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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

When esophageal disruption occurs in the presence of preexisting esophageal disease or is associated with sepsis or fluid and electrolyte imbalance, aggressive and definitive therapy often provides the only chance for patient salvage. Twenty-four adults (average age, 59 years) with intrathoracic esophageal perforations underwent esophagectomy: 15, transhiatal esophagectomy without thoracotomy; and 9, transthoracic esophagectomy. Restoration of alimentary continuity with an immediate cervical esophagogastric anastomosis was carried out in 13 patients. Eleven underwent a cervical or anterior thoracic esophagostomy, and 10 of them had a subsequent colonic (7) or gastric (3) interposition from 4 to 32 weeks (average time, 8.6 weeks) later. The perforations were due to esophageal instrumentation (9 patients), acute caustic ingestion (2), emesis (2), intrathoracic esophagogastric anastomotic disruption (2), and other causes (9). Preexisting esophageal disease in 20 patients included chronic strictures (10 patients), reflux esophagitis (3), esophageal cancer (3), achalasia (2), diffuse spasm (2), and monilial esophagitis (1 patient). Ten patients were operated on within 12 hours after the injury; 3, within 12 to 24 hours; and 11, within three to 45 days (average interval, 6.6 days). There were three hospital deaths (13%). Nineteen of the 21 survivors were able to swallow comfortably until the time of death or latest follow-up. Aggressive diagnosis and aggressive treatment of life-threatening esophageal perforations are advocated. Conservative procedures (repair, diversion, or drainage) for a perforation with preexisting esophageal disease often inflict more morbidity than esophageal resection, which eliminates the perforation, the source of sepsis, and the underlying esophageal disease. The decision to restore alimentary continuity in a single stage must be individualized.
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PMID:Esophagectomy for esophageal disruption. 229 75

In short, bacterial sepsis is associated with a number of peripheral manifestations involving the skin and soft tissues. The pathogenesis of the lesions observed is not fully understood and is almost certainly multifactorial. In ecthyma gangrenosum, the presence of large numbers of gram-negative bacilli in the walls of small blood vessels without a substantial inflammatory response suggests that either the bacteria themselves or bacterial products are responsible for tissue damage. Endotoxin probably plays a prominent role in producing these lesions. That Pseudomonas and Aeromonas species seem to cause ecthyma out of proportion to their prevalence as a cause of bacteremia might suggest that the endotoxin of these organisms has a special predilection for skin and subcutaneous structures. More likely, it indicates that other bacterial substances, such as exotoxins or proteases, are involved. The absence of PMN leukocytes is thought to play a permissive role, allowing unopposed bacterial proliferation. Lesions of symmetric peripheral gangrene characteristically do not have bacteria present. The presence of intravascular fibrin accumulation probably resembles the generalized Shwartzman phenomenon. However, the gangrenous lesions themselves more likely result from systemic hypotension and the resulting hypoperfusion of the tissues than from vessel obstruction. In lesions associated with vigorous inflammatory response, bacterial products may damage tissue either directly or by attracting leukocytes that, in turn, release substances that cause further tissue damage. An etiologic role for endotoxin or the gram-positive bacterial cell wall is likely, since endotoxin is known to produce similar lesions in the localized Shwartzman reaction. Favoring a role for other bacterial substances is the predisposition of V. vulnificus to cause cellulitis or of C. fetus to cause inflammation of the major vessels during sepsis; the mechanisms for these reactions are entirely unknown. It is interesting that in most instances in which peripheral lesions are caused by sepsis, either a large number of bacteria or an intense inflammatory response by PMNs is present, but not both. In both kinds of lesion, the tendency to involve blood vessels by different pathogenetic mechanisms contributes to the evolution of the disease process. In intensely inflamed lesions, veins and arteries can be shown histologically to be occluded. In the absence of inflammation, bacterial invasion of vessel walls or simply the presence of bacterial products adjacent to the vessel may produce spasm. As noted, the pathogenetic significance of thrombosis observed in the lesions of DIC remains unclear.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cutaneous manifestations of bacterial sepsis. 252 95

8 patients suffering from severe head injury (Glasgow Coma Scale score of 3-5) were treated with the calcium influx blocker nimodipine (2-3 mg/h) for a traumatic cerebral vasospasm. In every case the spasm involved the frontal region of the circle of Willis with the first two segments of the anterior and middle cerebral artery. Control angiograms, recorded in 6 patients, revealed a dilated or normalized lumen of the vessels that the first angiography had revealed to be spastic. The intracranial and the mean arterial pressure were not altered by nimodipine during simultaneous neurosurgical intensive care therapy (dexamethasone, mannitol, relaxation, and controlled respiration for 2-3 days). Monitoring of the somato-sensory evoked potentials (SEP) showed a distinct improvement of the cortical response within 7 days. One patient died of sepsis 8 days after the accident and one remained in a vegetative state. The remaining patients reached Glasgow Coma Scale scores of 13.0 +/- 1.1. within 8.6 +/- 2.2 days, the initial scores having been 4.1 +/- 0.8. One year after their accident all the patients were once again fully able to work. The survival quality was therefore better than that reported in the literature for patients in similar conditions. We conclude from these preliminary results that calcium influx blockers can be used successfully in the therapy of traumatic vasospasm and of severe head injuries. A study involving a larger number of patients is currently in progress.
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PMID:Treatment of cerebral vasospasm following severe head injury with the calcium influx blocker nimodipine. 401 Aug 64

The authors have reviewed 25 hips in 23 patients with cerebral palsy in which iliopsoas transfer had been performed for established dislocation or refractory progressive subluxation of the hip. The iliopsoas tendon was transferred either postero-laterally or antero-laterally, depending upon the degree of fixed flexion of the hip. An adductor release was performed in all cases and an open reduction when necessary. A painfree stable joint was produced except for one hip in which the iliopsoas tendon had become detached because of sepsis. The loss of flexor power at the hip due to the transfer is thought to be a small price to pay for the relief of pain and spasm and the increase in function.
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PMID:Iliopsoas transfer in the management of established dislocation and refractory progressive subluxation of the hip in cerebral palsy. 716 45

The case notes of all children admitted during the preceding five years for observation with painful hips (509 patients) were analysed to determine significant diagnostic factors and thus to design and admission policy. Most orthopaedic disorders (62 patients) were apparent on the initial radiographs, with the important exception of osteomyelitis/septic arthritis (21 patients). The remaining 426 patients were diagnosed by exclusion as having an irritable hip. The latter two groups were similar with respect to age, sex, and duration and nature of symptoms. A number of clinical features and laboratory investigations recorded within 12 hours of admission, however, were shown to have significant discriminative value. These were severe spasm, tenderness, pyrexia > or = 38 degrees C, and an erythrocyte sedimentation rate of > or = 20 mm/hour (the white cell count was not significant). Combination of any two of these produced a specificity and sensitivity for sepsis of 91% and 95% respectively (95% confidence interval 0.64 to 0.97). A protocol designed from this data analysis is now being tested and is expected to result in a significant reduction in admission rates.
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PMID:Management of irritable hip: a review of hospital admission policy. 806 94

Acute renal failure (ARF) in burn disease results in a range of phenomena important not only from theoretical, but also from practical point of views, whose causes are manifold. ARF is generally defined as a rapid renal failure resulting in accumulation of protein metabolism degradation products (catabolism). It has been known, for some time, that thermal agents do not produce only local skin damages, but also disturb the integrity of the whole organism producing major functional damages of all organs and systems. Most frequently organs affected by burn disease are the following: the lungs, the heart, the kidney, the liver and blood coagulation systems. There are many factors influencing the renal function during the burns. The most important are: decreased cardiac output, respiratory failure with hypoxia and acidosis, toxaemia and sepsis [1, 4, 6 7, 8-10, 12, 19]. ARF in burn disease may be early due to hypovolaemia and hypoperfusion of the kidneys or late, occurring after a week as a consequence of infection and endotoxaemia. Development of ARF in burn disease is a very unfavorable prognostic sign necessitating a complex evaluation. Anuria in an early phase of burn disease may indicate the development of ARF, particularly if urine findings are positive to haemoglobin, proteins, myoglobin, which is of the utmost importance in deep burns inflicted by high voltage current. The immediate cause of anuria in burn disease may be a reflex transfer and penetration of the large quantities of toxic materials into the circulation form the region affected by burns leading to the spasm of afferent glomerular arteriolae producing sudden discontinuation of glomerular filtration. After burns, sudden increase in the osmotic activity ensues in the affected tissue. Some low molecular links may result, and such particles tend to change the osmotic balance and stimulate the development of oedema, and if not excreted, they increase osmolarity. In 20-30% of the patients with burn disease anuria is absent [2, 5, 11, 14, 18, 20]. The genesis of burn disease-associated anaemias is therefore multifactorial. These factors are the following: haemorrhage, haemolysis and etrythropoiesis level decrease. In massive burns, large amounts of non-specific inflammatory components are produced as well: prostaglandins, histamine, quinines leukocyte phenomena, bacterial toxins, etc. [1, 6, 13-16]. The study based on a years-long treatment of our patients with burn disease included on 100 patients. The youngest of the patients was 14 years old, and the oldest 65 years. The percent of burns-affected body surface ranged from 25% to 75%. In 3/4 of the patients the picture of an early renal failure developed, with oliguria immediately after infliction of the burns with rapid increase of serum urea and creatinine levels, while in 1/4 of the patients ARF occurred on the eighth day following the infliction of the burns. "late form of acute renal failure". Among our series with burn disease, anuria was present in 34.0% of patients and oliguria in 25.0%. ARF (early phase) occurred in 59 patients, 38 patients had no sing of ARF, while late ARF developed only in 3 patients. ARF-associated mortality rate was high among these patients (23%), being 6% among anuric patients with ARF and 17% in patients with ARF with anuria. Seventy-seven percent of the patients survived, and their serum and urine analyses performed upon subsequent out-patient follow-up examinations ranged within normal values. Such high percentage of survival among our patients included in the study is based on an early diagnosis of ARF, understanding of pathophysiology of shock associated with burn disease, adequate therapeutic approaches, including both medicamentous treatment and extracorporeal haemodialysis along with early surgical management (Shema 1, 2). For the time being, haemodialysis is the most effective therapeutical procedure in the treatment of ARF, although the mortality rate of dialyzable patients
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PMID:[Acute renal insufficiency caused by burn injury]. 910 56

Intravascular therapy is essential in the care of acutely ill infants and children, but it is not without risks. The purpose of this article is to discuss potential intravascular, extravascular, and systemic complications related to peripheral and central intravascular therapy in infants and children. The formation of thrombi, infiltration, and sepsis are the most common complications. Less common complications are phlebitis, arterial spasm, catheter retention, catheter embolus, air emboli, dysrhythmias, and hemorrhage. Financial implications of long-term negative outcomes and nursing liability are discussed, and a proposed standard of preventative nursing care for intravascular therapy is presented.
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PMID:Negative outcomes of intravascular therapy in infants and children. 950 72

Access to the central venous circulation for chemotherapy infusion has traditionally been achieved surgically via the subclavian or jugular routes. With ongoing improvements in technical management, alternative means of central venous access have been developed such as arm-port or forearm-port implantation under imaging guidance. Venous arm port devices implantation was attempted in 200 cancer patients under fluoroscopic guidance, after arm venography. The 4% failure rate was due to the inability to perform the arm venogram, venous spasm or presence of a large contrast medium hematoma (rolling vein). Median follow-up was 180 days (range 4-671) and the complication rate was 13.3% (0.7/1,000 patients-day). Twenty-six complications occurred and were due to venous thrombosis (n = 3), large brachial hematoma (n = 1), local (n = 7) and systemic sepsis (n = 1), skin dehiscence (n = 4), fissuration (n = 4), dislocation (n = 2), obstruction (n = 2), and twist of the port (n = 2), leading to a 8.5% removal rate. Main indications for arm port implantation may be breast cancer, previous arm or cervical venous thrombosis, morbid obesity, respiratory insufficiency, previous surgical failure and the irradiated neck.
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PMID:[Brachial fluoroscopically guided implantation of venous port devices in oncology patients]. 1220 84

Reactive oxygen species (ROS) cause damage to the structure and function of tissues. Therefore tissues have systems that eliminate ROS. Bilirubin is one antioxidant that reacts with ROS to produce oxidative metabolites. Biopyrrins are one of the metabolites, the level of which in urine reflects oxidative stress. They are measured by non-competitive inhibition ELISA that employs anti-bilirubin antibody (24G7) and the results are corrected for the urinary concentration of cereatinine. Some reports suggested that psychological stress increased oxidative stress markers. Urinary biopyrrins were also elevated by speech stress, and the subjective stress score recorded by the speakers correlated with the level. The result suggests that bilirubin might eliminate ROS generated by psychological stress. From the beginning of the study of biopyrrins, their urinary level has been known to be increased by surgical stress. Furthermore, it was significantly higher in a major operation patient group than in a minor one, and correlated with operation duration. Sepsis increased the level in surgical patients. Ischemia-reperfusion elevates ROS and, as a result, biopyrrin production. An increase in urinary biopyrrins was observed in a coronary spastic angina group after a spasm provocation test, and the level in myocardial infarction patients with NYHA (New York Heart Association) classification became higher. Correlation between urinary biopyrrins and plasma B-type natriuretic peptide (BNP) was also reported. Research that determines the structures of biopyrrins and their clinical application are in progress.
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PMID:[Oxidative stress related diseases and biopyrrins]. 1579 50

In this review, hospital case records of 202 adult tetanus managed between January 1990 and December 2001 in a tertiary institution in Southwestern Nigeria were reviewed. The mean age of the patients was 36.1+/-17.8 years with male:female ratio of 2.2:1 and an overall mortality rate of 64%. Patients with unfavourable outcomes spent 4.5+/-0.41 days compared with 16.6+/-1.2 days by those who survived. Factors associated with poor prognosis are age >60 years (P=0.029), incubation period <7 days (P=0.007), period of onset <48 h (P=0.0001), tachycardia with pulse rate >120/min (P=0.001) and spasm (P=0.002). Gender (P=0.11), post-injury vaccination (P=0.48) and types of antibiotics administered (P=0.49) were not significantly associated with increased mortality. The three most common complications were aspiration pneumonitis, sepsis and urinary bladder obstruction while complications with highest mortality (100%) were sepsis and cardiac arrest.
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PMID:A 12-year review of cases of adult tetanus managed at the University College Hospital, Ibadan, Nigeria. 1771 9


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