Surgical treatment of long-segment tracheal anomalies in infants and children.

BACKGROUND: Tracheal stenosis in combination with vascular and/or cardiac anomalies is a life-threatening condition in infants and children presenting with severe symptoms of airway obstruction. The optimal surgical treatment of these cases remains controversial. OBJECTIVES: We present here a group of infants and children with combined tracheal malformations and vascular and/or cardiac anomalies. More than 30 % of the stenotic trachea was resected in a subgroup of the patients. A reconstruction with end-to-end anastomosis was achieved on the basis of extensive mobilization of the whole tracheobronchial tree and use of CPB. METHODS: The clinical outcome in 37 children with a median age of 8 (1 - 72) months was analyzed retrospectively. The patients presented with severe airway obstruction in combination with congenital heart defects and/or vascular anomalies. Cardiac catheterization, bronchoscopy and thoracic computer tomography were performed prior to operation. The operations were performed under CPB and consisted of tracheal resection with end-to-end anastomosis or external stabilization. Associated intracardiac and vascular anomalies were repaired simultaneously. RESULTS: All but 1 patient survived and had a straightforward recovery. The patients were extubated under bronchoscopic control with a median intubation time after airway repair of 12.2 days. The average follow-up was 8.4 years (1 - 14 years) and the surviving patients did not show signs of restenosis clinically. A segment longer than 30 % of the tracheal length was resected and reconstructed with end-to-end anastomosis in 57 % of the patients (12 of 21 patients). CONCLUSIONS: Our experience demonstrates that resection of tracheal stenosis and end-to-end anastomosis can be achieved successfully even in cases with stenosis of more than 30 % of the total tracheal length. The use of CBP allowed extensive mobilization of the tracheobronchial tree and resection with end-to-end tension-free anastomotic reconstruction.

Coronary fistula of right coronary artery to vena cava superior and ectasia of pulmonary artery.

We report on a patient with coronary heart disease, a coronary fistula of right coronary artery to vena cava superior and pulmonary hypertension. Combined with coronary artery revascularization, the coronary fistula was closed successfully.

Long-term results after repair of truncus arteriosus communis in neonates and infants.

BACKGROUND: We reviewed our experience of truncus arteriosus communis (TAC) repair. METHODS: Between 05/90 and 10/01, 16 patients underwent complete repair of TAC (primary repair: group I, 12 patients, secondary repair: group II, 4 patients). Age was 2.4 months [5 days-8.8 months] (median [range]) in group I, and 8.3 [5.6-13.5] years in group II. Continuity from the right ventricle to the pulmonary artery was achieved using a valved conduit. All patients had regular follow-up examinations. RESULTS: There was one early death in each group (12.5%). Follow-up was 9 [1.2-12.7] years. Valved conduit failure occurred in 8 patients (67 %) in group I (group II, 1 patient, 33 %) requiring replacement at 2.5 [0.3-4.3] years (group II, 5.8 years). Severe neo-aortic valve regurgitation after truncal valve repair was observed in one patient, requiring valve replacement at 8.5 years in association with repeat homograft replacement (group I). Actual echocardiographic examination revealed normal ventricular function. Moderate conduit dysfunction was noted in 2 patients (group I). CONCLUSIONS: Complete repair of truncus arteriosus communis can be performed with excellent long-term results.

The index of pulmonary vascular disease in children with congenital heart disease: relationship to clinical and haemodynamic findings.

OBJECTIVE: We asked whether a scoring system [index of pulmonary vascular disease (IPVD)] that quantifies the individual pulmonary vascular pathology would relate to postoperative survival in patients with congenital heart disease and pulmonary hypertension (PH). METHODS: Lung biopsy specimens from 28 patients at a median age of 6 months (1 month to 21 years) were analysed qualitatively and morphometrically. The IPVD and other morphometric parameters were related to haemodynamic findings and survival. RESULTS: Mean pulmonary artery pressure (PAP) was 44 mmHg (15-72 mmHg), and the resistance to pulmonary perfusion was 5 U x m(2) (0.9-14 U x m(2)). There were three early (in-hospital) and three late deaths during the follow-up period of 2.5 years (6 months to 7 years). Incipient plexiform lesions were observed in one infant with trisomy 21 and complete atrioventricular septal defect (cAVSD). An IPVD score above the upper critical limit (>2.2) was not observed during the first year of life. On discriminant analysis, morphometric parameters could not predict mortality ( P=0.08). CONCLUSIONS: The IPVD is not helpful to predict surgical mortality during the first year of life. Patients with trisomy 21 and cAVSD may show advanced pulmonary vascular disease in infancy.

Downregulation of myocardial contractility via intact ventriculo--arterial coupling in the brain dead organ donor.

OBJECTIVE: To test the hypothesis that altered loading conditions play a key role in hemodynamic instability and cardiac dysfunction in the brain dead (BD) organ donor. METHODS: BD was induced by inflation of a subdural balloon catheter. In the first part of the study, left ventricular function was assessed in a canine in situ cross-circulated heart model (n=6). Pre- and afterload and coronary perfusion pressure were kept identical in all hearts throughout the experiment. In the second part of the study, hearts (n=6) were investigated in vivo allowing the interaction between left ventricular contractility and arterial load. Left ventricular pressure--volume loops were obtained by a combined conductance-pressure catheter and the slope of the endsystolic pressure--volume relationship (Ees), arterial elastance (Ea), stroke work (SW), pressure--volume area, ventriculo--arterial coupling ratio (VAC) and mechanical efficiency (Eff) were calculated. RESULTS: Induction of BD led to a hyperdynamic response in both models with a significant increase of most hemodynamic parameters. In the in situ isolated heart model, left ventricular contractility returned to baseline without any further deterioration. In contrast, in the intact circulation the hemodynamic parameters declined significantly in comparison to baseline 4 h after BD (Ees: 4.07+/-0.51 vs. 8.06+/-1.09 mmHg/ml, P<0.05, Ea: 3.17+/-0.39 vs. 4.42+/-0.30 mmHg/ml, P<0.05). However, VAC (0.78+/-0.09 vs. 0.65+/-0.14 n.s.) and Eff (73.4+/-2.1 % vs. 76.8+/-3.7 %, n.s.) remained constant over the time. CONCLUSION: BD induction leads to an initial hyperdynamic reaction followed by hemodynamic instability. The facts that no cardiac dysfunction occurred if loading conditions were kept constant and the ventriculo--arterial coupling ratio and mechanical efficiency remained constant in the intact animal model indicate that decreased contractility reflects to decreased arterial elastance after brain death. Therefore, reduced contractile function after brain death at a decreased afterload may contribute to stroke work optimization.

Role of neural and humoral factors in hyperdynamic reaction and cardiac dysfunction following brain death.

BACKGROUND: Although hemodynamic instability and cardiac dysfunction after brain death are reported in the potential organ donor, the underlying mechanisms, for example, neurohumoral changes, myocardial injury, and altered loading conditions, have not been differentiated in clinical and experimental settings. In the present study, we performed a load-independent analysis of cardiac function, focusing on the influence of brain death-associated neural and humoral factors. METHODS: In a canine in situ cross-circulated heart model, brain death was induced by inflation of a subdural balloon catheter. Preload, afterload, and coronary perfusion pressure were kept identical in all hearts throughout the experiment. In Group H (humoral factors), the hearts of healthy dogs were perfused with blood from brain-dead support dogs (n = 6). In Group N (neural factors), the hearts of brain-dead dogs were perfused with blood from healthy support dogs (n = 6). In Group H + N (humoral and neural factors), the hearts of brain-dead dogs were perfused parabiotically in situ with the animals' own blood (n = 6). Systolic and diastolic pressure-volume relationships and coronary blood flow were measured. RESULTS: Induction of brain death led to a significant hyperdynamic response in all groups, with a maximal reaction in Group H + N followed by Group H and Group N. After the initial hyperdynamic phase, cardiac function returned to baseline within 15 minutes and remained stable in all groups for the 2-hour observation period. CONCLUSIONS: (1) Both neural and humoral factors contribute to the initial hyperdynamic reaction after brain death, and only in combination do they cause a maximal hemodynamic effect. (2) If loading conditions and perfusion pressure are kept constant, no cardiac dysfunction occurs after brain death. This indicates that poor cardiac function in the potential donor may reflect altered loading conditions and impaired coronary perfusion rather than neurohumorally mediated direct myocardial injury.

Vascular tracheobronchial compression syndromes-- experience in surgical treatment and literature review.

Between January 1988 and December 1997 a total of 22 patients (age: 8 days-46 years) were operated for vascular airway compression syndromes with respiratory insufficiency. Vascular anomalies in tracheal compression were double aortic arch in 7 patients, (2 previously operated elsewhere), right aortic arch + left ligamentum arteriosum in 1, and pulmonary artery sling in 3. Three of these patients had secondary long-segment tracheomalacia. Compression of trachea and a main bronchus existed in 2 patients with right aortic arch + left ligamentum. Isolated main bronchus obstruction was present in 9 patients (abnormal insertion of ligamentum arteriosum in 1, status post (s.p.) previous operation for PDA in 4, s. p. surgery for coarctation in 1, right aortic arch + left ligamentum arteriosum in 2, and right lung aplasia + left ligamentum in 1). 3 of these cases had secondary long-segment bronchomalacia. All patients had a complex respiratory anamnesis [long-term intubation in 7, s.p. tracheostomy in 2 (over 3 months - 3 years), and progressive respiratory insufficiency in 13). In tracheal compression, surgical correction included transsection of the underlying ring or sling components (with additional anterior aortic arch translocation in 5 patients resection-reimplantation of left pulmonary artery in 3, segmental tracheal resection in 1, and external tracheal suspension in 2). In the 2 cases with compression of the trachea and a main bronchus, aortic "extension" by a prosthetic tube was necessary. In isolated main bronchus obstruction, surgical decompression basically consisted of transsection of the ligamentum arteriosum or resection of its scarry remnant forming the "corner point" of a compression between aorta and pulmonary artery. In 3 patients with secondary long-segment malacia, additional external bronchus suspension was performed. Effective decompression and re-expansion of the airway segment concerned was achieved, and was demonstrated by intraoperative endoscopy in all patients. There were 3 postoperative deaths (sepsis 2; massive, irreversible edema of the tracheal mucosa 1). Of the 19 surviving patients 16 could be extubated between the 1st and 17th (mean = 7.5) postoperative day. In 1 case the preoperative long-term tracheostomy had to be left in place for inoperable additional laryngeal stricture. 2 patients had to be reoperated (segmental cervical tracheal resection after 5 months for primary long-term intubation-related subglottic stenosis in 1, esophageal decompression for residual dysphagia after 57 months related to a traction phenomenon at the right descending aorta in the other), both with gratifying results. In all other patients clinical, endoscopic, and radiographic examinations (follow-up = 2 months - 6 years) demonstrate good results.

Myocardial performance after brain death: studies in isolated hearts.

OBJECTIVES AND METHODS: Brain death related hemodynamic instability and/or cardiac dysfunction is frequently described in the potential organ donor which may lead to exclusion of the heart from transplantation. The underlying mechanisms are controversely discussed. Therefore, in the present study, potential brain death associated cardiodepressant factors were evaluated separately in cross-circulated canine heart models. Brain death was induced by inflation of a subdural balloon catheter. Loading conditions and coronary perfusion pressure were kept identical in all cross-circulated hearts throughout the experiment. RESULTS: Induction of brain death led to a significant hyperdynamic response in all groups, with a maximal effect by the combination of neural and humoral pathways. After the initial reaction all hemodynamic parameters returned to baseline and remained stable until the end of experiments. Even if the hearts were explanted from brain dead donors with typical hemodynamic deterioration in vivo, they showed no significant differences in comparison to the other groups including healthy controls ex vivo. CONCLUSIONS: Therefore we conclude, that hemodynamic instability in the potential donor may rather reflect altered loading conditions and impaired coronary perfusion than neuro-humorally mediated direct myocardial injury.

Modulation of coronary perfusion pressure can reverse cardiac dysfunction after brain death.

BACKGROUND: Brain death results in a rapid decline in left ventricular function, which has clinical relevance for organ transplantation. The aim of the present study was to investigate coronary perfusion changes during brain death and their role in cardiac dysfunction. METHODS: In an in situ isolated canine heart model, brain death was induced by inflation of a subdural balloon catheter. The heart was perfused separately with the animal's own blood by a pressure-controlled roller pump that was coupled to the measured aortic pressure. Myocardial contractility was estimated by the slope of the end-systolic pressure-volume relation. RESULTS: Induction of brain death resulted in a transient hyperdynamic response, followed by a significant decrease in systemic vascular resistance, coronary blood flow, and the end-systolic pressure-volume relation (p<0.05). However, if coronary perfusion pressure was decoupled from aortic pressure and elevated to pre-brain death levels, coronary blood flow and the end-systolic pressure-volume relation were also restored to baseline levels. CONCLUSION: Severe impairment of coronary blood flow may contribute to decreased contractility after brain death that can be reversed by modulation of coronary perfusion pressure.

Influence of brain death and cardiac preservation on systolic and diastolic function and coronary circulation in the cross-circulated canine heart.

Previous studies have demonstrated hemodynamic instability and cardiac dysfunction in the brain-dead organ donor. It remains unclear if primary cardiac dysfunction is responsible for hemodynamic deterioration or decreased cardiac function is secondary to brain death-associated altered loading conditions. Therefore in the present study the effects of brain death on hemodynamics and cardiac function were analyzed in vivo in an open chest model and ex vivo in a cross-circulated heart preparation. In a second protocol, the impact of brain death-associated hemodynamic changes on postischemic graft function was investigated. Brain death was induced injecting saline in a subdural Foley catheter. Induction of brain death led to a hyperdynamic reaction followed by hemodynamic deterioration with a decrease of systemic vascular resistance and myocardial contractility. If the hearts were explanted and assessed ex vivo, no differences were found between control and brain-dead hearts. Furthermore, both control and brain-dead hearts showed full functional recovery after 4 hours of hypothermic ischemic storage. Despite hemodynamic deterioration in situ after brain death, there were no differences between the postischemic function of control and brain-dead hearts. These results indicate that myocardial dysfunction is not irreversible and may be secondary to altered loading conditions, and that the recovery of cardiac function after long-term hypothermic storage is not impaired by the hemodynamic changes observed in situ after brain death induction. These data may also indicate that potential donor hearts might not be excluded from transplantation on the basis of impaired hemodynamic characteristics, especially if they are evaluated by load-dependent parameters.

Effects of brain death on myocardial function and ischemic tolerance of potential donor hearts.

BACKGROUND: An increasing number of experimental and clinical studies reports hemodynamic instability in the donor organism after brain death. However, the relative importance of brain death-related cardiac dysfunction on posttransplantation cardiac function and the reversibility of the observed changes remain controversial. In this study a load-independent analysis of cardiac function after brain death was performed. Special interest was focused on a possible interactive influence of brain death and cardiac preservation on postischemic cardiac function. METHODS: In 12 anesthetized dogs, brain death was induced by inflation of a subdural balloon; 12 sham-operated animals served as control subjects. After a 2-hour observation in situ, the hearts were explanted and perfused parabiotically either immediately or after hypothermic ischemic preservation (4 hours, 4 degrees C). Heart rate, cardiac output, left ventricular pressure, the maximum of left ventricular pressure development and aortic pressure were measured in situ. In addition, the slope of the end-systolic pressure-volume relationship, coronary blood flow, and myocardial oxygen consumption were estimated in the cross-circulated hearts. RESULTS: In spite of a brain death-associated hemodynamic deterioration in situ (expressed as low mean aortic pressure and significant decrease of maximal dP/dt), myocardial function was similar to control after explantation, if assessed ex vivo. Furthermore, after hypothermic ischemic preservation and reperfusion, complete functional recovery of control and brain-dead hearts could be observed. CONCLUSIONS: These data indicate that hemodynamic instability after brain death may rather reflect altered loading conditions than irreversible myocardial damage or primary cardiac dysfunction. Furthermore, there is no evidence for a brain death-related impairment of ischemic tolerance.

Right ventricular function after brain death: response to an increased afterload.

OBJECTIVE: A major cause of early postoperative morbidity and mortality after cardiac transplantation is right ventricular (RV) failure which is attributed to the inability of the donor's RV to acutely compensate for the recipient's elevated pulmonary vascular resistance. This study was performed to determine: (1) the acute effects of brain death on the RV function; and (2) the adaptation potential of the RV to a progressive increase in RV afterload. METHODS: In 13 anesthetized, open-chest dogs (eight with brain death vs. five control with sham operation), brain death was induced by inflation of a subdural balloon catheter. Heart rate, RV systolic and end-diastolic pressure (RVSP, RVEDP), pulmonary arterial pressure (PAP), and cardiac output (CO), and pressure-length loops (sonomicrometry) were recorded. Afterload increase was induced 2 h after brain death induction by constriction of the pulmonary artery with an increase in RVP from 25 to 50 mmHg in 5 mmHg steps. RESULTS: Cushing phenomenon occurred within a few minutes after brain death induction, with a significant increase of HR (229 +/- 10 vs. 89 +/- 6 min(-1), P < 0.001), CO (3.2 +/- 0.2 vs. 1.7 +/- 0.1 l/min, P < 0.001), PAP (30.4 +/- 2.5 vs. 15.5 +/- 1.3 mmHg, P < 0.01) RVSP (55 +/- 5 vs. 23 +/- 2 mmHg, P < 0.001) and RVEDP (7.4 +/- 0.9 vs. 3.3 +/- 0.6 mmHg, P < 0.001). All these values were also significantly (P < 0.01) higher than the time corresponding values of the control group. The analysis of the pressure-length loops showed a hypercontractile state. Within 15-60 min, all parameters turned to baseline and remained stable for up to 2 h. When afterload was increased progressively, RVEDP increased markedly in the brain death and slightly in the control group (9.4 +/- 0.7 vs. 4.2 +/- 1.1 mmHg, P < 0.01, at RVSP = 50 mmHg). On the other hand, the increase of peak positive dP/dt was significantly higher in the control group (430 +/- 37 vs. 644 +/- 55 mmHg/s, P < 0.01, at RVP = 50 mmHg). However, global RV pump function characterized by CO and stroke work was similar in both groups. While regional RV contractility remained unchanged in the brain death group in terms of pressure-length relationships, RV contractility significantly increased in the control group. CONCLUSION: (1) Brain death per se does not result in an acute impairment of RV function. (2) While control animals adapt to an increased afterload by the homeometric, as well as the heterometric regulation, after brain death, an increase in RV preload follows elevations in RV afterload by the Frank-Starling mechanism subserving the increased stroke work required to ensure unchanged pump function.

The role of coronary perfusion changes in cardiac dysfunction associated with brain death.

BACKGROUND: Previous studies described a hemodynamic instability in the potential organ donor which has clinical relevance for cardiac transplantation. The possible pathophysiological link between altered loading conditions, coronary perfusion, and cardiac function after brain death has not been investigated yet. Therefore this study was undertaken to investigate the role of coronary perfusion changes during brain death in cardiac dysfunction. METHODS: Dogs on cardiopulmonary bypass provided iso-volumetric left-ventricular (LV) contractions. By protocol, coronary perfusion pressure was kept at the level of mean aortic pressure. LV pressure, LV dP/dt, the slope of end-systolic pressure-volume relationship (Emax), coronary blood flow (CBF), and myocardial oxygen consumption (MVO2) were measured. Brain death was induced by a subdurally placed balloon-catheter. RESULTS: Induction of brain death led to a transient hyperdynamic response with a significant increase of aortic and LV pressure, dP/dt, Emax, CBF, and MVO2. Thereafter, aortic pressure and, parallelly, LV pressure, dP/dt, Emax, CBF, and MVO2 decreased significantly. However, if coronary perfusion pressure was decoupled from aortic pressure and elevated to pre-brain death level, CBF and myocardial contractility were restored to baseline level. CONCLUSION: The impairment of coronary blood flow may contribute to decreased contractility after brain death.

External stabilization of long-segment tracheobronchomalacia guided by intraoperative bronchoscopy.

BACKGROUND: Symptomatic obstruction of long-segment tracheal or bronchial portions either related to congenital instability or secondary to vascular compression are rare malformations, which remain difficult to manage. A method of external tracheal or bronchial stabilization is described. METHODS: From July 1992 to April 1995, 7 children (age range, 4 months to 4 years; mean age, 19 months) and 1 adult (age, 46 years) were operated on for severe respiratory insufficiency. In 4 cases of congenital tracheal instability, 2 children had associated type IIIb esophageal atresia. Both children with esophageal atresia had previous operations (two and three times, respectively): 1 child had aortopexy and division of a patent ductus arteriosus and another child had distal tracheal resection elsewhere, both without relief of malacia. All children were intubated and ventilated since birth for 11 to 15 months. Secondary tracheobronchomalacia due to vascular compression was seen in 4 patients caused by double aortic arch (n = 2) and persisting ligamentum arteriosum after previous ligation of a patent ductus arteriosus (n = 2), with 1 child ventilated thereafter for 5 months. Operation was performed with the aid of extracorporeal circulation in all patients but 1, and consisted of transection of vascular rings and persistent ligamentum Botalli (n = 5), closure of multiple ventricular septal defects (n = 1) and extensive mobilization of the tracheobronchial tree as well as the great arteries. External stabilization of the severely dysplastic distal trachea (n = 6) or left main bronchus (n = 2) was achieved by suspending the malacic segment within an oversized and longitudinally opened ring-reinforced polytetrafluoroethylene prosthesis. Multiple plegeted sutures were placed extramucosally to the dysplastic tracheal wall and the dyskinetic pars membranacea, as well as to the polytetrafluoroethylene prosthesis in a radial orientation. Guided by simultaneous video-assisted bronchoscopy, reexpansion of the collapsed segments was achieved by gentle traction on the sutures while tying. RESULTS: Stenosis-free tracheobronchial reexpansion was achieved in all patients, as seen on repeated bronchoscopies during hospitalization and thereafter. All patients were extubated within 1 to 12 days after the operation. There was one late death, unrelated to the procedure, in a 31-month-old child 20 months after the operation. All other patients are free of stridor and in excellent clinical condition 21 to 54 months (mean, 38 months) thereafter. CONCLUSIONS: The presented method of bronchoscopically guided external tracheobronchial suspension within a ring-reinforced polytetrafluoroethylene prosthesis immediately relieves severe malacia of the trachea or main bronchi in infants as well as adults without necessitating resection. Midterm preliminary data suggest that growth potential of the affected segment exists within the oversized polytetrafluoroethylene prosthesis.

Is the brain death related endocrine dysfunction an indication for hormonal substitution therapy in the early period ?

Experimental studies in animals have suggested that brain death (BD) -- related endocrinological dysregulations lead to a significant depression of cardiac pump and muscle function, however, the discussion about the relative extent of this influence remains controversal. The aim of the present study was to assess in an open chest animal model the short time course (5 hours) of hormonal (epinephrine, norepinephrine, T3, T4, ACTH, cortisol, insuline) and metabolic (glucose, lactate) changes in 10 brain dead dogs with special respect to the hemodynamic stability and myocardial pump function. After the onset of BD the concentrations of all hormonal parameters showed a significant decrease. Despite these changes, and in contrast to other studies, an adequate pump function (filling pressures, cardiac output) and muscle function (LVdp/dt) could be maintained by exclusive volume substitution without the use of hormonal or pressor agents. We conclude that in the present model a sufficient pump and muscle function can be maintained by adequate volume substitution, exclusively. The significant fall in adrenal and thyroid hormones had no direct effects on heart functional parameters in the first 5 hours after experimental BD induction.

Cardiocirculatory effects of acutely increased intracranial pressure and subsequent brain death.

Hemodynamic instability and functional impairment of the donor heart are currently reported problems in organ transplantation. Actual shortage of potential donor hearts continues to raise controversial discussion about adequate donor management with regard to graft quality. In an experimental open chest model, physiopathologic effects of acutely induced, irreversible intracranial hypertension (AIIHT) were investigated in situ with respect to hemodynamics, cardiac pump and muscle function, and hormonal parameters. Acutely induced irreversible intracranial hypertension was induced by rapid inflation of a subdural balloon catheter in 10 anesthetized dogs, four animals serving as controls. The observation period in both groups was 300 min. Cardiocirculatory stability was maintained by continuous crystalloid volume substitution without the use of inotropic or pressor agents. After AIIHT, three characteristic hemodynamic response phases have been observed: 1) The "acute hyperdynamic phase" lasting up to 15 min with marked increases of heart rate (HR), left ventricular pressure (LVP), cardiac output (CO) and myocardial contractility indices, 2) At the end of the "early restabilization phase", (60 min), these parameters returned close to control levels, except HR (+50%) and systemic vascular resistance (SVR) (-40%), 3) During the "late restabilization phase", filling pressures, LVP and CO remained within control limits at low SVR, contractility indices showed a decreasing tendency. All assessed plasmatic hormones (Catecholamines, triiodothyronine (T3), thyroxine (T4), adrenocorticotropic hormone (ACTH), cortisol and anti-diuretic hormone (ADH) showed a continuous fall to levels significantly below control over the phases of restabilization. Acutely induced irreversible intracranial hypertension leads to multifactorial hemodynamic and hormonal changes. At low SVR, cardiac pump function was preserved exclusively by continuous volume substitution, while myocardial contractility indicated a slight decrease. From this observed hemodynamic and functional state within the donor organism, no reliable prediction on graft functional capacity can be made.