Biomedical subjects

T Hackert

Publications and source records attributed to T Hackert.

12 recordsLinked to original sources

PubMed2006

Problems and costs associated with alcohol and drug abuse in emergency medicine.

Preclinical care refers to patients with life-threatening conditions. It remains unclear how alcohol and drug abuse contribute to the frequency and severity of emergency cases. This study evaluated the influence of these psychotropic substances on preclinical emergencies and the social security costs arising from this. The records of 400 emergency patients were analyzed prospectively regarding type and severity of emergency, intake of psychotropic substances before the emergency, and their influence on patients' outcome. Psychotropics were detected in 19% of patients; 84% of these patients (vs. 55% overall) were scored below 4 (not life threatening) on the National Advisory Committee for Aeronautics scale and therefore did not require a physician on-site. Alcohol or drug intake frequently causes emergencies with physicians on-site; retrospectively 84% of these interventions were thus found to be unnecessary, caused by difficulties in recognizing the severity of the disorder, especially in mental or respiratory disorders. Extrapolated to Germany overall this means 675,000 drug-related emergencies yearly, costing euro 310,000,000.

Alcoholism↗

PubMed2005

Platelet function in acute experimental pancreatitis induced by ischaemia-reperfusion.

BACKGROUND: Ischaemia-reperfusion (IR)-associated microcirculatory changes play a major role in acute post-transplantation pancreatitis. The pathophysiological role of platelets in these events is unknown. The aim of this study was to examine platelet adhesion and function during early reperfusion after pancreatic ischaemia. METHODS: Rats were subjected to warm pancreatic ischaemia by cross-clamping of the pancreatic vessels for 1 h. After 1 h of reperfusion, platelet-endothelium interaction was evaluated after platelet separation and staining by fluorescence microscopy. Amylase levels and pancreatic histology were evaluated 24 h after reperfusion. Animals treated according to an identical protocol, but without ischaemia, served as controls. RESULTS: Mild pancreatitis had developed by 24 h after IR; serum amylase levels were significantly higher than those in control animals. The numbers of adherent platelets in capillaries and venules were significantly increased, and platelet velocity in capillaries was significantly decreased, in the IR group compared with controls. There was significantly more oedema and inflammation in pancreatic tissue after IR. CONCLUSION: Warm ischaemia for 1 h followed by reperfusion for 24 h caused mild pancreatitis in this experimental model. The pancreatic microcirculation was characterized by pronounced platelet-endothelium interaction in capillaries and venules. These results suggest that platelet activation may play an important role in acute post-transplantation pancreatitis.

Acute Disease↗

PubMed2005

Surgery in the treatment of acute pancreatitis--open pancreatic necrosectomy.

Management of acute necrotizing pancreatitis has changed significantly over the past years. Early management is non-surgically and solely supportive. Today, more patients survive the early phase of severe pancreatitis due to improvements of intensive-care-medicine. Pancreatic infection is the major risk factor with regard to morbidity and mortality in the late phase of severe acute pancreatitis. Whereas early surgery and surgery for sterile necrosis can only be recommended in selected cases, pancreatic infection is a well accepted indication for surgical treatment. Surgery should ideally be postponed until four weeks after the onset of symptoms as necrosis is well demarcated at that time. Four surgical techniques can be performed with comparable results regarding mortality: necrosectomy combined with (1) open packing, (2) planned staged relaparotomies with repeated lavage, (3) closed continuous lavage of the retroperitoneum, and (4) closed packing. However, closed continuous lavage of the retroperitoneum, and closed packing seem to be associated with a lower morbidity compared to the other two approaches. Advances in radiologic imaging, new developments of interventional radiology and other minimal access interventions have revolutionized the management of many surgical conditions over the past decades. However, minimal invasive surgery and interventional therapy for infected necrosis should be limited to specific indications in patients who are critically ill and otherwise unfit for conventional surgery. Open surgical debridement is the "gold standard" for treatment of infected pancreatic and peripancreatic necrosis.

Debridement↗

PubMed2003

Accuracy of diagnostic laparoscopy for early diagnosis of abdominal complications after cardiac surgery.

BACKGROUND: In the early postoperative period after major cardiac surgery using extracorporal circulation, abdominal complications can have serious consequences with a mortality rate of up to 70%. Early diagnosis and the timely institution of therapy are the most important factors to improve the outcome; however, clinical evaluation of the abdomen is difficult in these patients. Diagnostic laparoscopy is a minimally invasive procedure with low procedure-associated morbidity, even in critically ill patients. The aims of our study were to investigate the safety of laparoscopy in critically ill patients suspected to have intraabdominal pathology following cardiac surgery and to evaluate the accuracy of diagnostic laparoscopy compared to laparotomy in this setting. METHODS: A total of 17 patients were included (13 male, four female, age 52-80 years) in the early (3-30 days) postoperative period after cardiac surgery using extracorporal circulation (10 ACVB, four valve replacement, one aorto-coronary-venous-bypass (ACVB)+ valve replacement, two cardiac transplantation). Clinical and laboratory findings included distended abdomen (17 of 17), elevated white blood cells (12 of 17), elevated C-reactive protein (CRP) (13 of 17), and elevated lactate levels (11 of 17). The decision to perform laparotomy was taken in all patients on the basis of their clinical condition. Diagnostic laparoscopy was always performed immediately before laparotomy. The laparoscopic findings were then compared to the laparotomy findings. RESULTS: In one patient, laparoscopy showed no abnormal findings, this was confirmed on laparotomy. Five patients were found to have massive distension of the large bowel without ischemia on both laparoscopy and laparotomy. Colonic ischemia of the right hemicolon was found laparoscopically in six patients, which was confirmed in all cases by open resection and histological workup. Three patients suffered from acute cholecystitis, which was correctly diagnosed by laparoscopy in all cases. In one patient, laparoscopy revealed fibrinous peritonitis without other findings. Open exploration failed to identify the cause of the peritonitis in this patient. Laparoscopy showed no pathological findings in one patient, but laparotomy then revealed necrotizing pancreatitis confined to the lesser sac. There was one laparoscopy-associated intraoperative complication (6%) in this series. CONCLUSIONS: Diagnostic laparoscopy is a minimally invasive procedure that can be performed at low intraoperative risk in critically ill patients and has a high sensitivity (94%) for the correct diagnosis of intraabdominal complications after major cardiac surgery. These results suggest that bedside laparoscopy should be considered for all patients with equivocal abdominal symptoms in this setting.

Aged↗

PubMed2002

Specimen retrieval in laparoscopic colon surgery.

In the past decade, for benign as well as malignant colon diseases, minimally invasive surgery has gained more and more importance in colon surgery. Specimen retrieval after colonic resections is difficult due to the large size of the specimen usually resected. To date there is no standardized retrieval technique for the different procedures. Four incision sites are common for transabdominal specimen retrieval: left or right lower quadrant transrectal portside incision; periumbilical midline incision, and transverse suprapubic incision. Perineal incisions are used for retrieval following low anterior resection or abdomino-perineal extirpation. Three major complications are described in the literature: wound infection (0-9%); hernias (0-2%), and incision site recurrence (0-1.3%). There are no significant differences between the different incision sites with regard to the occurrence of complications. In laparoscopic surgery for malignant diseases retrieval is usually performed using a plastic bag, whereas retrieval can be performed hand-assisted without a bag during surgery for benign diseases. Wound edge protectors are recommended by several authors, yet there is no standard system which is accepted broadly. In conclusion, specimen retrieval in laparoscopic colon surgery is not standardized. The morbidity rate for specific retrieval complications ranges between 0 and 9%, yet there are no randomized controlled studies or evidence-based data regarding different retrieval approaches and systems.

Colonic Diseases↗

PubMed2001

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.

Animals↗

PubMed2000

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.

Animals↗

PubMed2000

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.

Animals↗

PubMed1999

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.

Analysis of Variance↗

PubMed1999

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.

Animals↗

PubMed1998

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.

Animals↗

PubMed1998

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.

Animals↗