Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the time it has taken medicine to develop the techniques to describe the circulatory changes of severe infections, both pattern and process have been profoundly influenced by the use of intravenous fluids, vasopressors, antibiotics, steroids, mechanical ventilation and haemoflltration. Constant features of severe sepsis include a reduction in peripheral vascular tone on both the arterial and venous sides of the circulation, a defect in oxygen utilisation resulting in lactic acidosis, and varying degrees of myocardial dysfunction. These events have a temporal progression, the precise pattern observed depending on the tempo of the infection, the influence of therapeutic manoeuvres, the age and comorbidities of the patient, and the time the observations are made in the course of events. Early sepsis is accompanied by a decrease in systemic vascular resistance and a metabolic acidosis. The clinical picture includes fever, tachycardia, tachypnoea, respiratory alkalosis and an increased cardiac output with warm, dry peripheries and a bounding pulse. Advanced sepsis involves varying degrees of venous and myocardial contractile failure, and is characterised by progressive acidaemia, respiratory failure and marked sympathetic adrenergic activation. In the absence of vigorous fluid resuscitation, the cardiac output is decreased and the patients are cold, clammy peripherally shut down, and frequently confused, obtunded or comatose. In infections with a silent primary focus (predominantly involving Gram-negative organisms), this stage is frequently the first to attract the attention of attending staff. Late sepsis is characterised by profound acidaemia, vascular hypo-responsiveness, multiple organ failure and death.
 ...
PMID:The haemodynamics of human septic shock. 1116 73

Lactic acidosis has been described in persons with HIV infection particularly in association with the use of nucleoside reverse transcriptase inhibitors (NRTIs). Little is known about the epidemiology of this problem. We reviewed the records of all HIV-infected adults with elevated lactate levels admitted to Barnes-Jewish hospital from 1996 to 1998. There were 37 patients identified with elevated lactate levels. The annual rate of elevated lactate levels was 22.6, 33.9, and 30.8 per 1,000 admissions in 1996, 1997, and 1998, respectively. The median age of the patients was 40.4 years; median CD4(+) count was 148 cells/mm(3); and the median HIV-1 RNA level was 4,401 copies/ml. The median lactate level was 4.5 mmol/liter (range, 2.2-19 mmol/liter). Twenty-nine patients (78%) had elevated lactate levels at admission. Elevated lactate levels were associated with sepsis (48.7%), pancreatitis (13.5%), liver failure (8.1%), multiorgan failure (8.1%), and other conditions. Five patients had lactic acidosis associated with the use of antiretroviral medications; one patient with unexplained lactic acidosis and four patients with pancreatitis. The mortality rate was 45.9% (17/37). Higher lactate levels were associated with increased mortality. In conclusion, elevated lactate levels were uncommon but not rare in hospitalized patients with HIV infection. Sepsis was the most commonly associated condition and antiretroviral medications were the second most frequently associated factor. There was no significant increase in the annual rate of lactic acidosis during this 3-year period.
 ...
PMID:Elevated lactate levels in hospitalized persons with HIV infection. 1117 1

Sepsis-associated purpura fulminans is defined as septicemia, shock, disseminated intravascular coagulation and circulatory failure leading to multiple organ dysfunction. 40-70% of patients with sepsis-associated purpura fulminans die. Early prognostic factors in adults have not been well delineated yet. Aim of our study was 1) to evaluate currently used scoring systems for meningococcal septicemia in the setting of sepsis-associated purpura fulminans and 2) to assess if other parameters are feasible as early prognostic factors. From 1.1 1994-31.12.1998 twelve patients (female: 7; mean age: 31 (21; 43) years) were studied. Six patients (50%) died within 2 hours and 7 days after admission despite standard intensive treatment. On admission non-survivors had a more pronounced degree of disseminated intravascular coagulation compared to survivors (platelet count 18000 (15000; 45000) G/l vs. 119.000 (111000; 152000) G/l, (p = 0.03); fibrinogen 67 (50; 108) mg/dl vs. 356 (234; 483) mg/dl, (p = 0.02); PTZ 28% (20%; 30%) vs. 44% (35%; 51%), (p = 0.05); aPTT 120 (120; 128) sec vs. 46 (44; 69) sec, (p = 0.001). Severity of lactic acidosis was significantly higher in non-survivors than in survivors (pH 7.08 (6.92; 7.21) vs. pH 7.4 (7.25; 7.4), (p = 0.02); lactate 13.5 (11; 15) mval/l vs. 6.0 (4.4; 6) mval/l, (p = 0.02); data presented as median (25-75% interquartile range). In our patients the Glasgow Meningococcal Septicemia Prognostic Score (GMSPS) and the Niklasson-Score failed to distinguish between survivors and non-survivors (GMSPS 7 (6; 11) vs 7.5 (7; 9) out of 15; predicted mortality according to Niklasson-Score 73% vs 88%). There was no difference in the APACHE II Score (22 (18.5, 24) vs 22 (20.25, 26)). The severity of disseminated intravascular coagulation assessed by routine laboratory parameters and the degree of lactic acidosis on admission were the strongest predictors of outcome in patients with sepsis-associated purpura fulminans. Scoring systems developed for patients with meningococcal septicemia are of limited value in the setting of sepsis-associated purpura fulminans.
 ...
PMID:Sepsis-associated purpura fulminans in adults. 1125 35

Severe lactic acidosis has been increasingly reported as a potentially fatal complication of HIV treatment. We report on an asymptomatic HIV-infected woman treated with stavudine, lamivudine and indinavir for one year. She was hospitalized because of progressive dispnoea, oedema, cyanosis and severe lactic acidosis. Arterial blood pH was 6.98, bicarbonate 4.4 mmol/l (normal value 22-26), blood lactate: 29.7 mmol/l (normal value <2.2). Hepatic function was normal. She had an impressively rapid response (within a few hours) to empirical treatment with thiamine (100 mg i.v.). No evidence of sepsis or malabsorption were identified and vitamin B1 level was not tested before thiamine infusion. Three months later she was re-started successfully on nelfinavir plus nevirapine. The rapid response to thiamine infusion deserves a careful attention and such an approach should be considered in similar cases as a support treatment of this potentially life-threatening complication of HIV therapy.
 ...
PMID:Severe lactic acidosis and thiamine administration in an HIV-infected patient on HAART. 1136 26

Because of several factors, including a change in the hormonal behavior, the postoperative period is at high risk for the diabetic patient to present a metabolic complication. On the other hand, a diabetic metabolic disorder may be secondary and reveal a severe underlying complication (sepsis...). Ketoacidosis is the consequence of an absolute or relative lack of insulin and occurs mainly in insulin dependent diabetic patients. Its incidence should be very low during the postoperative period since insulin protocols are systematically used. The main clinical and biological signs are a polypnea, signs of dehydration, an hyperglycemia associated with a high anion gap metabolic acidosis and the presence of ketoacids in the urine. Its treatment is mainly based on an active rehydration and an insulin and potassium supply. Sodium bicarbonate should not be used systematically any more, even during severe acidosis. Hyperosmolar non ketotic states affects insulin nondependent and older diabetic patients for the most part and occurs under similar conditions than ketoacidosis, revealing most of the time a severe underlying complication. Clinical and biological manifestations include a severe dehydration, alterations in consciousness and a major hyperglycemia associated to a moderate or mild metabolic acidosis. Its main treatment is an active rehydration and insulin plus potassium in a second time. Hypoglycemia is usually the consequence of a mistake in the diabetes care and in the insulin management. Every sickness or consciousness disorder occurring in a diabetic patient treated with insulin should lead to perform a blood glucose measurement. In case of severe manifestations, glucose should be administered in emergency, orally if the patient is conscious or intravenously if he is not. Lactic acidosis occurring during the postoperative period in a diabetic patient is usually non specific of diabetic disease and reflects the existence of an underlying complication (sepsis, hemorrhage, hypoxia,...), as it would in an non diabetic patient. Lactic acidosis due to a treatment with metformin is now very rare and occurs almost only in patients having a contraindication to the use of metformin.
 ...
PMID:Acute postoperative metabolic complications of diabetes. 1137 21

Profound hypothermia (core temperature of less than 28 degrees C) is a life threatening state and a medical emergency associated with a high mortality rate. The prognosis depends on underlying diseases, advanced or very early age, the duration prior to treatment, the degree of hemodynamic deterioration, and especially, the methods of treatment, including active external or internal rewarming. This is a case study of an 80-year-old female patient with severe accidental hypothermia (core temperature 27 degrees C). She was found in her home lying immobile on the cold floor after a fall. The patient was in a profound coma with cardiocirculatory collapse, and the medical staff treating her was inclined to pronounce her deceased. On her arrival at the hospital, she was resuscitated, put on a respirator and actively warmed. Very severe metabolic disorders were found, including a marked metabolic acidosis composed of diabetic ketoacidosis (she had suffered from insulin treated type 2 diabetes mellitus) and lactic acidosis with a very high anion gap (42) and a hyperosmotic state (blood glucose 1202 mg/dl). There were pathognomonic electrocardiographic abnormalities, J-wave of Osborn and prolonged repolarization. Slow atrial fibrillation with a ventricular response of 30 bpm followed by a nodal rhythm of 12 bpm and reversible cardiac arrest were recorded. The pulse and blood pressure were unobtainable. Despite the successful resuscitation and hemodynamic and cognitive improvement, rhabdomyolysis (CKP 6580 u/L), renal failure and hepatic damage developed. She was extubated and treated with intravenous fluids containing dopamine, bicarbonate, insulin and antibiotics. Her medical condition gradually improved, and she was discharged clear minded, functioning very well and independent. Renal and liver tests returned eventually to normal limits. Progressive bradycardia, hypotension and death due to ventricular fibrillation or asystole commonly occur during severe hypothermia. Respiratory and metabolic, sometimes lactic, acidosis, lethargy and coma, hypercoagulopathy, hyperosmolar state, acute pancreatitis and renal and hepatic failure are frequent complications of hypothermia. Underlying predisposing causes of hypothermia are diabetic ketoacidosis, cerebrovascular disease, mental retardation, hypothyroidism, pituitary and adrenal insufficiency, malnutrition, acute alcoholism, liver damage, hypoglycemia, sepsis, hypothalamic dysfunction, sepsis and polypharmacy, and especially, the use of sedative and narcotic drugs. Our case demonstrates once again that CPR once begun should continue until the successful rewarming because "no one is dead until warm and dead".
 ...
PMID:[Severe accidental hypothermia in an elderly woman]. 1175 73

We report the survival of a multiply injured patient with exanguinating haemorrhage and an arterial pH of 6.5, following a road vehicle crash. The previously healthy 38 years old male driver veered off the motorway and collided with a tree. The ambulance arrived at the scene 9 min after being called by an eyewitness and, following rapid extrication from the wreckage; the patient arrived in hospital 27 min later (with a GCS of 6), and was immediately intubated. The patient had suffered near-complete amputation of the left leg at upper femoral shaft level, along with multiple distal fractures and open wounds. He also sustained a head injury and closed displaced fractures of left radius and ulna. The patient received 2 l of crystalloids in the pre-hospital phase. Once in hospital the haemorrhage was controlled with a pressure dressing and intra-venous fluids were kept to a minimum until he was taken promptly to theatre. His initial arterial blood sample revealed a pH of 6.57, pCo(2) of 9.18 kPa, a pO(2) of 70.11 kPa and a base excess of -27.5 mmol l(-1). The co-oximeter Hb was 5.8 g dl(-1). Haemorrhage was controlled in theatre where he was transfused a total of 30 U of blood, 1 pack of platelets, 12 U of fresh frozen plasma, 3.5 l of crystalloids and 1.5 l of colloid. Sodium bicarbonate was administered three times. He subsequently remained ventilated in intensive care unit (ICU). Over the following week he survived sepsis, disseminated intravascular coagulation and myoglobinuria (with transient renal failure) attributable to rhabdomyolysis secondary to muscle necrosis. He later underwent diversion colostomy and disarticulating amputation of the left femur after several debridements. After 6 weeks on ICU he made an excellent recovery will full return of his mental abilities. In this case, the serial arterial blood samples obtained were reliable. The lactic acidosis observed was the result of profound tissue hypo-perfusion and its rate of clearance seems to have greater prognostic value than its peak or initial value. Several factors may have contributed to the patient's survival: rapid retrieval from the scene; early intubation with excellent subsequent oxygenation (thus avoiding the dangerous combination of hypoxia and acidosis with synergistic influence on cardiac depression) and limited initial fluid resuscitation in the emergency department with prompt surgical intervention and vigorous restoration of organ perfusion after surgical haemostasis. Immediate operative haemostasis, coupled with restricted fluid administration beforehand and vigorous restoration of organ perfusion afterwards is now replacing the old resuscitation paradigm. Perhaps this shift in practice has helped this patient to survive.
 ...
PMID:Survival with an arterial pH of 6.57 following major trauma with exsanguinating haemorrhage associated with traumatic amputation. 1200 26

One of the most important achievements in the contemporary intensive care management is introduction of continuous renal replacement therapy (CRRT). The most common indications for CRRT are acute renal failure complicated with heart failure, volume overload, hypercatabolism, acute or chronic liver failure, and/or brain swelling. Less common indications include systemic inflammatory response (SIRS), sepsis, multiorgan failure (MOF), adult respiratory distress syndrome, crush syndrome, tumor lysis syndrome, lactacidosis, and chronic heart failure. Methods of CRRT could be used during or after open heart operations, heart, lung or/and liver transplantation in adults and children. Modern approach to treatment of acute renal failure introduces dialysis early in the course of disease in order to avoid complications on other organs. Sepsis, SIRS and septic shock are still major therapeutic problems in intensive care units with a mortality rate over 50%. Numerous uncontrolled and several controlled clinical studies have demonstrated that CRRT could remove inflammatory substances including cytokines, activated components of the complement, and derivatives of the arachidonic acid. Hemodynamic stability and gas exchange in the lungs were significantly improved. These is due not only to removal of inflammatory substances but also to other nonspecific hemodynamic effects (control of body temperature, fluid and metabolic balance). Besides the convection, cytokines could be removed from the plasma with adsorption on the membrane of dialyzer or hemofilter. Prophylactic use of CCRT in patients with normal renal function, without disturbances in fluid excretion and with normal hemodynamics is still controversial, while the possible benefit is not higher than the risks of invasive therapeutic method, and there is no evidence that prophylactic CCRT could prevent development of acute renal failure in these patients. However, current knowledge of MOF pathophysiology justifies the use of CRRT in patients with signs of heart failure, disturbances in metabolic and fluid homeostasis and sepsis, and in patients with the risk of developing acute respiratory failure or MOF, despite the mild impairment of renal function according to laboratory results.
 ...
PMID:[Indications for continuous renal function replacement therapy]. 1287 69

Metabolic acidosis frequently complicates sepsis and septic shock and may be deleterious to cellular function. Different types of metabolic acidosis (e.g., hyperchloremic and lactic acidosis) have been associated with different effects on the immune response, but direct comparative studies are lacking. Murine macrophage-like RAW 264.7 cells were cultured in complete medium with lactic acid or HCl to adjust the pH between 6.5 and 7.4 and then stimulated with LPS (Escherichia coli 0111:B4; 10 ng/ml). Nitric oxide (NO), IL-6, and IL-10 levels were measured in the supernatants. RNA was extracted from the cell pellets, and RT-PCR was performed to amplify corresponding mediators. Gel shift assay was also performed to assess NF-kappa B DNA binding. Inc easing concentrations of acid caused increasing acidification of the media. Trypan blue exclusion and lactate dehydrogenase release demonstrated that acidification did not reduce cell viability. HCl significantly increased LPS-induced NO release and NF-kappa B DNA binding at pH 7.0 but not at pH 6.5. IL-6 and IL-10 expression (RNA and protein) were reduced with HCl-induced acidification, but IL-10 was reduced much more than IL-6 at low pH. By contrast, lactic acid significantly decreased LPS-induced NO, IL-6, and IL-10 expression in a dose-dependent manner. Lactic acid also inhibited LPS-induced NF-kappa B DNA binding. Two common forms of metabolic acidosis (hyperchloremic and lactic acidosis) are associated with dramatically different patterns of immune response in LPS-stimulated RAW 264.7 cells. HCl is essentially proinflammatory as assessed by NO release, IL-6-to-IL-10 ratios, and NF-kappa B DNA binding. By contrast, lactic acidosis is anti-inflammatory.
 ...
PMID:Lactic and hydrochloric acids induce different patterns of inflammatory response in LPS-stimulated RAW 264.7 cells. 1469 14

A 15-year-old female with short intestine syndrome due to chronic intestinal pseudo-obstruction associated with kidney failure underwent a multivisceral (stomach-duodenum-jejunum-ileum-pancreas-liver) and kidney transplant. She had required parenteral nutrition for the last 5 years, with numerous complications such as sepsis from the central catheter, deep venous thrombosis, severe liver dysfunction, pancytopenia due to bone marrow failure, and severe malnutrition. Surgery lasted 15 hours and was free of complications other than hypothermia, which worsened after revascularization of the grafts. Replacement of 6 units of blood products and crystalloids was required. Biochemical and hemodynamic variables were stable, apart from the development of hypernatremia, hyperglycemia, and lactic acidosis. The anesthetic approach included preoperative assessment of problems related to chronic parenteral nutrition (liver dysfunction, coagulopathy, and restricted venous access), the prevention of hypothermia, correction of electrolyte imbalance and the acid-base status, treatment of reperfusion syndrome, and the replacement of fluids and blood products to maintain circulatory homeostasis and assure sufficient splanchnic perfusion.
 ...
PMID:[Anesthesia for a pediatric multivisceral transplant]. 1507 2


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>