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

Critical surgical illness, commonly accompanied by shock, sepsis, multiple transfusions, and renal failure, is usually associated with low total calcium and/or low or normal ionized calcium. A seminal case of hypercalcemia in a surgical intensive care unit (SICU) patient prompted the review of 100 patients with longer than average SICU days (greater than 12) to determine the incidence, associated factors, and possible etiologies of this condition. Ten patients had elevated measured, and five others had elevated calculated, ionized calcium (5.9 +/- 0.25 mg%), an incidence of 15%. Compared to the 85 patients who did not develop hypercalcemia, this population had a significantly higher frequency of the following: renal failure, dialysis, total parenteral nutrition (TPN) usage greater than 21 days, bacteremic days greater than 1, transfusions greater than 24 units, shock greater than 1 day, SICU days greater than 36, and antibiotics used greater than 7. In addition, this group had significantly more days of hypocalcemia early in their hospital course. There was no difference in sex, age, mortality, or incidence of respiratory failure. Two patients studied in depth had renal failure requiring dialysis and no malignancy, milk-alkali syndrome, hyperthyroidism, or hypoadrenalism. Parathormone (PTH) concentrations were high normal or elevated (N terminal 20 and 21 pg/ml; C terminal 130 microliters Eq/ml and 1009 pg/ml) at the time of elevated calcium (total 9.2 to 14.6 mg%; ionized 4.9 to 8.2 mg%). Immobilization does not increase PTH. In renal failure, PTH elevation is a consequence of hypocalcemia rather than hypercalcemia. Moreover, five patients did not have renal failure. Shock, sepsis, and multiple transfusions containing citrate may lower total and/or ionized calcium and thus stimulate PTH secretion. Whatever the mechanism, approximately 15% of critically ill surgical patients develop hypercalcemia, which may represent a new form of hyperparathyroidism.
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PMID:Hypercalcemia in critically ill surgical patients. 393 94

The oncology patient can experience medical or surgical emergencies as a result of effects of the primary tumor, metastases, or systemic effects of the disease. Emergencies unrelated to the primary oncologic diagnosis, such as acute myocardial infarction, drug overdose, or gastrointestinal hemorrhage, also may occur. For this reason routine emergency protocols and diagnostic procedures should be followed in the treatment of oncology patients. We review the major oncologic-related emergencies, including central nervous system and spinal cord compression, airway obstruction, cardiac tamponade, gastrointestinal obstruction, adrenal insufficiency and hypercalcemia, sepsis, and coagulopathies. Medical and surgical emergencies in the oncology patient should be treated aggressively in the emergency department because a determination about the quality of life of the patient, or the reversibility of the acute process, often cannot be answered quickly in the emergency setting.
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PMID:Emergency evaluation of the cancer patient. 646 53

Bilateral adrenal hemorrhage and acute adrenal insufficiency in three acutely ill patients occurred as a complication of pneumonia in two and recent abdominal surgery in the third. The diagnosis was unsuspected in each case before abdominal computed tomography (CT), which showed bilateral adrenal masses. CT was done for suspected intraabdominal sepsis. Adrenal insufficiency was confirmed by endocrine studies, and each patient promptly recovered with steroid replacement therapy. Follow-up CT showed diminution or disappearance of the masses and density changes consistent with resolving hematomas.
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PMID:CT of bilateral adrenal hemorrhage with acute adrenal insufficiency in the adult. 660 97

To determine if concentration of plasma arginine vasopressin (AVP) is inappropriate for the plasma Na+ concentration in hyponatremic burned patients, we obtained 32 plasma samples from 20 patients with total burn size (TBS) 15 to 80% of body surface on or after postburn day (PBD) 4 in the morning following all-night recumbency. In the 25 samples (17 patients) with hyponatremia, AVP was elevated, 1.6 to 14.3 (normal less than 0.5) pg/ml. Most patients with normal serum Na+ had normal AVP values. Out of the total, nine patients (12 samples) without renal failure or sepsis, selected also for hyponatremia and urinary Na+ greater than or equal to 20 mEq/L, were considered separately. BUN of 11.7 +/- 1.8 mg/dl and plasma glucose of 130 +/- 5.6 mg/dl, Na+ of 130 +/- 1.1 mEq/L, calculated osmolality of 272 +/- 1.6 mosm/kg, and cortisol of 20.4 +/- 1.6 micrograms/dl were associated with a 24-hour fluid intake of 4.3 +/- 0.26 L and urinary output of 2.7 +/- 0.33 L, Na+ of 80 +/- 14 mEq/L, and osmolality of 520 +/- 73 mosm/kg (mean +/- SE). In all of the plasma samples, AVP was markedly elevated (6.9 +/- 1.1 pg/ml). In another study, four hyponatremic burned patients were given a standard water load. Excretion of the water was delayed, and further dilution of the initially hypotonic plasma resulted in a fall of urinary osmolality and plasma AVP. Cutaneous thermal injury can cause resetting of the mechanism linking plasma tonicity and AVP secretion resulting in dilutional hyponatremia. This syndrome occurs in the absence of gross physiologic perturbations such as volume depletion or adrenal insufficiency.
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PMID:Inappropriate vasopressin secretion (SIADH) in burned patients. 683 44

There is increasing evidence that the hypercortisolemia in inflammatory diseases suppresses the elaboration of proinflammatory cytokines, thus protecting the host from its own defence reactions. In severe sepsis and septic shock cortisol levels are usually elevated, but some patients may have relative adrenal insufficiency. This may contribute to the overwhelming systemic inflammatory response syndrome. We evaluated the impact of low-dose hydrocortisone infusion (10 mg/h) on the course of the systemic inflammatory response syndrome. This dose corresponds to a maximum secretory rate of cortisol achieved in corticotropin-stimulated healthy humans. In a prospective observational study 57 surgical patients with severe sepsis or septic shock were studied, of which in addition to the conventional treatment 12 patients were infused with low-dose hydrocortisone, and 45 were treated without any corticosteroid. In the longitudinal analysis the systemic inflammatory response--as judged by body temperature, cardiovascular response, and kinetics of inflammatory mediators such as phospholipase A2, C-reactive protein, and neutrophil elastase--started to differ in favor of the hydrocortisone-treated patients after 2 days of treatment (P < 0.05, Mann-Whitney U test). The difference disappeared after withdrawal of exogenous cortisol. Shock reversal was achieved in all patients treated with low-dose hydrocortisone. The data provide evidence that low-dose hydrocortisone infusion attenuates the systemic inflammatory response in human septic shock. From an immunological point of view a relative cortisol deficiency may contribute to the amplified immune response in systemic inflammatory diseases. A randomized clinical trial must clarify the impact of low-dose hydrocortisone infusion on the clinical course and outcome of septic shock patients.
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PMID:Low-dose hydrocortisone infusion attenuates the systemic inflammatory response syndrome. The Phospholipase A2 Study Group. 786 82

Continuous hemofiltration (CHF) procedures (a total of 33 with overall duration 2495 hours and replacement of 2221 kg of fluid) were conducted in 23 patients (12 males and 11 females) aged 30.5 +/- 2.5 years suffering from severe acute renal failure (ARF). CHF efficacy was judged by the kinetics of urea and creatinine. With parenteral feeding the patients received protein and amino acids 1.2-1.5 g/day/kg b.m. The death of 13 patients resulted from sepsis, hemorrhage, shock, adrenal insufficiency. The filtration speed 15.6 +/- 0.6 (7-34) ml/min allowed replacement of 21.7 +/- 1.3 (8-49) kg or 0.49 +/- 0.03 of body fluid a day. The highest rate of hemofiltration was used on day 1, this reducing plasma urea from 35.7 +/- 2.5 (7.5-55.0) to 27.5 +/- 2.0 mmol/l (p < 0.05) and creatinine from 742 +/- 77 (182-1800 to 539 +/- 44 mumol/l (p < 0.05). Subsequently urea and creatinine were maintained in the plasma at the levels 26.8 +/- 1.0 mmol/l and 539 +/- 73 mumol/l, respectively. Urea eliminated with the filtrate amounted to 591 +/- 53, creatinine 13.5 +/- 4.0 mmol or 0.49 +/- 0.02 and 0.65 +/- 0.07 of the overall pools, respectively. In anuria urea generation reached 525 +/- 35 (108-1071) mmol/day, that of creatinine 9.6 +/- 1.4 (1.2-14.0) mmol/day, being on the average less than filtrate elimination of these substances. It is believed that CHF contributes to balanced treatment of severe ARF in spite of parenteral introduction of large quantities of protein and amino acids.
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PMID:[Urea and creatinine kinetics during the continuous hemofiltration of patients with acute kidney failure]. 794 Nov 23

Mild infection or sublethal dose of endotoxin elicits a brief elevation of GH and PRL in the serum. These hormones have proinflammatory and immunostimulatory effect. In severe trauma, sepsis and shock, GH and PRL are suppressed, whereas glucocorticoids and catecholamines are elevated. Under these conditions an acute phase response is initiated by tissue derived (cytokine) hormones, namely IL-1, IL-6, TNF alpha, and several others, which elicit a neuroendocrine response and initiate major metabolic alterations. There is fever and catabolism prevails, whereas the synthesis of acute phase proteins in the liver, cell proliferation in the bone marrow, and protein synthesis by leukocytes is elevated. This is an emergency reaction to save the organism after the local immune/inflammatory response has failed to contain and eliminate the infectious agent. During sepsis and endotoxin shock the systemic activation of the complement system and of leukocytes releasing enzymes and highly toxic cytokines seriously threaten survival. Glucocorticoids suppress proinflammatory cytokine production and potentiate the secretion of acute phase proteins. Some of these proteins, such as C reactive protein, or LPS binding protein, are designed to combine with microorganisms and trigger their destruction by the activation of complement system and of phagocytes. The increased production of some complement components also helps host resistance. The rise in serum fibrinogen promotes blood clotting which can serve to isolate the invading agent by triggering thrombosis in infected tissues. A number of enzyme inhibitors are produced as acute phase proteins, which are likely to serve to curb the nonspecific damage inflicted by enzymes released from activated phagocytes and from damaged cells into the circulation during sepsis and shock. Catecholamines are also elevated, which serve to inhibit inflammatory responses and to promote, even initiate, the acute phase response. If the acute phase reaction fails to protect the host, shock will develop. Patients with subclinical adrenal insufficiency succumb to septic shock almost invariably if glucocorticoid therapy is not given. However, glucocorticoid treatment of septic patients with normal adrenal function has not been helpful. The use of antibiotics to control infection did not lead to spectacular success either because of the emergence of resistant bacterial strains or the enhanced release of endotoxin by this therapy. The new approaches to prevent and treat septic shock involve the use of antibodies capable of neutralizing LPS and of cytokines and the inhibition of cytokine action by antagonist agents.
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PMID:Neuroendocrine defence in endotoxin shock (a review). 797 6

We examined the incidence, diagnosis and therapy of acute adrenal insufficiency, secondary to adrenal hemorrhage. This insufficiency resulted in temperature irregularities. hemodynamic instability, and a large volume resuscitation requirement post-operatively. The case illustrates that a high level of suspicion should be maintained in a clinical scenario that mimics sepsis or myocardial insufficiency in the intensive care unit.
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PMID:Acute adrenal insufficiency resulting from adrenal hemorrhage as indicated by post-operative hypotension. 801 90

The case of a patient with abdominal crisis and shock without any discernible origin who died 36 hours after hospital admission despite maximal therapy is described. Gram-negative sepsis, peritonitis and haemochromatosis with hepatic siderosis was the post-mortem diagnosis. We consider spontaneous peritonitis arising from translocation of normal intestinal flora (E. coli) through the intact wall of the gut combined with the impaired ability of the reticulo-endothelial system to remove endotoxin to be the causative factors. It is unknown whether the adrenal insufficiency due to siderophilic adrenal hypophysis and adrenal glands contributed to the fulminant course of the disease. Undiagnosed liver cirrhosis and especially haemochromatosis should therefore be included in the differential diagnostic considerations in patients presenting with these symptoms, and in whom no obvious cause for a septic focus can be found.
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PMID:[Septic shock with acute abdomen in idiopathic hemochromatosis]. 835 6

Patients with end-stage liver disease have significant mortality often associated with intercurrent episodes of bleeding or sepsis. Intact adrenal function is essential in such situations. In order to test the hypothesis that adrenal insufficiency might be present in severe liver disease, hypothalamic-pituitary adrenal function was evaluated in patients with end-stage liver disease awaiting transplantation. The study had a prospective, open comparative design with patients restricted to those having non-alcoholic liver disease in order to avoid the confounding direct effects of alcohol on adrenocortical function. Fifty-one consecutive patients with end-stage, non-alcoholic liver disease undergoing evaluation for liver transplantation and 40 healthy controls were studied. Patients who had used corticosteroids (n = 8) or who were unable to complete the investigations (n = 5) were excluded leaving 38 patients eligible for analysis. Adrenal function was evaluated under basal conditions by single morning measurements of plasma total and free cortisol, corticosteroid-binding globulin, dehydroepiandrosterone sulfate and by adrenal stimulation indirectly using insulin-induced (0.1 U/kg, i.v.) hypoglycaemia and/or directly by adrenocorticotrophic hormone (ACTH); 250 micrograms tetracosactrin, i.v.) stimulation. Compared with healthy controls, patients with liver disease had a 64% reduction in maximal increments of plasma cortisol to indirect adrenal stimulation via insulin-induced hypoglycaemia and a 39% reduction to direct adrenal stimulation by ACTH (all P < 0.001). There was a significant negative correlation between the severity of underlying liver disease as assessed by Child-Pugh scores and peak control responses to ACTH (r = -0.647, P < 0.0001) and insulin-induced hypoglycaemia (r = -0.597, P < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypothalamic-pituitary adrenal function in end-stage non-alcoholic liver disease. 839 Aug 70


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