Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 51-year-old woman suddenly developed severe pain in the chest and back, also dyspnea. On admission, she was in a state of preshock. Plain X-ray indicated the lack of the left aortic arch and poor pneumatization in the whole right lung. The thoracic fluid was transparent with yellowish tinge and was contaminated with neither any bacterium nor tubercle bacillus. The response to the Rivalta's reaction was negative. The possibility of pleurisy was, therefore, denied. The ECG and blood biochemical data on the second day suggested the possibility of myocardial ischemia. Plain chest X-ray on the fourth day revealed an increased right pulmonary pneumatization and an enlarged mediastinal shadow toward the aortic arch. Upper pulmonary CT showed a mass on the right side. Enhanced CT disclosed a dissepiment in the center, which was high medially and somewhat low laterally. It was diagnosed as a false lumen due to the lateral displacement of the right aortic arch. Hepatic CT disclosed the tapering of the abdominal aorta from right to left in the prevertebral region. These findings indicated that the aorta descended from the right aortic arch along the right side of the spine and crossed the spine dextrosinistrally at the hepatic level. In addition, dissociant aneurysm was observed in the right aortic arch. Echocardiography showed no evidence of dissociant aneurysm at the aortic base. Chest X-ray, CT and echocardiography showed the dissociation of the aorta from the aortic arch to the abdominal aorta. Thus the diagnosis of De Bakey type III was established. Clinically, DIC and multiorgan disorders were manifested but after medical treatments, the clinical course was uneventful.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A dissecting aortic aneurysm involving a right-sided aortic arch]. 273 81

In spite of all the scientific and technical advances in recent years, shock that is not rapidly correctable with fluid can have a morbidity rate exceeding 80%. Consequently awareness of such precipitating factors as sepsis and early diagnosis and treatment are essential. Treatment should be rapid and should follow a previously outlined protocol. Such protocols should include correction of the precipitating problem and aggressive resuscitation to assure adequate ventilation and oxygenation of the blood and optimal oxygen delivery to the tissues. Fluid and blood should be given as needed until filling pressures begin to rise rapidly with further fluid infusion. With hemorrhagic shock in previously healthy individuals, a hemoglobin level of 10.0 g/dL is usually adequate. In older, septic, or cardiogenic shock patients, a hemoglobin level of 12.5 to 14.0 may be preferable. If an optimal preload does not increase cardiac output to normal or higher levels, inotropic agents should be used. If shock still persists, one must be sure that the arterial pH is not excessively high or low. Glucocorticoids may then be given in low dose (200 mg hydrocortisone) in case some degree of adrenal insufficiency is present. They can also be given in high doses (equivalent to 150 mg/kg hydrocortisone) early in septic shock primarily to prevent excess complement activation and to preserve membrane integrity. Vasopressors may occasionally be required if there is excessive vasodilation, especially if there is persistent hypotension in the presence of high-grade coronary or cerebral artery stenosis. Vasodilators may be used to try to correct myocardial ischemia (nitroglycerin), excessive preload (nitroglycerin), or excessive afterload (nitroprusside or hydralazine). Combinations of vasodilators and inotropic agents may be required in some patients with high systemic vascular resistance and persistently low cardiac outputs. Mechanical assist with IABP can be of great value in persistent cardiogenic shock. Diuretics may occasionally help prevent renal failure in patients who are persistently oliguric after blood flow and pressure are restored. Heparin is occasionally of value if DIC develops with no concomitant fibrinolysis. Antibiotics are important in septic shock and may also be important if persistent shock has reduced gastrointestinal mucosal integrity so that bacteria and bacterial products can enter the portal system.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Science and shock: a clinical perspective. 389 56

Pre-operative and operative complications in 2266 patients having undergone transurethral resection of prostate (TURP) for the past 20 years at Kitasato University Hospital were analyzed. They consisted of 2008 benign prostatic hyperplasia and 258 prostate cancer patients. Seven hundred and fifty four patients showed some of physical disorders prior to TUR:hypertension in 147 cases, diabetes mallitus in 87, ischemic heart disease in 46, chronic obstructive lung disease in 41 and others. Operative and postoperative complications of TURP were seen in 308 cases (13.6%). Perforation of the prostatic capsule was seen in 100 cases (4.4%) and bladder perforation into intraperitoneal cavity in 6 cases (0.3%). Transurethral fulgulation for postoperative hemorrhage was conducted on 79 cases (3.5%). Hyponatremia lower than 130 mEq/L was noted in 14 cases (0.6%). Severe urinary tract infection leading to bacteremia was observed in 9 cases (0.4%). Postoperative epididymitis was evident in 20 cases (0.8%). There was postoperative urinary incontinence in 19 cases, 3 of which was treated with Teflon-paste injection successfully. One patient had to undergo AMS-800 artificial sphincter implantation. The number of postoperative urethral stricture patients requiring urethral dilatation or internal urethrotomy was 12 (0.5%) and postoperative bladder neck contracture was seen in 20 cases (0.9%). One patient (0.04%) who developed DIC after profuse postoperative hemorrhage died on the 37th postoperative day. The efficiency of TURP depends not so much on the skill of cutting as on the speed and accuracy of orientation and haemostasis. The quick recognition of anatomical landmarks will assure effective and safe resection.
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PMID:[Pre-operative, operative and postoperative complications in 2266 cases of transurethral resection of the prostate]. 768 90

From March 1993 to February 1993, 36 patients with chronic renal failure underwent cardiac surgery with intraoperative hemodialysis (HD). We examined and compared the medium term results of those patients cased upon the time periods of operation and types of heart disease. With respect to the time periods of operation, the 1st term (n = 12) was between March 1985 and February 1989, and the 2nd term (n = 24) was between March 1989 and February 1993. Concerning types of disease, Group A was comprised of 24 patients with ischemic heart disease, and Group B was comprised of 12 patients with valvular or congenital heart disease. Only one early death was observed in the 1st term (8.3%: LOS). As for late death, 5 cases were observed in the 1st term (45.3%), and 2 cases were observed in the 2nd term (8.3%). The actuarial survival rate (post 3 years) was 72.7% in the 1st term and 91.3% in the 2nd term. In each case, the survival rate of the 2nd term was significantly better than the that of the 1st term (p < 0.025). When compared cased upon the types of disease, the actuarial survival rate (post 6 years) was 84.6% in Group A, and 45.5% in Group B, respectively. This difference was statistically significant (p < 0.05). Causes of late death were cerebral hemorrhage in 5 cases, sudden and unknown in one and DIC in the remaining one patient. There were many postoperative complications in this series in addition to the above stated fatal ones. The majority of them, however, were successfully treated, if early diagnosis of them was obtained. During the perioperative period through the long-term period, incidents of fatal hemorrhage among patients on chronic dialysis were reduced by 1) strict management of hypertension; 2) HD without use of Heparin; and 3) with respect to patients who required Warfarin after valve replacement, through the careful anti-coagulant therapy which maintained the thrombo-test (TT) value at precise levels.
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PMID:[Cardiac surgery in patients on chronic hemodialysis]. 891 Oct 41

A 27-year-old woman (38 week pregnant) was admitted to an obstetric hospital with an acute severe abdominal pain. At that time, the fetal heart sound was not audible. The diagnosis of placental abruption was made and she underwent an emergency cesarean section (C/S) under general anesthesia. She had anemia which became worse in the first few hours after C/S, requiring blood transfusion. ST depression was also present in the ECG during this period. Subsequently, we found an increase in myocin light chain, but not in troponin-T. On the 2nd postoperative day, pulmonary edema appeared and DIC was suspected. We treated her with nitrates, diuretics, protease inhibitors and oxygen by mask. She was discharged on 14th postoperative day with no other complications. Cardiac echogram showed no abnormalities, but a borderline change was seen in her exercise ECG. Depression of the ST segment has been reported in C/S patients, but this does not indicate myocardial ischemia (MI) nor treatment is necessary in most cases. In our case, the diagnosis was not conclusive, but in view of the risks associated with MI, patients with placental abruption should be managed strictly as if they have MI.
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PMID:[Myocardial ischemia during cesarean section in a patient with placental abruption]. 1088 50

Systematic evaluations of anemia, thrombocytopenia, and coagulopathy are essential to identifying and managing their causes successfully. In all cases, clinicians should evaluate RBC measurements alongside WBC and platelet counts and WBC differentials. Multiple competing factors may coexist; certain factors affect RBCs independent of those that affect WBCs or platelets. Ideally, clinicians should examine the peripheral blood smear for morphologic features of RBCs, WBCs, and platelets that provide important clues to the cause of the patient's hematologic disorder. Thrombocytopenia arises from decreased platelet production, increased platelet destruction, or dilutional or distributional causes. Drug-induced thrombocytopenias present diagnostic challenges, because many medicines can cause thrombocytopenia and critically ill patients often receive multiple medications. If they suspect type II HIT, clinicians must promptly discontinue all heparin sources, including LMWHs, without awaiting laboratory confirmation, to avoid thrombotic sequelae. Because warfarin anticoagulation induces acquired protein C deficiency, thereby exacerbating the prothrombotic state of type II HIT, warfarin should be withheld until platelet counts increase to more than 100,000/microL and type II HIT is clearly resolving. The presence of a consumptive coagulopathy in the setting of thrombocytopenia supports a diagnosis of DIC, not TTP-HUS, and is demonstrated by decreasing serum fibrinogen levels, and increasing TTs, PTs, aPTTs, and fibrin degradation products. Increasing D-dimer, levels are the most specific DIC parameter and reflect fibrinolysis of cross-linked fibrin. Elevated PTs or a PTTs can result from the absence of factors or the presence of inhibitors. Clinicians should suspect factor inhibitors when the prolonged PT or aPTT does not correct or only partially corrects following an immediate assay of a 1:1 mix of patient and normal plasma. In addition to factor inhibitors, antiphospholipid antibodies (e.g., lupus anticoagulant) can produce a prolonged aPTT that does not correct with normal plasma but is overcome by adding excess phospholipid or platelets. Paradoxically, a tendency to thrombosis, not bleeding, accompanies lupus anticoagulants and the antiphospholipid antibody syndrome. Transfusion of red blood cells, platelets, or plasma products is sometimes warranted, but clinicians must carefully weigh potential benefits against known risks. In critically ill patients, administering RBCs can enhance oxygen delivery to tissues. Among euvolemic patients who do not have ischemic heart disease, guidelines recommend a transfusion threshold of HGB levels in the range of 6.0 to 8.0 g/dL; patients who have HGB that is at least 10.0 g/dL are unlikely to benefit from blood transfusion. The use of rHuEPO to increase erythropoiesis offers an alternative to RBC transfusion, assuming normal, responsive progenitor cells and adequate iron, folate, and cobalamin stores. Future research should examine whether clinical outcomes from rHuEPO use in critically ill patients are important and cost-effective. Because platelets play an instrumental role in primary hemostasis, platelet transfusions are often important in managing patients who are bleeding or at risk of bleeding with thrombocytopenia or impaired platelet function. Platelet transfusions carry risks, and decisions to transfuse platelets must consider clinical circumstances. Most important, platelet transfusions are generally contraindicated if the underlying disorder is TTP or type II HIT, because platelet transfusion in these settings may fuel thrombosis and worsen clinical signs and symptoms. Plasma products can correct hemostasis when bleeding arises from malfunction, consumption, or underproduction of plasma coagulation proteins. Choice of plasma product for transfusion depends on clinical circumstances. FFP is the most commonly used plasma product to correct clotting factor deficiencies, particularly coagulopathies that are attributable to multiple clotting factor deficiency states as in liver disease, DIC, or warfarin anticoagulation. PCC or rFVIIa that is administered in small volumes may provide advantages over FFP when coagulopathies require quick reversal without risk of volume overload. Factor concentrates can replace specific factor deficiencies. Recombinant FVIIa bypasses inhibitors to factors VIII and IX and vWF. Use of rFVIIa in managing hemostatic abnormalities from severe liver dysfunction; extensive surgery, trauma, or bleeding; excessive warfarin anticoagulation; and certain platelet disorders requires further study to determine optimal and cost-effective dosing regimens. Recombinant activated protein C reduces mortality from severe sepsis that is associated with organ dysfunction in adults who are at high risk for death (APACHE scores of at least 25). In severe sepsis, levels of protein C decrease, as do fibrinogen and platelet levels. Because of its anticoagulant effect, however, drotrecogin alfa may induce bleeding. Guidelines for drotrecogin alfa use must take into account bleeding risks.
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PMID:Critical issues in hematology: anemia, thrombocytopenia, coagulopathy, and blood product transfusions in critically ill patients. 1471 Jun 93