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.

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.

Plasma ionized calcium in brain-dead patients.

BACKGROUND: The mechanism of brain death-induced myocardial dysfunction remains debatable. Hypocalcemia is known to induce reversible myocardial dysfunction. However, the incidence of hypocalcemia and its effect on myocardial function during brain death is unknown. METHODS: In 54 consecutive brain-dead patients, we measured plasma total and ionized calcium concentrations, QT and corrected QT intervals, and left ventricular ejection fraction area (LVEFa), using transesophageal echocardiography. RESULTS: 49 (91%) of brain-dead patients had a decrease in total plasma total calcium concentration but only 19 (35%) had a decrease in plasma ionized calcium. Corrected total plasma calcium failed to predict ionized calcium concentration and QT intervals were not significantly different in normo and hypocalcemic patients. The LVEFa was not significantly different between normo and hypocalcemic patients (53 +/- 13 versus 50 +/- 20%), and no correlation was found between LVEFa and ionized calcium (R = 0.02, NS). Hypocalcemic patients required greater doses of dopamine (8.2 +/- 5.2 versus 5.0 +/- 3.4 micrograms.kg-.min-1, p < 0.02) to maintain arterial pressure. Hypocalcemia was associated with a higher volume loading and a lower plasma protide concentration which reflected hemodilution. CONCLUSION: A decrease in plasma ionized calcium is not frequent, rarely severe, and probably not the main mechanism of myocardial dysfunction in brain-dead patients. Hypocalcemic patients required higher doses of dopamine, suggesting a decrease in systemic resistance. Only direct measurement of ionized calcium can assess plasma calcium ion status in brain-dead 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.

Fiberoptic bronchoscopy in brain-dead organ donors.

Criteria for selecting lung donors include normal chest X-ray and adequate gas exchange, but normal bronchoscopy is not always required. Thus, we conducted a prospective study of fiberoptic bronchoscopy in 72 brain-dead donors scheduled for multiple organ procurement. Chest X-ray was considered normal in 37 donors (51%), and PaO2 was > 400 mm Hg with an FIO2 of 100% in 34 donors (47%). Fiberoptic bronchoscopy was normal in only 24 donors (33%). In the remaining 48 donors, inhalation of gastric contents (n = 26) or blood (n = 17), pulmonary contusion (n = 5), or purulent bronchial secretions (n = 4) were noted. In the 26 donors with normal chest X-ray and PaO2 > 400 mm Hg with FIO2 of 100%, bronchoscopy was abnormal in 10 donors (38%). In 33 donors, arteriovenous difference in oxygen content (2.4 +/- 0.8 ml O2/100 ml), and pulmonary shunt (0.30 +/- 0.11, range 0.13-0.49) were measured. In the 15 donors with PaO2 > 400 mm Hg, pulmonary shunt was 0.23 +/- 0.07 (range 0.13-0.35). Our study suggests that chest X-ray and arterial blood gas analysis are not sufficient, and that fiberoptic bronchoscopy should be routinely performed to select potential lung donors. Even in brain-dead donors, only the measurement of pulmonary shunt can precisely assess pulmonary gas exchange.

Changes in hepatic flow induced by continuous positive pressure ventilation in critically ill patients.

To quantify the influence of continuous positive pressure ventilation (CPPV) on hepatic plasma flow (HPF) in 8 critically ill patients submitted to controlled ventilation, we measured simultaneously HPF by the indocyanine green dye (IGD) clearance and cardiac output (CO) by the thermodilution technique, while increasing PEEP from 0--20 cm H2O. CPPV induced a significant decrease in HPF which was related to the level of PEEP. A linear correlation was documented between HPF and CO; HPF remained a constant fraction of CO during CPPV. These results suggest that the decrease in CO is the most likely mechanism of the fall in HPF during CPPV.

Hemodynamic and metabolic effects of morphine in the critically ill.

To assess the effects of i.v. injection of morphine, 0.5 mg/kg, hemodynamic studies were performed on 24 critically ill patients under controlled ventilation. An esophageal balloon was used to estimate intrapleural pressure and transmural cardiac filling pressures were calculated. After injection of morphine, there were significant decreases in heart rate (13%), cardiac index (18%), stroke index (17%) and arterial pressure (15%) and there was a nonsignificant increase in esophageal pressure (15%). Transmural cardiac filling pressures decreased significantly (21% for the pulmonary wedge pressure); intravascular filling pressures were unchanged. Oxygen consumption decreased significantly, by 21%, in 10 patients with initially elevated oxygen consumption and by 9% in 14 patients with initially normal oxygen consumption. The oxygen extraction ratio was unchanged, suggesting that the decrease in oxygen consumption was caused by decreased oxygen demand rather than by inadequate oxygen delivery. These results indicate that the hemodynamic effects of morphine (0.5 mg/kg) administered to critically ill patients were associated with a significant decrease in oxygen consumption, which probably reflected sedation and analgesia.

Cardiovascular response to the i.v. administration of morphine in critically ill patients undergoing IPPV.

The haemodynamic changes following the administration of morphine 0.15 and 0.30 mg kg-1 i.v. were studied in 11 patients, free from known cardiac disease. All patients were acutely ill and their lungs were being ventilated mechanically. In those patients receiving 0.15 mg kg-1, the only haemodynamic change was a slight and transitory decrease in the systolic arterial pressure. In contrast, several changes were observed in patients receiving 0.30 mg kg-1: an immediate and prolonged decrease in the cardiac index was noted along with transient decreases in heart rate, stroke volume index, arterial pressure and left stroke work index. These results suggest that the haemodynamic cost of morphine 10 mg is negligible but could be significant when 20 mg has been administered and must be weighed against its beneficial effects in the critically ill patient.