Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In patients with deep venous thrombosis, there is a recent trend towards surgical thrombectomy to avoid late complications. However, up to 10% of these patients suffer from severe intraoperative pulmonary embolism, 30 to 40% of whom die on the operating table. Treatment options for massive pulmonary embolism include embolectomy (high mortality), transvenous thrombus fragmentation techniques, and thrombolytic therapy. However, while thrombolysis is recommended as the treatment of choice for PTE, it is usually considered contraindicated in surgical patients because of bleeding complications. We report on 5 cases of severe pulmonary thromboembolism with marked cardiogenic shock during venous thrombectomy. Three patients were treated successfully by intraoperative thrombolysis alone or in combination with mechanical fragmentation of the embolus using a catheter technique under fluoroscopy (one case). Diagnosis was established by a sudden decrease of mean arterial pressure (from 83 to 45 mmHg), a marked increase of mean pulmonary artery pressure (MPAP) (from 16 to 43 mmHg), hypoxaemia (SaO2 < 90%), an increased arterial-to-end-tidal CO2-difference (from 7 to 42 mmHg), and/or pulmonary angiography (2 cases). All patients had to be treated with high dosages of catecholamines (norepinephrine 0.5 microgram.kg-1.min-1 or epinephrine 0.1 microgram.kg-1.min-1, and dopamine 6-15 micrograms.kg-1.min-1). Three patients required CPR prior to or during thrombolytic therapy. Thrombolysis was started intraoperatively with rt-PA with dosages ranging from 20 to 90 mg, applied in single injections (5-75 mg) followed by infusions (5 or 10 mg.h-1) for up to 8 hours.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Intraoperative thrombolysis with rt-PA in massive pulmonary embolism during venous thrombectomy]. 781 77

More than 50% of all congenital haemangiomas are located on the head and neck. Because most orofacial haemangiomas exhibit the tendency to grow rapidly, they are often treated by embolisation and excision. CASE REPORT. The case of a 5-year-old patient is presented, who was admitted to the hospital for embolisation and immediate surgery of a haemangioma of the right side of the face and upper lip. After the injection of 2 ml fibrin glue she suddenly developed hypotension, tachycardia, a low oxygen saturation, and a low end-tidal carbon dioxide partial pressure. There was no failure of the breathing circuit and no airway obstruction could be found. Most likely these symptoms were due to transport of the fibrin glue from the haemangioma into pulmonary vessels. The therapy included the administration of heparin and antihypotensive drugs. After stabilisation, the patient was transferred to the intensive care unit for 1 day without further complications. CONCLUSION. Pulmonary embolism after injection of fibrin glue into an orofacial haemangioma has not previously been reported, but it should be considered that systemic complications can occur after injecting substances for embolisation into vessel-rich tissues.
 ...
PMID:[Possible lung embolism following embolization of a hemangioma with fibrin glue]. 797 88

Massive intraoperative embolism is a life-threatening condition that may lead to immediate death. Important for the survival of the patient are rapid diagnosis and prompt surgical embolectomy. Case report. Nineteen days after a traffic accident, a 67-year-old patient who had complex ligamentous injuries was operated upon on both knees during general anaesthesia. The operation progressed uneventfully for the first 30 min when the patient's systolic blood pressure became slightly unstable and decreased to 85 mm Hg despite administration of ephedrine and infusion of hetastarch. This was followed 30 min later by an immediate drop to values that were undetectable on an oscilloscope. The pulse oximeter no longer detected a signal at the finger-tip and the end-tidal CO2 decreased to 1 kPa (7.5 mm Hg). To confirm the diagnosis of an acute pulmonary embolism, we performed transoesophageal echocardiography (TEE) and found a large amount of free-floating material in the right atrium, a dilated and hypokinetic right ventricle, and a collapsed left ventricle (Fig. 1 a). Embolectomy was immediately started using the inflow-occlusion technique supported by cardiopulmonary bypass (CPB). All emboli were removed from the right atrium and pulmonary artery (Fig. 1 b). During closure of the sternotomy, heart function was monitored by TEE and we again noted large emboli in the right atrium (Fig. 1 c). To remove these, we reinstated CPB and then placed an inferior vena cava filter. The final TEE control showed free heart chambers with good contractility (Fig. 1 d).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Massive intraoperative pulmonary embolism. Diagnosis and control following embolectomy with transesophageal echocardiography]. 804 74

Myxedema coma is characterized by severe lack of thyroid hormones, unconsciousness and serious restriction of vital functions. The mortality rate still ranges between 50 and 80%. In patients with inapparent hypothyroidism myxedema coma occasionally follows surgery, anesthesia or severe infection. A case of myxedema coma following surgery is reported. CASE REPORT. A 46-year-old woman was anesthesized for hip replacement. The intraoperative cardiovascular situation was characterized by hypotension and tachycardia. On the first postoperative day, unexpectedly a cardiac arrest occurred. Resuscitation with high doses of epinephrine was successful. There was no evidence of myocardial infarction, hypoxia and pulmonary embolism as causative factors for cardiac arrest. A pulmonary artery catheter was inserted and showed low cardiac output. Catecholamines and intravascular fluids were administered without hemodynamic improvement. In the next 5 days pneumonia was followed by ARDS and acute renal failure. After successful treatment of these complications the patient remained in deep coma. An intracerebral disease could be excluded by computerized tomography. Evaluation showed low thyroid hormones (T3; T4) and elevated TSH. The diagnosis of a myxedema coma was assumed. After failure of oral therapy with L-thyroxine (0.025-0.05 mg/day) for 10 days, intravenous therapy with 0.5 mg L-thyroxine was performed. Thirty-six hours later the patient regained consciousness, without cardiac complications. The patient progressed uneventfully under oral therapy with 0.1 mg L-thyroxine and was discharged from the hospital 6 weeks later. DISCUSSION. Pathophysiology and symptomatology of a case of postoperative myxedema coma are described (Tables 1-4). In this patient, the following symptoms occurred: low thyroid hormones (T3; T4), elevated TSH, deep coma, decreased ventilatory response to CO2, diminished myocardial contractility under catecholamine stimulation, impaired renal water excretion. After failure of oral substitution of L-thyroxine, intravenous therapy had to be performed in spite of the high risk of further cardiac complications in this patient. This led to complete recovery with normal neuropsychological and cardiopulmonary parameters. CONCLUSION. Myxedema coma is a rare complication in postoperative care, but in cases of inexplicable unconsciousness thyroid failure should be excluded. If myxedema coma is evident, intravenous therapy with L-thyroxine should be performed under the conditions of extended monitoring.
 ...
PMID:[Myxedema coma as a rare postoperative complication]. 848 Sep 6

Twenty-five patients with acute pulmonary embolism without other pulmonary or heart diseases were analyzed for pulmonary hypertension. Doppler echocardiography was used to determine the systolic pressure of the pulmonary artery (PAPs) from the maximal velocity of the tricuspid regurgitation using corrected Bernoulli's formula (PAPs = 1.23 x 4 Vmax2 - 0.09). Pulmonary hypertension was found in 84% (21/25) of the patients with acute pulmonary embolism. PAPs values ranged between 34 and 90 mmHg (X = 54 +/- 7.5 mmHg) and hypocapnia with carbon dioxide partial pressure, PaCO2, ranged from 26 to 34 mmHg (X = 30 +/- 2 mmHg). PAPs showed a significant negative correlation with oxygen partial pressure (r = -0.87, P < 0.01). According to the findings of lung scintigraphy, all patients with pulmonary hypertension had submassive pulmonary embolism with perfusion abnormalities in two segments (X = 5 +/- 2 segments). It is concluded that pulmonary hypertension may be expected in more than 80% of the patients with submassive acute pulmonary embolism, and hypoxemia and hypocapnia. Doppler echocardiography is a noninvasive method useful in the diagnosis and follow-up of pulmonary hypertension in patients with acute pulmonary embolism.
 ...
PMID:[Pulmonary hypertension in acute pulmonary embolism]. 864 78

Patients with severe pulmonary embolism can suffer progressive hypercapnia refractory to supramaximal mechanical ventilation, and may require open-thoracic or transvenous emergency embolectomy in addition to anticoagulation and/or thrombolysis. The functional recovery of gas exchange would be signaled by an increase in pulmonary CO2 elimination and decrease in CO2 retention; such data could guide the course of operative embolectomy. Accordingly, we studied five chloralose-urethane anesthetized, mechanically ventilated dogs with open thoraces in which the right pulmonary arteries (RPAs) were reversibly occluded with cloth snares. After waiting for steady state, we abruptly released the snare to restore RPA perfusion and experimentally simulate resolution of pulmonary embolism. For 70 min we serially measure the CO2 volume exhaled per breath (VCO2,br), arterial, mixed venous, and end-tidal PCO2 (PACO2, PVCO2, PETCO2), cardiac output (QT), and the alveolar dead space fraction (VDalv/VTalv = [PaCO2 - PETCO2/PaCO2). RPA reperfusion caused VCO2,br to significantly and abruptly increase from 8.9 +/- 2.7 to 11.6 +/- 3.6 mL; 70 min later VCO2,br had returned to baseline. PaCO2 and PVCO2 steadily decreased during 70 min of RPA reperfusion. PETCO2 increased from 25 +/- 5 to 33 +/- 5 mm Hg immediately after RPA reperfusion, as VDalv/VTalv decreased from 54% +/- 10% to 32% +/- 12%, but PETCO2 was still significantly greater than baseline at 70 min of RPA reperfusion. QT did not significantly change. We conclude that intraoperative measurement of VCO2,br should immediately detect and follow the resolution of CO2 retention in the lung and peripheral tissues after RPA reperfusion. PETCO2 could not detect the decrease of VCO2,br back to baseline because PETCO2 does not measure exhaled volume or the PCO2 waveform.
 ...
PMID:Carbon dioxide elimination measures resolution of experimental pulmonary embolus in dogs. 869 1

To test how large pulmonary embolism changes non-steady state CO2 kinetics, the right pulmonary artery (RPA) was occluded in 5 anesthetized, ventilated, thoracotomized dogs. By 1 min after RPA occlusion, CO2 volume exhaled per breath (VCO2,br) decreased from 9.3 +/- 2.8 to 7.0 +/- 2.6 ml and end-tidal PCO2 (PETCO2) decreased from 28.7 +/- 4.2 to 21.8 +/- 3.3 Torr. During the ensuing 70 min, VCO2,br increased back to baseline but PETCO2 was still 13% less than baseline. Both PaCO2 (41.5 +/- 1.7 to 55.1 +/- 8.1 Torr) and PvCO2 (48.2 +/- 1.9 to 62.8 +/- 6.5 Torr) steadily increased and approached equilibrium by 45 min of RPA occlusion. Cardiac output did not significantly change. In summary, RPA occlusion immediately decreased VCO2,br by 25%, due mostly to increased alveolar VD (VDalv). Then, VCO2,br recovered back to baseline as CO2 accumulated in tissues and lung. In contrast, elevated VDalv caused persistent decreased PETCO2, which did not detect recovery of VCO2,br nor increase in PaCO2 during RPA occlusion.
 ...
PMID:How does experimental pulmonary embolism decrease CO2 elimination? 893 Nov 81

We present the case of a young comatose female patient in whom a massive pulmonary embolism was diagnosed by pulmonary angiography. During the angiography, not only successful thrombolytic therapy with recombinant human tissue-type plasminogen activator (rt-PA) (100 mg) was performed, but measuring of the pulmonary artery pressures, oxygen and carbon dioxide levels was also possible. Thrombolysis seems to be a good alternative to surgical thrombectomy.
 ...
PMID:[Rt-PA thrombolysis in the treatment of massive pulmonary embolism]. 898 7

Main circulatory (heart frequency, HF, intra-artery pressure, AP ECG) and respiratory (arterial oxyhemoglobin saturation SaO2, end-tidal CO2) arterial gas-analysis (HGA) parameters were recorded continually during cemented hip arthroplasty in 70 consecutive non-selected patients. The use of cement did not cause any change in the parameters obtained in 21 of the cases, reduction in arterial oxygen pressure (PaO2) ranging from 11% to 38% was observed in 44 cases, associated with simultaneous reduction in ETCO2 in 11 cases. The reduction in ETCO2 was an isolated finding in 5 of the patients. AP decreased by more than 10% in only 2 cases and there was arrhythmia in another 2 cases. These findings are strongly suggestive of pulmonary embolism encouraging the hypothesis of gas embolism previously suggested by other authors. In patients with little coronary or pulmonary reserve use of cement means an increased risk of severe hemodynamic complications.
 ...
PMID:Pulmonary embolism associated with use of bone cement during hip arthroplasty. 914 25

Although the factors associated with mortality, such as forced expiratory volume in one second (FEV1), arterial oxygen tension (Pa,O2) and pulmonary arterial pressure, have been well described, there is limited information on the circumstances of death in patients with chronic obstructive pulmonary disease (COPD). The aim of this study was to investigate the causes and circumstances of death in patients with COPD and chronic respiratory failure (Pa,O2 < 8.0 kPa (60 mmHg) breathing air), treated with long-term oxygen therapy (LTOT). Ten European centres participated in the study and data were collected from patients both during a period of clinical stability and at the time of death. Of the 215 patients evaluated (161 males and 54 females; aged 66 +/- 10 yrs), the major causes of death were: acute on chronic respiratory failure (38%); heart failure (13%); pulmonary infection (11%); pulmonary embolism (10%); cardiac arrhythmia (8%); and lung cancer (7%). Seventy five percent of patients died in hospital. There was no difference in the number of patients who died in the morning, afternoon and night hours. Twenty percent of the total died during sleep and in 26% death was unexpected. A lower arterial carbon dioxide tension (Pa,CO2), less oxygen usage per 24 h, and increased incidence of arrhythmias were seen in those patients who died suddenly. Drug therapy was not related to unexpected death. The majority of patients with chronic obstructive pulmonary disease on long-term oxygen therapy died from chronic or acute on chronic respiratory failure. Prevention and treatment of respiratory failure in patients with chronic obstructive pulmonary disease is likely to have the greatest impact in reducing mortality.
 ...
PMID:Causes of death in patients with COPD and chronic respiratory failure. 915 11


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>