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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eight patients admitted to a University hospital with acute surgical problems and related adrenal insufficiency were reviewed and three are presented in detail. Surgical stress and continued sepsis played major roles in the lack of responsiveness to usual modes of therapy until the adrenal insufficiency was corrected. The patients fell into three major clinical categories of adrenal insufficiency. Chronic illness and sepsis are shown to affect steroid production and metabolism, as well as adrenal responsiveness to ACTH. Pharmacologic amounts of steroids are often needed in patients with shock, gram negative sepsis and prolonged illnesses, even if normal or elevated serum cortisols are present. Therapeutic trials of cortisol administration are shown to be confusing when not accompanied by easily performed diagnostic tests of adrenal function. It is emphasized that a pretreatment serum cortisol should be obtained whenever possible. The evaluation of adrenal function is of lifelong importance to the patient.
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PMID:Occult adrenal insufficiency in surgical patients. 16 92

Bilateral adrenal gland hemorrhage was found in 22 of 2,000 (1.1%) consecutive general hospital autopsies. Clinical features of these 22 patients with diffuse or focal bilateral adrenal hemorrhage have been analyzed and compared with previous series. In our experience, patients with this postmortem finding rarely manifest features of adrenocortical insufficiency and appear instead to die as a consequence of concomitant overwhelming illness, such as septicemia, body surface burns or cardiovascular catastrophe. Two-thirds of the current series had impaired renal function at the time of adrenal hemorrhage and three patients had pituitary gland necrosis. Experimental and clinical observations indicate that the "stressed" adrenal gland--under substantive endogenous or exogenous ACTH stimulation--is unusually susceptible to hemorrhage. While our own experience indicates that bilateral adrenal hemorrhage can infrequently be implicated as a factor contributing to patients' death, the possibility of adrenocortical insufficiency must be considered in patients at risk for adrenal hemorrhage. Such patients are those who are azotemic and have bacteremia, burns, or recent cardiovascular catastrophe, particularly when the latter is managed with anticoagulant administration. In these patients, unexplained clinical deterioration or the appearance of findings consistent with adrenocortical insufficiency mandate measurement of serum cortisol concentration and institution of stress-level corticosteroid replacement therapy until a diagnosis of acute adrenocortical insufficiency can be established or refuted.
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PMID:Adrenal hemorrhage in the adult. 20 58

Delay in healing of the perineal wound is a major cause of disability in patients after excision of the rectum. The outcome of primary suture in 76 patients treated at St Mark's Hospital between 1967 and 1976 was correlated with a number of factors describing the patients, their preparation for surgery and details of surgical technique and management. The perineal wound healed by first intention in 33 patients. The remaining 43 patients regarded as failures included 7 with delayed breakdown after initial healing. The results showed that women fared better than men. Excision of the rectum following colectomy and ileostomy was associated with failure of the perineal wound to heal in 9 out of 10 patients. Treatments with peroperative ampicillin and topical antibacterial agents were both correlated significantly with success. Preoperative sepsis and operative contamination were followed by perineal sepsis and wound breakdown on 16 out of 21 occasions. Discriminant analysis showed that topical and peroperative antibacterial treatments, sex, preoperative sepsis and finally ACTH were the most important variables in descending order of importance. The prediction of success and failure by this procedure was 72.4 per cent correct.
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PMID:Primary suture of the perineal wound following rectal excision for inflammatory bowel disease. 35 37

Cushing's syndrome may be caused by pituitary ACTH, ectopically produced ACTH, adrenocortical tumor or medication. Cushing's disease, due to excessive pituitary ACTH resulting in adrenocortical hyperplasia, remains a complex endocrine disorder for which no single treatment is wholly satisfactory. Twenty-two patients with surgically treated Cushing's syndrome are presented: Four with benign adrenocortical adenoma, two with adrenocortical carcinoma and 16 with adrenocortical hyperplasia. The four benign adenomas were excised with the one death due to respiratory failure and sepsis. Both patients with carcinoma and liver metastases died of their tumors. Of the 16 patients with adrenocortical hyperplasia and Cushing's disease, eight underwent subtotal adrenalectomy and thereafter eight had total intra-abdominal adrenalectomy with autotransplantation of adrenal tissue to the thigh. There was one operative death. Total adrenalectomy has now replaced subtotal resection in most clinics. All eight of the patients who had adrenal autotransplantation exhibited biopsy or functional evidence of some degree of graft survival. On patient stopped steroid replacement permanently and another developed recurrent Cushing's syndrome from the grafts. Of a total of 26 reported patients with adrenal autotransplants surveyed, 22 exhibited evidence of graft survival, 16 were able to discontinue steroid replacement therapy and three eventually developed recurrent Cushing's syndrome from the transplants. There is now strong evidence that most patients with Cushing's disease harbor a pituitary basophil ademona, and in the future the initial surgical attack may be directed to the pituitary rather than to the adrenals.
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PMID:Surgical management of Cushing's syndrome with emphasis on adrenal autotransplantation. 68 95

Hypoglycemia (h.) in the postneonatal period was predominantly observed in male infants and children. The incidence was 0,51/1000 hospitalizations. The majority of cases was found in the agegroup around 2 years. Concomitant diseases (mostly infections of the upper respiratory tract or gastrointestinal tract) were found in 30 out of 43 hospitalizations. Convulsions and coma were the most frequent symptoms which were found in 43%. In 30% some degree of somnolence was obvious. Hypoglycemia was not considered in the differential diagnosis in any case by the physician treating first. Only 7 out of 34 cases a complicated biochemical work up resulted in an etiological diagnosis: one leucininduced h.; one ketotic h,; one h. in dystrophy and bronchopneumonia with septicemia; one h. in meningococcic septicemia; one h. in adrenal insufficiency; one h. in isolated ACTH-deficiency; one ethyl-induced h.; one h. in polynesy of pancreas; one h. in insulinoma; one h. in diabetes mellitus under insulintherapy.
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PMID:[On the syndrome of childhood-hypoglycemia. II. Hypoglycemia in the postneonatal period (author's transl)]. 89 35

The effects of cyclosporine administration on the adrenocortical response to the severe stress of burn wound sepsis were studied in Wistar rats. Animals were treated with cyclosporine (10 mg/kg/day) or saline by gavage for 10 days, then subjected to 30% scald burns with wound inoculation with Pseudomonas. Animals were sacrificed on Postburn Days (PBDs) 1, 4, and 7 for determination of serum corticosterone and ACTH levels and adrenal weights and histology. Adrenal glands from animals sacrificed on PBD 7 were also analyzed for DNA, RNA, and protein content. Cyclosporine treatment without injury had no significant effect on body weight gain, adrenal mass, or baseline ACTH or corticosterone levels. During sepsis, cyclosporine-treated animals demonstrated a significantly diminished adrenocortical response compared to those given only saline. Serum corticosterone levels in the cyclosporine group were 45, 53, and 62% lower on PBDs 1, 4, and 7, respectively, than in saline-treated controls (P < 0.01 on each day). ACTH levels were 43 and 36% lower in cyclosporine-treated animals on PBDs 4 and 7, respectively, compared to the saline-treated group (P < 0.05 on each day). Adrenal hyperplasia occurred in both groups by PBD 7, but increases in adrenal mass and in histologic changes associated with hyperplasia (lipid depletion, vascular dilation) were less pronounced in cyclosporine-treated animals compared to those receiving saline, while adrenal composition remained similar between the two groups. Thus, cyclosporine administration is associated with an attenuated adrenocortical response to the stress of sepsis due to diminished circulating levels of ACTH.
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PMID:Effect of cyclosporine on adrenocortical response to injury and infection. 138 13

Profound nonhemorrhagic shock developed in one postoperative and two trauma patients. Cardiovascular collapse was characterized by severe hypotension (systolic blood pressure less than 80 mm Hg), hyperdynamic cardiac indices (CI greater than 4 L/min/m2), low systemic vascular resistance (SVR less than 500 dyne.sec/cm5.m2), and multiple organ failure. Sepsis was not found by culturing of specimens or visual inspection at laparotomy. Screening cortisol levels were low (less than 2 micrograms/dL in two patients) and did not respond appropriately to synthetic ACTH (cosyntropin) challenge. Administration of exogenous glucocorticoids promptly and dramatically reversed shock and organ failure in two patients. Oral glucocorticoid and mineralocorticoid supplementation were required at hospital discharge. Acute adrenal insufficiency is rare after trauma, but may produce life-threatening cardiovascular collapse, mimicking the "septic" shock state. Cosyntropin stimulation testing confirms the diagnosis and is accurate in traumatized patients. Outcome is dependent upon early recognition and exogenous glucocorticoid administration. Appropriate endocrine evaluation prevents unnecessary use of steroids in a population of trauma patients who are already in a state of immunosuppression.
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PMID:Acute adrenal insufficiency presenting as shock after trauma and surgery: three cases and review of the literature. 173 82

The use of increased dosages of glucocorticoids during periods of physiologic stress in allograft recipients represents a clinical dilemma in that the short-term exogenous therapy required may significantly impair wound healing and immunocompetence. To investigate whether "stress steroids" are actually necessary, a prospective study was conducted in 40 renal allograft recipients admitted with significant physiologic stress. Stress categories included sepsis, metabolic abnormalities, and surgery. These patients received only their baseline prednisone immunosuppression (5-10 mg/day) and no supraphysiologic or stress doses of glucocorticoids. The clinical course of the patients revealed no evidence of adrenal insufficiency. There was no mortality, increase in hospital stay, or eosinophilia. Five episodes of hyponatremia and seven instances of hypotension were attributed to primary disease processes and responded promptly to specific treatment without steroid supplementation. Biochemical evaluation during stress revealed suppression of ACTH levels in 74.5% of episodes, elevation of urinary free cortisol levels in 79.1% of episodes, and elevation of isolated serum cortisol levels in 55.9% of episodes. This suggested that these patients had physiologically adequate adrenal function. The cosyntropin stimulation test overestimated the incidence and degree of clinically significant adrenal dysfunction (63% of patients) and was not a useful indication of a requirement for additional glucocorticoids. We conclude that functional adrenal suppression is uncommon in renal allograft recipients receiving baseline prednisone immunosuppression (5-10 mg/day) and that the demands of physiologic stress are met by a combination of endogenous adrenal function plus exogenous, baseline, immunosuppressive doses of glucocorticoids. Supra-physiologic or high doses of so-called "stress steroids" are not required. The cosyntropin stimulation test has significant clinical limitations and did not serve to alter clinical care.
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PMID:Adrenal suppression and steroid supplementation in renal transplant recipients. 184 49

Tumor Necrosis Factor (TNF) has been implicated in the early metabolic events following acute tissue injury or sepsis; it increases blood levels of glucocorticoids and glucagon or the cellular responses to the hormones. To examine whether stress-related hormones have any effect on macrophage activation by TNF, human monocyte-derived macrophages were exposed to somatostatin (S), ACTH, angiotensin (An), insulin (I), epinephrine (E), and glucagon (G) at physiologic concentrations. 125I-TNF binding as well as the ability of TNF to activate macrophages to kill an intracellular pathogen (Mycobacterium avium) were measured. While treatment with recombinant interferon gamma increased the number of TNF receptors by 53 +/- 8%, E, I, G, S, ACTH and An decreased the number of receptors by 81 +/- 6%, 83 +/- 6%, 15 +/- 5%, 83 +/- 4%, 17 +/- 4% and 21 +/- 4%, respectively. Treatment with I, E, and S also decreased the ability of macrophages to kill M. avium by 30 +/- 1%, 20 +/- 6%, and 51 +/- 2%, respectively. These in vitro results suggest that stress hormones influence TNF-mediated activation of macrophages.
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PMID:Effect of stress-related hormones on macrophage receptors and response to tumor necrosis factor. 197 Oct 32

Decreased cytosolic [Ca2+] and impaired Ca2+ release in response to an IP3 challenge are among perturbations in hepatocyte Ca2+ homeostasis associated with endotoxemia and sepsis. These changes are consistent with the accompanying alterations in appropriate physiologic functions, e.g., activation of glycogen phosphorylase and gluconeogenesis, mediated by [Ca2+]c and defective phosphorylation of relevant enzymes. Attenuation of IP3 binding to the subcellular fractions that are imputed to be targets of IP3 and a decrease in the size of the IP3-sensitive pool of releasable Ca2+ are underlying components of the mechanism of the reduced Ca2+ release upon IP3 stimulation and its metabolic sequelae. ET treatment leads to a significant increase in Ca2+ associated with the cell surface compartment of adipocytes, a reduction in 45Ca2+ uptake by endoplasmic reticulum and higher cytosolic [Ca2+] under basal conditions and upon ACTH stimulation than that observed in cells of control rats. The reduced 45Ca2+ uptake is also manifest in adipocytes of septic rats. Alterations in adipocyte metabolism induced by ET include increased oxidation of glucose to CO2 (an insulin-like effect) and increased lipolysis upon NE and ACTH stimulation.
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PMID:Altered Ca2+ homeostasis and functional correlates in hepatocytes and adipocytes in endotoxemia and sepsis. 225 82


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