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Biomedical subjects

G Heberer

Publications and source records attributed to G Heberer.

At least 37 records · Page 2Linked to original sources

Prostaglandin E2 (PGE2)-dependent suppression of interleukin alpha (IL-2) production in patients with major trauma.

The depression of interleukin-2 synthesis represents a major dysfunction within the cascade of immunologic defects induced by mechanical and thermal trauma. This study was undertaken to elucidate the negative control mechanisms that were responsible for the deficiency of IL-2 production in polytraumatized patients. Peripheral blood mononuclear cells (PBMC's) from 29 patients (average age, 35.8 years; average ISS, 35) were separated on post-trauma days 1, 3, 5, 7, 10, 14, and 21 and cultured as untreated cells (C), cells treated with indomethacin (C + INDO), and cells depleted of adherent cells (C-AC). Cell cultures were assayed for proliferative responses to PHA, IL-2 synthesis, PGE2 production, gamma-interferon levels, and phenotyping studies. On all days post-trauma there was found a marked reduction of IL-2 production compared to controls with a highly significant nadir from day 5 to day 10 with an almost 80% inhibition of IL-2 (p less than 0.005). C + INDO cells showed increases of IL-2 synthesis over untreated cells ranging from 48% (Day 1) to 220% (Day 7). Removal of adherent cells (C-AC) did not reverse the suppression of IL-2 production. gamma-interferon levels were depressed in parallel with IL-2 levels but did not increase with C + INDO. The phenotyping of the PBMC's showed highly significant suppression of OKT3+, OKT4+, and IL-2R+ lymphocytes as well as a highly significant elevation of the monocyte (p less than 0.005) count. There was a highly significant increase of PGE2 synthesis from monocytes, due to the monocytosis and to a higher capacity of synthesis of the individual cells following trauma. PGE2 levels peaked on Day 5 and 7 post-trauma at 400% of control (p less than 0.005). These data suggest that the suppression of IL-2 synthesis post trauma is caused mainly by two factors: the excessive PGE2 output of inhibitory monocytes and inadequate function in immature and/or blocked lymphocytes. The partial restoration of IL-2 synthesis by indomethacin suggests that blockade of the cyclo-oxygenase pathway as an immunomodulating therapy may reverse some of the immunologic abnormalities in multiple trauma patients.

Adult

Traumatic aneurysms of the descending thoracic aorta.

From July 1979 to December 1985 we observed 51 patients with traumatic lesions of the descending thoracic aorta. Twenty-nine had acute ruptures, mostly accompanied by multiple injuries, and 27 had to be operated upon immediately. Twenty-two patients (19 males, 3 females) had chronic traumatic aneurysms of the descending thoracic aorta (more than six weeks after trauma). Mean age at the time of trauma was 24 years. Mean age at time of surgery was 36.5 years. Twelve patients were symptomatic. All were treated surgically. At surgery, complete aortic disruption was found in 15 patients and partial rupture in seven. We did not use aortic shunting of any kind, only aortic cross-clamping. Hypertension was controlled by intravenous drug infusion. The ruptured aortic segment was replaced in all cases by prosthetic Dacron graft. There were no operative deaths. One patient (age 77) died 11 weeks after surgery from multiple organ failure. One case of postoperative paraplegia was observed. This patient recovered almost completely from his neurological deficit.

Adult

[Results of repair and direct reconstructive procedures of the sphincter system].

Direct sphincter repair gives good surgical results. In 8 out of 10 patients operated on, incontinence was clearly improved. In 15 patients posterior repair was performed simultaneously with posterior rectosigmoidal resection because of rectal prolapse. 14 patients had been incontinent. Incontinence was improved clearly in 7 patients, remained unchanged in 4 and worsened in 3. However, the good clinical results did not correspond completely to those achieved by perfusion manometry.

Anal Canal

Altered hormonal activity in severely ill patients after injury or sepsis.

We studied the hormonal millieu and possibility of altered thyroid function in 25 patients in a surgical intensive care unit (ICU) who had severe life-threatening illnesses. Sixteen patients had septic complications and nine patients had multiple-system injuries. On admission to the ICU, serial measurements were begun of thyroxine (T4), triiodothyronine (T3), T4-binding globulin, thyrotropin (thyroid-stimulating hormone [TSH]), corticotropin (adrenocorticotropic hormone [ACTH]), cortisol, prolactin, human growth hormone, catecholamine, insulin and glucose, lactate, retinol-binding protein, prealbumin, and transferrin levels. All patients initially had low normal levels of T4 (4.5 +/- 2 micrograms/dL) and T3 (55 +/- 26 ng/dL), with normal TSH levels (2.3 +/- 2.3 microU/mL) (the "low T3 syndrome"). The 11 surviving patients had their levels increase to normal before leaving the ICU (T4, 7.0 +/- 2.1 micrograms/dL; T3, 110 +/- 48 ng/dL; and TSH, no change). The 14 patients who died showed further decreases before death (T4, 2.6 +/- 2.1 micrograms/dL; T3, 30.6 +/- 23.5 ng/dL; and TSH, 0.9 +/- 0.7 microU/mL). The corticotropin, cortisol, prolactin, and growth hormone levels were normal throughout the study. Catecholamine levels were high initially and decreased in surviving patients. Epinephrine levels increased greatly in nonsurvivors before death, and the norepinephrine-epinephrine ratio decreased from 5.7:1 to 2:1. After protirelin (thyroid-releasing hormone [TRH]) stimulation, the TSH level increased either minimally or not at all in six patients who eventually died. This indicates hypothalamic-pituitary dysregulation or suppression, and altered release and/or peripheral metabolism of T4. Whether this represents a deficiency of thyroid hormone for cell and organ function remains to be established.

Adolescent

[Surgery].

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Female

Multiple organ failure in polytrauma patients.

To determine limitations in survival and problems of single and multiple organ failure (SOF, MOF) following trauma in Bavaria, we reviewed 433 consecutive patients with multiple injuries treated at the Klinikum Grosshadern from 1978 through 1982. Most patients were young and were injured in traffic accidents. The overall mortality was 18% (78 deaths): 38 deaths were due to CNS injuries (49%), six from miscellaneous causes (7%), 15 associated with SOF (19%), and 19 associated with MOF (25%). There were 50 patients with SOF and 34 with MOF. Two MOF patterns were found: a rapid single-phase (15 patients) due to trauma and shock; and a delayed two-phase MOF (19 patients) due to trauma, shock, and sepsis. Mortality for the MOF group was 56%. The lung was the predominant organ to fail represented in all SOF and MOF cases. Cimetidine and pirenzipin prevented stress bleeding in all but four patients. Significant factors leading to MOF were shock, massive blood transfusions, sepsis, and errors in treatment. The temporal sequence of organ failure was lung, clotting system, kidney, and liver. Sepsis was ultimately the cause of death in eight MOF patients (42%). Earlier pulmonary and cardiovascular support beginning at the scene of the accident, and prevention and better treatment of head injury, respiratory failure, and sepsis are critical factors for increasing survival after injury.

Abdominal Injuries