were reduced following embolisation of the insufficient pelvic veins. These symptoms are also known as the pelvic congestive syndrome. The exact correlation between insufficiency of the pelvic veins and the complaints mentioned above has not yet been determined, but it seems that in most patients the symptoms diminish or disappear following embolisation of the insufficient pelvic veins. When patients complain of chronic pelvic pain of unknown aetiology, one should look for atypical
varices
and vulval
varices
and consider pelvic-vein insufficiency as a possible cause.
...
PMID:[Women with pelvic complaints and atypical varicose veins, varicose veins of the vulva and insufficiency of the pelvic veins; treatment with embolisation]. 1600 43
Nutcracker syndrome is caused by compression of the left renal vein between the aorta and the superior mesenteric artery where it passes in the fork formed at the bifurcation of these arteries. The phenomenon results in left renal venous hypertension. The syndrome is manifested by left flank and
abdominal pain
, with or without unilateral haematuria. Other common presentation is as "pelvic congestion syndrome" characterized by symptoms of dysmenorrhea, dyspareunia, post-coital ache, lower
abdominal pain
, dysuria, pelvic, vulvar, gluteal or thigh
varices
and emotional disturbances. Likewise compression of the left renal vein can cause left renal-to-gonadal vein reflux resulting in lower limb
varices
and varicoceles in males. Its diagnosis is based on history and physical examination, basic lab tests to exclude other causes of haematuria, cystoscopy and ureteroscopy to confirm unilateral haematuria and exclude other causes of this sinister symptom. Sequence of imaging has more or less been rationalised to USS with Doppler studies, CT or MR angiography and finally phlebography with renal vein and IVC manometery to confirm the diagnosis.
...
PMID:Current trends in the diagnosis and management of renal nutcracker syndrome: a review. 1678 Nov 73
Portal vein thrombosis (PVT) consists of two different entities: acute PVT and chronic PVT. Acute PVT usually presents as
abdominal pain
. When the thrombus extends to the mesenteric venous arches, intestinal infarction can occur. Chronic PVT is usually recognized after a fortuitous diagnosis of hypersplenism or portal hypertension, or when there are biliary symptoms related to portal cholangiopathy. Local risk factors for PVT, such as an abdominal inflammatory focus, can be identified in 30% of patients with acute PVT; 70% of patients with acute and chronic PVT have a general risk factor for PVT, most commonly myeloproliferative disease. Early initiation of anticoagulation therapy for acute PVT is associated with complete and partial success in 50% and 40% of patients, respectively. A minimum of 6 months' anticoagulation therapy is recommended for the treatment of acute PVT. For patients with either form of PVT, permanent anticoagulation therapy should be considered if they have a permanent risk factor. In patients with large
varices
, beta-adrenergic blockade or endoscopic therapy seems to prevent bleeding as a result of portal hypertension, even in patients on anticoagulation therapy. In patients with jaundice or recurrent biliary symptoms caused by cholangiopathy, insertion of a biliary endoprosthesis is the first treatment option. Overall, the long-term outcome for patients with PVT is good, but is jeopardized by cholangiopathy and transformation of underlying myeloproliferative disease into myelofibrosis or acute leukemia.
...
PMID:Nonmalignant portal vein thrombosis in adults. 1695 67
This paper presents the hypothesis, that pain and functional disturbances of organs which lie on the midline of the body might be caused by a venous congestion of these organs. Cause of their congestion is the participation of these organs (vertebral column, skull, brain, spinal medullary, uterus, prostate, left ovary/testis, urinary bladder rectum, vagina, urethra) in the collateral circulation of the left renal vein. In many patients with complaints of the above mentioned organs the left renal vein is compressed inside the fork formed by the superior mesenteric artery and the aorta. This so called nutcracker phenomenon is incompletely understood today. It can lead to a marked reduction of left renal perfusion and forces the left renal blood to bypass the venous compression site via abundant collaterals. These collaterals are often not sufficient. Their walls become stretched and distorted -
varices
with inflamed walls are formed. These dilated veins are painful, interfere with the normal organ's function and demand more space than usual. This way pain in the midline organs and functional derangement of the midline organs can occur. The term "midline congestion syndrome" seems appropriate to reflect the comprehensive nature of this frequent disorder. The rationale for this hypothesis is based on the novel PixelFlux-technique (www.chameleon-software.de) of renal tissue perfusion measurement. With this method a relevant decline of left renal cortical perfusion was measured in 16 affected patients before therapy (left/right ratio: 0.79). After a treatment with acetylsalicylic acid in doses from 15 to 200mg/d within 14-200 days a complete relief of so far long lasting therapy-resistant midline organ symptoms was achieved. Simultaneously the left/right renal perfusion ratio increased significantly to 1.24 (p=0.021). This improvement of left renal perfusion can be explained by a better drainage of collateral veins, diminution of their wall distension, thereby decline of their intramural inflammation, reduction of their mass effects (especially by the replaced spinal fluid inside the spinal canal and the skull), and altogether a reduction of pain and functional derangement in the affected midline organs. The proposed theory might influence the current understanding of such frequent and difficult to treat diseases as chronic back pain, headaches, frequent cystitis, enuresis,
abdominal pain
, flank pain and might spur new theories of arterial hypertension, placental insufficiency, prostate diseases and myelopathies.
...
PMID:From the nutcracker-phenomenon of the left renal vein to the midline congestion syndrome as a cause of migraine, headache, back and abdominal pain and functional disorders of pelvic organs. 1732 37
A 74-year-old man with compensated hepatitis C virus-related liver cirrhosis was admitted for the treatment of small hepatocellular carcinoma (HCC) by radiofrequency ablation therapy (RFA). As a routine pretreatment examination, gastrointestinal endoscopy was performed, and large nodular
varices
were observed in the gastric fornix, with telangiectasia on top of the
varices
. As soon as the RFA was completed, prophylactic balloon-occluded retrograde transvenous obliteration (B-RTO) was performed. Seven days after the B-RTO, the patient complicated of upper
abdominal pain
. Gastrointestinal endoscopy was performed, and a deep ulcer, located at the top of the tumor-shaped gastric
varices
, was found. The ulcer showed rapid healing after 1-week administration of a proton pump inhibitor (PPI). A severe ulcer after a B-RTO procedure, is extremely rare, because sclerosing agents rarely flow into the gastric mucosa. The ulcer in this patient was deep and large, and it may have been due to direct mucosal damage caused by the sclerosing agent, because mucosal telangiectasia on top of the
varices
was observed before the B-RTO. It is likely that, in this patient, the mucosal vessels communicated with the submucosal large
varices
, and ethanolamine oleate (EOI) flowed into the gastric mucosa via this communication. Based on our experience, we recommend periodic follow-up endoscopy.
...
PMID:Gastric ulcer after prophylactic balloon-occluded retrograde transvenous obliteration. 1738 Feb 86
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