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

The clinical course of a 26 year old female patient with acute liver necrosis and coma due to hepatitis B is reported. The disturbances of conciousness had improved. The patient survived 41 days after the beginning of the coma and developed liver cell regeneration and an acute post-hepatitic liver cirrhosis. As a grave complication a septicemia with aspergillus was observed. The patient died because of gastro-intestinal hemorrhage. At autopsy there were no signs of brain edema. The treatment consisted in: daily infusions with coenzyme A, nicotinamid-adenin-dinucleotide, alpha lipoic acid and cocarboxylase to improve the metabolic disorders and the clinical picture; mannitol intravenously to prevent and to treat cerebral edema; 33 charcoal-hemoperfusions to remove toxic substances of acute liver failure. Treatment of the aspergillus infection with 5-fluorocytosine and amphotericine B and infusion of concentrated ascites led to a decompensation of liver functions. From this observation the following conclusions can be drawn: after an acute viral hepatic necrosis, new synthetic functions and improvements of the disturbed intermediary metabolism in regenerated liver-cells can eventually be seen only after twenty-four to thirty days. With systematically applicated mannitol infusions it is possible to treat cerebral edema effectively.
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PMID:Treatment of fulminant hepatic failure with infusions of Co-factors and mannitol and charcoal-hemoperfusions during Forty-one days. 50 61

In childhood hyperpyrexia is the most important factor causing the irreversibility of shock. The combination of high fever and circulatory impairment is more frequent during the first years of life. This behaviour is due to the high resistance of the arterial system in infancy. Marked general vasoconstriction increases the risk of a reduction in circulation and of heat loss, and causes hypoxia and rise of fever. The further course of shock is largely determined by microcirculatory failures. Under hyperpyrexia the disturbance of homeostasis can be intensified by shivering, blocking of perspiratio sensibilis, hyperosmolarity, brain edema, and DIC. In most cases of meningococcal sepsis shock and DIC begin with vasoconstrictive centralisation of circulation. The high-output-shock is extremely rare in children with high fever. The control of all important functions of a febril child in shock is the best baseline for the treatment. It is necessary in all shock patients in hyperpyrexia to reduce the fever and to repair the peripheral circulation. The therapy consists of antipyretic drugs, physical cooling, infusions of buffer-bases, dopamine, antibiotics and so on. In DIC heparin or streptokinase are indicated. In severe circulatory impairment combined with high fever prednisone is useful, in brain edema dexamethasone. The fatality rate of our cases has been diminished by a systematic therapy of hyperpyrexia and shock from 10 to 3 percent.
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PMID:[Hyperpyrexia and shock (author's transl)]. 77 99

In neurosurgical patients with renal failure, dialysis entails specific problems, chief of which is increased intracranial pressure and progressive brain edema as a result of rapid lowering of the serum osmolality. Another major problem is a tendency to hemorrhage, in response to either systemic heparinization or insufficient dialysis. The authors describe the results obtained with hemodialysis (HD), continuous arteriovenous hemofiltration (CAVH), continuous ambulatory peritoneal dialysis (CAPD), continuous peritoneal dialysis (CPD), and intermittent peritoneal dialysis (IPD). Nine patients were treated with HD, one with CAVH, five with CAPD or CPD, and two with IPD. Three of the six patients treated with continuous dialysis (CAVH, CAPD, and CPD) died, whereas intermittent dialysis (HD and IPD) carried an 82% mortality rate (nine of 11 patients). The causes of death were progressive brain edema in three cases, intracranial hemorrhage in three, gastrointestinal bleeding in three, overhydration due to insufficient dialysis in one, septicemia in one, and rupture of a cerebral aneurysm in one. Continuous dialysis appeared to be superior to intermittent dialysis in these neurosurgical patients in that it produced less brain edema and was less often associated with hemorrhage due to insufficient dialysis. In HD and CAVH, systemic heparinization was also thought to account for the high incidence of hemorrhage. However, CAVH with short half-life anticoagulants may be useful in patients who have abdominal complications and are therefore not suitable candidates for peritoneal dialysis.
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PMID:[Comparison of five modes of dialysis in neurosurgical patients with renal failure]. 248 92

In Norway a hyperendemic situation has persisted since 1974 as regards meningococcal disease, with an adjusted annual incidence of almost 10 per 100,000 inhabitants. 80% of the cases are caused by group B meningococci, and the lethality has been about 10%. This article summarises the new Norwegian guidelines for the diagnosis and management of systemic meningococcal disease. Clinical signs and symptoms are described, together with criteria for the classification of cases into four main categories: I Distinct meningitis; II Severe sepsis; III Simultaneous distinct meningitis and severe sepsis; IV Milder septicaemia and/or meningitis. This type of classification is useful when choosing treatment, and for prediction and evaluation of the outcome. Hospital departments should establish appropriate routines for the management of such life-threatening infections. In cases of suspected meningococcal disease, antibiotic treatment should be started within 15 minutes of admission. Initially, benzylpenicillin and chloramphenicol are recommended, to cover haemophilus infection as well. When the diagnosis has been confirmed chloramphenicol may be discontinued. Laboratory specimens are highly desirable, but sampling procedures should not delay start of treatment. As a main rule patients with meningitis should have a spinal puncture. In severe septicaemia, antibiotic treatment and management of shock are given priority. All patients should be closely monitored. The condition of the patient may deteriorate rapidly. Detailed advice is given on laboratory tests and patient monitoring, and also on the management of septic shock, adult respiratory distress syndrome (ARDS), brain edema, renal failure and coagulation disturbances (DIC).
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PMID:[Guidelines for the diagnosis and treatment of meningococcal disease at hospitals]. 274 27

Imipenem/cilastatin sodium (MK-0787/MK-0791) was evaluated for its safety, efficacy and pharmacokinetics in children. Thirty cases of bacterial infections were treated with MK-0787/MK-0791 at a daily dose of 40 to 222 mg/kg for 2.25 to 13 days. Clinical cure rate was 93% and bacteriological efficacy rate was 88%. Treated diseases included severe tonsillitis due to mixed anaerobic infections, pneumonia, sepsis, brain abscess and soft tissue infections. Two cases, one with periosteomyelitis due to methicillin-resistant S. aureus and the other with pulmonary abscess due to Haemophilus influenzae (other than type b), failed to respond to the MK-0787/MK-0791 therapy. The serum half-life of MK-0787 was 0.892 hour in children with normal renal functions. An episode of convulsions in a case of sepsis with bacterial croup and brain edema was considered to be associated with the MK-0787/MK-0791 therapy. From the present study, MK-0787/MK-0791 appears a safe and effective antibiotic when used in children with a variety of bacterial infections.
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PMID:[Clinical evaluation of imipenem/cilastatin sodium in children]. 346 75

The therapeutic goals for fluid replacement in 9 patients were studied. Five cases in sepsis, 2 in necrotizing pancreatitis and 2 in fat embolism were treated as dehydration or hypovolemia. Fluid replacement was performed with the view of obtaining the amelioration of circulation and urine output, even if CVP or PCWP had been elevated on admission. The values of CVP and PCWP, renal function and pulmonary function were assessed retrospectively. Out of 9 patients, one died of refractory shock, brain edema due to fat embolism and remaining one after recovery of shock. Out of 6 survivors, 2 showed oliguric renal failure, and 2 nonoliguric renal failure. The volume of administered fluid ranged from 5445 ml/10 hrs to 15820 ml/14 hrs and speeds of fluid administration were 545 ml/hr to 1248 ml/hr. CVP value on admission ranged from 4.0 to 22.0 cmH2O (3.0 to 16.3 mmHg), mean value 14.0 +/- 6.5 cmH2O. Through the course, the highest CVP and PCWP ranged from 12.5 to 26.5 (mean 19.8) mmHg and 14 to 36 (mean 20.9) mmHg, respectively. Out of 9 patients, 8 were suffering from respiratory distress, however, 7 recovered by PEEP except for one refractory shock. High values of CVP or PCWP could be recognized even if in hypovolemic shock and/or septic shock. Maintenance of higher values (18-20 mmHg) in CVP and/or PCWP during fluid resuscitation might be recommended because adequate fluid resuscitation could sustain the renal function, and result in good outcome.
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PMID:[Therapeutic goals for fluid management in profound shock]. 382 15

We studied prospectively the syndrome of brain edema after a large infarction in 12 patients. The major symptom was drowsiness, which began on the first to fourth day after the ictus and which was accompanied by asymmetry in pupillary size of 0.5 to 2.0 mm in eight patients, periodic breathing in seven, and Babinski's sign contralateral to the hemiparesis in five. These accompanying signs appeared several hours after drowsiness in some patients. Seven patients had brain death, one died of sepsis after recovering from brain swelling, and only four survived. In six patients in whom intracranial pressure was continuously measured, levels persistently above 15 mm Hg were associated with eventual brain death (four patients) and levels below 15 mm Hg were associated with survival (two patients).
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PMID:Brain edema after stroke. Clinical syndrome and intracranial pressure. 660 14

The pathophysiological processes of the nervous system observed in the reactions to aggressive external stresses like severe trauma, systemic infection and so on have been reviewed. As is generally understood, such stresses as tissue destruction lead to the metabolic changes via proprioceptive impulses to central nervous system and neuroendocrinological courses. Cytokines are well known to work to induce systemic inflammatory responses and also to be important components of sepsis syndrome, for example. In the early phase of septic encephalopathy without overt infection of the brain or the meninges, it is possible that cytokines cause capillary leakage with brain edema, interference with microcirculation and direct effects on tissue metabolism resulting in brain dysfunction. And besides, Interleukins are prove to be produced in a few hours post-injury in experimental model. In clinical settings, severe head injury patients, who are often complicated with respiratory or urinary infection and with bacterial translocation, can suffer not only from systemic inflammatory responses originated from the brain but also from septic encephalopathy mentioned above. Therefore multiply traumatized patients with damaged brain for instance might well have to be considered as the aggregation, or integration of the systemic insult from the aspect of aggressology.
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PMID:[The significance of neurological manifestations from the aspect of aggressology]. 894 Jun 84

Kinins are peptide hormones that exert pathophysiological as well as pronounced beneficial physiological effects, mainly by stimulation of bradykinin (BK) B(2) receptors. Owing to the strong proinflammatory properties of kinins resulting from vasodilation, plasma extravasation, activation of mast cells, fibroblasts and macrophages, stimulation of sensory neurons, and the release of nitric oxide, prostaglandins, leukotrienes and cytokines, kinins are believed to play an important role in a variety of inflammatory diseases and pain. Beneficial effects of BK B(2) receptor antagonists in perennial rhinitis, asthma and brain edema have already been shown in clinical trials. Recently, the potential therapeutic utility of BK B(2) receptor antagonists has been extended by the discovery of orally active, nonpeptide BK B(2) receptor antagonists and the identification of novel indications for their use. On the other hand, kinins also have been identified as potent antihypertensive and organ-protective peptides. They have been shown to have vasodilatory, antihypertrophic, antiaggregatory and fibrinolytic effects due to the BK B(2) receptor-mediated release of the autacoids nitric oxide, prostacyclin and tissue plasminogen activator. A recent finding is that kinins are also involved in ischemic preconditioning. Orally active, nonpeptide BK B(2) receptor agonists as potential novel therapeutic agents in cardiovascular medicine have also been identified. In conclusion, interaction with the BK B(2) receptor by either its blockade or its stimulation offers promising therapeutic approaches. BK B(2) receptor antagonists may prove to be useful in the treatment of asthma, rhinitis, arthritis, colitis, pancreatitis, sepsis, edema, tissue injury, pain and possibly infections, hepatorenal syndrome, Alzheimer's disease and lung cancer. BK B(2) receptor agonists have potential in the treatment of cardiovascular diseases like hypertension, cardiac hypertrophy, restenosis and myocardial infarction and diabetic disorders.
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PMID:Bradykinin B2 receptor as a potential therapeutic target. 1293 26

We report on two children with sepsis-associated encephalopathy. They presented with fulminant neurological damage on clinical, neuroimaging, and neurophysiological findings. At onset, both went into deep coma after status epilepticus, resulting in near brain death. Both patients showed diffuse brain edema on CT and severe brain dysfunction on electroencephalography within a day of onset. Brain magnetic resonance (MR) imaging of one patient on day 2 showed restricted diffusion in the basal ganglia and the subcortical white matter of the frontal and occipital lobes. Brain edema aggravated and lasted for a few months despite a variety of treatments. MR imaging in the chronic phase revealed cracking lesions extending to the cerebral white matter, the cerebellum, and the brainstem. MR angiography showed diminished intracranial major arteries. These serial neuroradiological findings suggested severe brain damage resulting from fulminant elevation of intracranial pressure, which mimicked "brain death" or "respirator brain".
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PMID:Fulminant sepsis-associated encephalopathy in two children: serial neuroimaging findings and clinical course. 2013 72


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