Comparison of stroke volume (SV) and stroke volume respiratory variation (SVV) measured by the axillary artery pulse-contour method and by aortic Doppler echocardiography in patients undergoing aortic surgery.

BACKGROUND: The goal of the study was to compare stroke volume (SV) and respiratory stroke volume variation (SVV) measured by pulse-contour analysis and aortic Doppler. METHODS: These were measured by pulse-contour analysis and thermodilution (PiCCO) and by aortic pulsed wave Doppler with transoesophageal echocardiography in patients undergoing abdominal aortic surgery. Simultaneous measurements were done at different times of surgery. All data were recorded on PiCCOwin software and videotape and analysed off-line by a blinded investigator. RESULTS: A total of 114 measurements were achieved in 20 patients. There was a good correlation and small bias between the PiCCO and the echo-Doppler values of the mean SV [r=0.885; bias=0.2 (8) ml], and between the minimum [r=0.842; bias=1 (9) ml] and maximum SV [r=0.840; bias=2 (10) ml] values. CONCLUSIONS: There is a fair correlation between pulse-contour analysis and aortic Doppler for beat-by-beat measurement of SV but not for calculation of SV respiratory ventilation.

Low negative predictive value of dobutamine stress echocardiography before abdominal aortic surgery.

BACKGROUND: According to previous studies, a negative dobutamine stress echocardiography (DSE) test before major vascular surgery indicates that postoperative myocardial necrosis is very unlikely. We believe that the use of new cardiac troponin assays which can detect small amounts of myocardial necrosis results in a lower DSE negative predictive value for myocardial necrosis. METHODS: A total of 418 consecutive patients were screened using the ACC/AHA Guideline for Perioperative Cardiovascular Evaluation for Noncardiac Surgery before scheduled abdominal aortic surgery. Of these 143 met ACC/AHA criteria for non-invasive testing and underwent DSE. Patients with a negative DSE were deemed to be fit for surgery. A positive DSE led to a coronary angiogram. DSE was negative in 110 (77%) and positive in 33 (23%) patients. Myocardial necrosis was monitored up to the third postoperative day by daily cardiac troponin I (cTnI) measurement and a daily 12-lead ECG. RESULTS: Coronary angiography showed artery stenosis in 27 (84%) of 32 patients with a positive DSE. The negative predictive value of DSE for cTnI elevation was 92.7% (95% CI 86.2-96.8%). This was significantly lower than the lowest value of negative predictive value for myocardial necrosis assessed in previous studies. CONCLUSION: A negative DSE prescribed before scheduled aortic surgery according to ACC/AHA guidelines does not rule out postoperative myocardial necrosis.

[Subdural haemorrhage following lumbar spinal drainage during repair of thoraco-abdominal aneurysm]. / Hématome sous-dural aigu après soustraction-drainage du LCR par voie lombaire chez deux patients opérés d'anévrismes thoraco-abdominaux.

Physicians in charge of patients undergoing thoracic or thoraco-abdominal aneurysmectomy, frequently use lumbar spinal drainage of the cerebrospinal fluid (CSF) to prevent paraplegia. Whereas the profit of this technique is a much debated question, we report 2 case reports of delayed sub-dural hemorrhage, after lumbar spinal drainage of CSF. Cross clamping of the aorta decreases the spinal cord artery pressure, increases the cerebral pressure and by alterations of distribution of the venous return, is responsible for an increase of the CSF pressure. This increase of the CSF pressure decreases the spinal cord driving pressure. Lumbar spinal drainage of CSF aims to improve the spinal cord driving pressure close to the normal (where driving pressure = aortic pressure - CSF pressure). The two case reports have to be added to the liability of a method of prevention that, as attractive that it is, did not give the proof of its efficiency to decrease the frequency and/or the severity of paraplegia after thoracic or thoraco-abdominal aneurysmectomy. At this time, this technique should be reserved to the patients with documented risk, as it is possible using preoperative spinal cord arteriography. The insertion and the withdrawal of the catheter must be done in the usual conditions of medullar puncture with regard to anticoagulant and antiplatelet agents

Evaluation of transesophageal echocardiography for diagnosis of traumatic aortic injury.

BACKGROUND: Traumatic aortic injury is a frequent cause of death after blunt trauma, but few patients survive to reach a trauma center. The role of transesophageal echocardiography (TEE) in the diagnosis of traumatic aortic injury remains debated. METHODS: Over a 9-yr period, 209 blunt trauma patients (mean age, 34 +/- 13 yr) were suspected of having traumatic aortic injury because of enlarged mediastinum and/or sudden deceleration, and underwent TEE and angiography (aortography and/or contrast-enhanced computed tomography. RESULTS: Traumatic aortic injury was diagnosed in 42 patients (20%). Angiography (aortography and/or contrast-enhanced computed tomography) was less accurate (sensitivity, 83%; specificity, 100%) than TEE (sensitivity, 98%; specificity, 100%) for the diagnosis of aortic injury because it failed to diagnose most minor injuries (intramural hematoma or limited intimal flap, n = 7). However, when considering only patients with major aortic injury (n = 33; i.e., those who might need surgery), angiography (sensitivity, 97%; specificity, 100%) and TEE (sensitivity, 97%; specificity, 100%) were equivalent. CONCLUSION: Transesophageal echocardiography is an accurate method for diagnosis of traumatic aortic injury. Nevertheless, the clinical implications of limited aortic injuries diagnosed by the technique have yet to be determined.

Administration of desmopressin in brain-dead donors and renal function in kidney recipients.

BACKGROUND: Diabetes insipidus is common among brain-dead donors and may lead to decreased graft function. The use of desmopressin to limit the consequences of diabetes insipidus is controversial. We assessed the effects of desmopressin administered to brain-dead donors on early and long-term graft function in kidney recipients. METHODS: In a randomised controlled study, 97 brain-dead donors received desmopressin as 1 microg bolus every 2 h when diuresis was more than 300 mL/h (desmopressin group n=49) or no desmopressin (control group n=48). In 175 kidney recipients (controls n=89, desmopressin group n=86) we measured serum concentrations of creatinine and haemodialysis requirements to assess early renal function in the first 15 days after transplantation. We assessed long-term results of transplantation (median time 45 months) for a homogeneous subgroup of 95 recipients (48 in the desmopressin group). FINDINGS: We found no significant differences between the two groups of brain-dead donors, except for final diuresis, which was lower in the desmopressin group than among controls. Haemodialysis requirement in controls and the desmopressin group (20 vs 23%, p=0.63) and serum creatinine concentrations (decrease from 903 micromol/L to 206 micromol/L vs 814 micromol/L to 193 micromol/L, p=0.14) did not differ significantly in the first 15 days after transplantation. Long-term graft survival was similar in the two groups (88 vs 87%). INTERPRETATION: Desmopressin can be given to brain-dead donors to limit the harmful effects of diabetes insipidus without any substantial effects to graft function in recipients.

Use of transesophageal echocardiography for diagnosis of traumatic aortic injury.

This prospective study was conducted to describe the signs on transesophageal echocardiography (TEE) associated with traumatic aortic injury (TAI). Twenty-eight patients with TAI underwent TEE, and they were compared with a control group of 30 thoracic trauma patients without aortic injury. The TEE signs were classified as direct or indirect signs, and the quality of imaging was assessed. Patients' TEE images were compared with their anatomic lesions. The direct signs were thick stripes (n=19), false aneurysm (n=7), aortic dissection (n=6), free-edge intimal flap (n=15), aortic wall hematoma (n=2), fusiform aneurysm (n=13), and complete aortic obstruction (n=2). The indirect signs included minor increases in aortic diameter (n=7), impairment of the aortic Doppler color flow (n= 18), and an increase of aorta-probe distance, indicating hemomediastinum (n=23). TEE allowed diagnosis of recently described limited intimal lesions frequently missed by other conventional methods, and permitted rapid diagnosis of complete rupture in which fast degeneration means that more time-consuming methods are not practicable. Significant blurring of the aortic outline was noted in 20% of cases and intraluminal artifacts were observed in 36% of cases, but neither sign impaired accurate diagnosis of TAI. The echocardiographic signs of aortic injury are complex and may be confined to a short section of the aorta. Therefore, examination by a physician highly trained in echocardiography is necessary in such cases.

Circulating cardiac troponin T in myocardial contusion.

STUDY OBJECTIVE: Myocardial contusion may induce life-threatening complications, but its diagnosis is difficult. Circulating cardiac troponin T is considered a highly sensitive and specific marker of myocardial cell injury. We investigate the value of cardiac troponin T measurement in the diagnosis of myocardial contusion. DESIGN: Prospective study. SETTING: Level 1 trauma center. METHODS: We prospectively measured circulating cardiac troponin T and performed echocardiography and continuous Holter monitoring in patients who had suffered blunt trauma. Myocardial contusion was diagnosed in patients who fulfilled one of the following criteria: (1) an abnormal echocardiography compatible with myocardial contusion; (2) severe cardiac rhythm abnormalities; (3) severe cardiac conduction abnormalities; and (4) hemopericardium. MEASUREMENTS AND RESULTS: One hundred twenty-eight patients were included and myocardial contusion was diagnosed in 29 patients. Patients with myocardial contusion had more severe trauma, experienced more frequently associated thoracic lesions, and had a lower left ventricular ejection fraction area (48 +/- 15 vs 61 +/- 10%; p < 0.001). Elevated circulating cardiac troponin T concentrations were significantly more frequent in patients with a myocardial contusion (31 vs 9%; p < 0.007). An elevated circulating cardiac troponin T concentration (> or = 0.5 microgram/L) was more accurate than MB fraction of creatine kinase (CK) (CK-MB) and CK-MB/CK ratio in the diagnosis of myocardial contusion, as shown by an area under the receiver operating characteristic (ROC) curve (AROC), which was significantly different from 0.50 (AROC = 0.69; 95% confidence interval, 0.56 to 0.80). However, this improvement was not clinically acceptable (sensitivity, 0.31; specificity, 0.91). CONCLUSIONS: Circulating cardiac troponin T measurement had a slightly greater diagnostic value than usual biological parameters (CK-MB, CK-MB/CK) in myocardial contusion. Nevertheless, it was concluded that an elevated circulating cardiac troponin T concentration has no important clinical value in the diagnosis of myocardial contusion.

The effects of triiodothyronine on hemodynamic status and cardiac function in potential heart donors.

Brain death is associated with altered cardiac function and low concentrations of circulating triiodothryronine (T3). However, the effects of T3 administration on hemodynamic status and cardiac function in potential heart donors remain controversial. Thirty-seven brain-dead patients were randomly and blindly allocated to receive an intravenous bolus of either 0.2 microgram/kg T3 (n = 19) or saline placebo (n = 18). Measurements included conventional hemodynamic and echocardiographic variables of cardiac volume conditions and systolic function of the left ventricle (fractional area change [FAC], velocity of myocardial fiber shortening) using a transesophageal probe, arterial and mixed venous blood gas parameters, and serum thyroid hormone concentrations. The mean concentration of T3 was 1.86 +/- 1.55 pmol/L, and only six patients (16%) had normal values of T3 in control conditions. There was no significant correlation between T3 concentration and FAC (R = 0.17, not significant). All patients receiving T3 had normalized serum T3 concentration (7.55 +/- 2.56 pmol/L) in contrast to patients receiving saline (1.48 +/- 1.26 pmol/L). No significant differences in hemodynamic and echocardiographic parameters were observed between the placebo and T3 groups. Indeed, FAC remained unchanged after T3 (44% +/- 17% vs 46% +/- 22%) or placebo (47% +/- 18% vs 50% +/- 14%) administration. In 20 patients with impaired left ventricular function (FAC < 50%), FAC remained unchanged after T3 (n = 10; 34% +/- 12% vs 30% +/- 10%) or placebo (n = 10; 38% +/- 12% vs 35% +/- 13%) administration. In 17 patients in whom organ harvesting was delayed, transesophageal echocardiography was performed 6 h later and no significant changes in FAC were noted in the T3 group (n = 8; 49% +/- 17% vs 44% +/- 17%) and the placebo group (n = 9; 51% +/- 18% vs 47% +/- 18%). In conclusion, T3 administration did not improve hemodynamic status and myocardial function in brain-dead patients, suggesting that the euthyroid sick syndrome is not the main determinant of myocardial dysfunction in these patients.

Systemic gas embolism complicating pulmonary contusion. Diagnosis and management using transesophageal echocardiography.

Systemic air embolism has been frequently reported after penetrating thoracic trauma. In blunt thoracic trauma, systemic air embolism has been rarely diagnosed, and then only after an invasive procedure such as thoracotomy. Transesophageal echocardiography has been recently introduced for the early assessment of trauma patients and is considered a sensitive noninvasive procedure to diagnose air embolism. We report three cases of systemic air embolism in patients with pulmonary contusion secondary to a blunt thoracic trauma requiring controlled ventilation. Transesophageal echocardiography was performed for evaluation of hemodynamic instability, and it showed air bubbles in the left atrium and left ventricle during the insufflation phase, which disappeared during apnea. A decrease in airway pressure (release of PEEP, low tidal volume, high frequency jet ventilation) significantly reduced the systemic air embolism. We concluded that systemic air embolism can occur after blunt thoracic trauma, and transesophageal echocardiography enables a rapid and accurate diagnosis that may be useful for therapeutic management.

Circulating cardiac troponin T in potential heart transplant donors.

BACKGROUND: Brain death may induce myocardial dysfunction, the mechanisms of which are not yet fully understood. Circulating cardiac troponin T is considered a highly sensitive and specific marker of myocardial cell injury. METHODS AND RESULTS: We prospectively measured circulating cardiac troponin T in 100 brain-dead patients and measured the left ventricular ejection fraction area (LVEFa), using transesophageal echocardiography. Sixty-one patients had normal LVEFa, 25 had moderate decrease in LVEFa (30% to 50%), and 14 had severe decrease in LVEFa (< or = 30%). Circulating cardiac troponin T concentrations were significantly higher (1.68 +/- 1.03 micrograms/L-1, P < .01) in patients with a severe decrease in LVEFa than in the two other groups (0.42 +/- 0.43 and 0.12 +/- 0.16 microgram/L-1, respectively), and there was a significant correlation between LVEFa and cardiac troponin T concentration (p = -0.59, P < .0001). An elevated circulating cardiac troponin T concentration (> or = 0.5 microgram/L-1) was more accurate (sensitivity, 1.00; specificity, 0.84) in predicting a severe decrease in LVEFa than an elevated CKMB value or an increased CKMB/CK ratio. CONCLUSIONS: An elevated circulating cardiac troponin T was associated with a severe decrease in LVEFa in brain-dead patients, suggesting that severe and potentially irreversible myocardial cell damage occurred. In contrast, CKMB determination was not useful. Since the quality of the donor's heart is considered an important prognosis factor in heart transplantation, the determination of circulating cardiac troponin T concentration could be useful to the heart transplantation team.

Cardiovascular consequences of severe hypophosphataemia in brain-dead patients.

Hypophosphataemia is known to induce reversible myocardial dysfunction, but the incidence of hypophosphataemia and its effect on myocardial function during brain death are unknown. In 90 consecutive brain-dead patients, we measured plasma concentrations of phosphate and left ventricular ejection fraction area (LVEFa), using transoesophageal echocardiography. In 15 severely hypophosphataemic (< 0.40 mmol litre-1), consecutive, brain-dead patients, haemodynamic status, LVEFa, and oxygen delivery and consumption were assessed before and after phosphorus loading (0.30 mmol kg-1). In 10 other brain-dead patients, urine elimination of phosphates was measured. Only 30 (33%) brain-dead patients had normal plasma phosphate concentrations, 22 (24%) had mild hypophosphataemia (0.40-0.80 mmol litre-1) and 38 (42%) had severe hypophosphataemia (< 0.40 mmol litre-1). There were no significant differences in LVEFa between these three groups (mean 53 (SD 16), 55 (12) and 51 (17)%, respectively) and no significant correlation between LVEFa and plasma phosphate concentration (r = 0.04). In 15 severely hypophosphataemic patients, phosphorus loading increased plasma phosphate concentration from 0.30 (0.10) to 1.06 (0.41) mmol litre-1, but did not modify haemodynamic status, LVEFa or oxygen delivery and consumption. In 10 other patients, urine phosphorus elimination was 16.8 (23.3) mmol/24 h while plasma phosphate concentration was at its highest level (0.80 (0.37) mmol litre-1), and only one of these patient had a slightly elevated phosphaturia. In conclusion, hypophosphataemia frequently occurs after brain death but has no significant cardiovascular consequences, suggesting that it is related to intracellular transfer and not phosphorus depletion.(ABSTRACT TRUNCATED AT 250 WORDS)

Diagnosis of traumatic mediastinal hematoma with transesophageal echocardiography.

In patients with blunt chest trauma, early diagnosis of mediastinal hematoma is important, because it could be associated with thoracic vessel injury. Mediastinal hematoma is generally evoked because of a widened mediastinum on chest radiograph, but radiologic diagnosis may lead to excessive angiography being performed. Transesophageal echocardiography (TEE) provides accurate views of the mediastinum and can be rapidly performed at the bedside. Thus, we conducted a prospective study to define TEE signs of mediastinal hematoma. TEE was performed in 22 thoracic trauma patients (trauma group) and in 20 brain-dead patients without thoracic trauma (control group). The positive diagnosis of mediastinal hematoma was made using thoracic surgery or computed tomographic scan. The specificity of TEE was 75 percent and sensitivity was 100 percent. In the trauma group, there was only one false positive but angiography discovered a traumatic aneurysm of the proximal right subclavian artery. No false negative was noted. We described three different TEE signs of mediastinal hematoma: (1) an increased distance between the probe and the aortic wall; (2) a double contour of the aortic wall; and (3) visualization of the ultrasound signal between the aortic wall and the visceral pleura. The distance between the esophageal probe and the aortic wall was the most accurate sign because it could be easily obtained; the threshold value for this distance was 3 mm. TEE appears to be an accurate method to diagnose traumatic mediastinal hematoma.

Early diagnosis of traumatic thoracic aortic rupture by transesophageal echocardiography.

Traumatic aorta rupture survival depends on early diagnosis requiring aortography. Aortography is the "gold standard" method, but it is time-consuming and may be dangerous in trauma patients with multiple organ injuries. Transesophageal echocardiography is a noninvasive technology that can be performed at the bedside. We report two cases in which transesophageal echocardiography enabled us to make the early diagnosis of thoracic descending aorta rupture.