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

A 68-year-old female on two-year chronic hemodialysis for chronic renal failure due to chronic pyelonephritis, was admitted to hospital for weakness, dulled sensorium and dizziness. On examination the patient was in a state of circulatory collapse, the electrocardiogram showed an accelerated idioventricular rhythm and laboratory analysis revealed extreme hyperkalemia (K+ 10.1 mmol/l). There were no common causes of shock, such as hypovolemia, sepsis, heart failure and presence of vasodilator drugs. The patient was treated with calcium gluconate, sodium bicarbonate and sodium chloride (to oppose the effects of hyperkalemia on the cell membrane to minimize cardiac and neuromuscular toxicity), insulin and dextrose (to increase the transport of K+ from the extracellular to the intracellular compartment), and hemodialysis (to remove K+ from the body). At the end of the hemodialysis session, the patient was in a clinically good condition, blood pressure was 160/90 mm Hg and the serum K+ concentration was normal. The case appeared to suggest that extreme hyperkalemia may have direct effects on vascular resistance, causing hypotension and shock.
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PMID:A life-threatening complication of extreme hyperkalemia in a patient on maintenance hemodialysis. 748 41

Septic shock following gram-negative infection is a leading cause of mortality in critically ill patients, accounting for nearly 200,000 deaths a year. The exaggerated production of tumor necrosis factor-alpha (TNF alpha) is known to contribute to hemodynamic collapse and the hematological dyscrasia associated with gram-negative sepsis. Although previous studies have shown TNF alpha antibodies and TNF immunoadhesins to be effective in experimental gram-negative sepsis, we postulated that administration of a novel construct of two modified soluble p55 receptors linked to polyethylene glycol (PEG-BP-30) would also attenuate the hemodynamic and hematologic alterations to lethal Escherichia coli septic shock in non-human primates. Nine adult female and male baboons (Papio anubis), weighing 10-17 kg, were anesthetized and invasively monitored. The nine animals were randomized to receive either 0.2 mg/kg body wt PEG-BP-30 (n = 3), 5.0 mg/kg body wt PEG-BP-30 (n = 3), or placebo (n = 3). One hour after pretreatment, animals were infused with 5-10 x 10(10) CFU/kg of live E. coli iv and vital signs were recorded for the next 8 hr. Arterial blood was drawn for baseline parameters and throughout the study to obtain total and differential white blood cell and platelet counts and cytokine levels (TNF alpha, IL-1 beta, IL-6, IL-8). E. coli bacteremic baboons receiving only placebo demonstrated a significant fall in mean blood pressure and leukopenia. Two of the three animals expired. In contrast, five of the six baboons receiving the PEG-BP-30 survived and these animals exhibited markedly attenuated declines in blood pressure and leukocyte numbers.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:PEG-BP-30 monotherapy attenuates the cytokine-mediated inflammatory cascade in baboon Escherichia coli septic shock. 763 Jan 20

We have previously reported that fresh frozen plasma (FFP) may induce a rapid irreversible shock when repeatedly infused in pigs challenged with Gram-negative sepsis. The aims of the present study were to elucidate the cardiovascular nature of the shock and determine the aetiologic role of tumour necrosis factor (TNF), complement activation and halothane anaesthesia. Three groups of anaesthetized piglets were inoculated with a lethal dose of live E. coli bacteria. Groups I (n = 8) and III (n = 8) were anaesthetized with halothane and group II (n = 8) with ketamine. Animals in groups I and II received repeated infusions of FFP, whereas animals in group III received repeated infusions of 7% albumin. Six animals in group I and four animals in group II died during the first plasma infusion. Survival time was significantly longer in group II (P = 0.04) compared to group I. No animals in group III died during the albumin infusions, and no adverse effects were observed during the infusions. In group I the plasma induced shock was characterized by abruptly falling mean arterial pressure, cardiac index, systemic vascular resistance index and left ventricular contractility. Concomitant increases were recorded in left ventricular filling pressure and central venous pressure. Group II demonstrated a similar, but delayed response. Plasma infusion was associated with a significant increase in terminal complement complex (TCC) (P < 0.03 in group I, P < 0.05 in group II) and depletion of serum ionized calcium. We conclude that FFP may induce fatal myocardial depression and circulatory collapse in severe sepsis. Complement activation may be of aetiologic importance.
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PMID:Fatal myocardial depression and circulatory collapse associated with complement activation induced by plasma infusion in severe porcine sepsis. 772 71

To overcome the hemorrhagic complications that may occur during extracorporeal circulatory support for post cardiotomy shock patients, a heparinized circuit was introduced into the percutaneous cardiopulmonary support system and decreased systemically administered heparin during bypass. Heparin coated percutaneous cardiopulmonary support with low dose systemic heparinization was instituted in 13 patients (6 men and 7 women, mean age 62.2 +/- 8.5 years) who experienced circulatory collapse after cardiac surgery. Of the 13 patients, 9 could not be weaned from cardiopulmonary bypass and 4 had circulatory collapse in the operating room or in the intensive care unit. The duration of support ranged from 1 to 66 hr (mean 27.4 +/- 26.7), and the flow rate ranged from 1 to 3 L/min (2.2 +/- 0.5). An activated coagulation time of about 150 sec was maintained with or without minimal systematically administered heparin. Of the patients cannulated, 77% (10 of 13) were successfully weaned from percutaneous cardiopulmonary support and 39% (5 to 13) were long-term survivors. The causes of death were sepsis in three, progressive heart failure in three, lower leg ischemia in one, and vital infection in one. From the results of clinical or post mortem examinations, there was no massive bleeding or evidence of thromboembolism in the major organs. From observations made within 12 hr of initiation of percutaneous cardiopulmonary support, there was no significant decrease in the number of platelets, but platelet count had significantly decreased 24 hr after initiation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heparin coated percutaneous cardiopulmonary support for the treatment of circulatory collapse after cardiac surgery. 785 34

Leukemia inhibitory factor (LIF) has recently been associated with septic shock in humans. In this study we sought to determine, in mice, the role of LIF in septic shock. During sublethal endotoxemia, serum LIF levels, as determined by radio-receptor competition assay, peaked at 2 h and were low (3 ng/ml), whereas in lethal Escherichia coli septic shock serum LIF levels rose progressively (> 30 ng/ml) in the premorbid phase coincident with the development of tissue injury. Single i.v. injections of high doses (up to 50 micrograms per mouse) of recombinant murine LIF had no obvious acute detrimental effects, whereas continued i.p. administration (30 micrograms per mouse per day) for 3-4 days induced a fatal catabolic state without evidence of preceding hemodynamic collapse or shock. Simultaneous or subsequent administration of high doses of LIF had no effect on mortality from sublethal and lethal E. coli septic shock, whereas prior administration conferred significant protection against lethality (P << 0.001 by log-rank test), an effect that was dose and interval dependent. This protective effect resembled endotoxin tolerance and was characterized by suppression of E. coli-induced serum tumor necrosis factor concentration (P < 0.05), reduction in the number of viable bacteria (P < 0.05), and prevention of sepsis-induced tissue injury. These observations suggest that systemic LIF production is part of the host response to both endotoxin and sepsis-induced tissue injury.
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PMID:Leukemia inhibitory factor protects against experimental lethal Escherichia coli septic shock in mice. 787 78

Langston and Sampson point out that the sine qua non of empyema management is early, adequate, and dependent drainage. Diagnostic thoracentesis followed by closed tube thoracostomy and conversion to open drainage, either by a large-bore tube or a rib-resection with a pleurocutaneous fistula, are initial procedures that may be continued for an extended period to control infection, obliterate loculations, and heal co-apted pleural surfaces secondarily. Clagett and Geraci have noted that postpneumonectomy empyema spaces can be "sterilized" and the initial drainage site can be closed after antibiotic instillation. Miller, however, reports success rates for this procedure only in the range of 25% to 33%. Our results are somewhat higher. Obliteration of the persistent space after control of infection by drainage can be accomplished by interposition of muscle flaps with closure of any bronchopleural fistulas and/or by thoracoplasty. As stated previously, myoplastic techniques to obliterate empyemas and close bronchial fistulas in tuberculous disease have a success rate of approximately 75%. Such techniques, however, not only assist in limiting the extent of thoracoplasty, but also may avoid the procedure entirely in some cases. Virkkula has emphasized that use of pedicled myoplasty does not necessarily obviate the need for thoracoplasty. Pairolero and colleagues reported that the use of selected thoracoplasty combined with muscle transposition afforded a 73% success rate for postpneumonectomy empyema and a 64% success rate for closure of persistent bronchopleural fistulas and precludes protracted drainage and/or extended thoracoplasty. Young and Ungerleider concluded that (1) thoracoplasty is more successful if it is applied for patients with parapneumonic rather than postresectional empyemas; (2) concomitant tailoring thoracoplasty has a higher rate of failure; (3) preliminary drainage followed by thoracoplasty has a higher success rate in eliminating the empyema than thoracoplasty alone; (4) first rib resection is indicated for apical collapse only; (5) preoperative preparation is important to control and manage underlying suppurative processes; and (6) thoracoplasty of any type should not be used as a desperation modality of therapy in which uncontrolled sepsis and inadequate drainage are present or in which cancer or unidentified sites of hemorrhage exist. Sequential management of the residual infected space can proceed along several pathways. Many patients with empyema are well-controlled with simple open drainage and with underlying lung reexpansion, either spontaneously or in association with decortication, and may never need thoracoplasty. Drainage and thoracoplasty alone may be effective not only in obliterating an empyema space but also in sealing a bronchopleural fistula.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Thoracoplasty. 795 86

The primary function of the heart and lungs is to generate a flow of oxygenated blood to respiring tissues to sustain aerobic metabolism. Teleologically, such a transport system has several basic requirements. It should be energy efficient, avoiding unnecessary cardiorespiratory work, but it should be sensitive to the fluctuating demands of cellular metabolism. Ideally, metabolic demand and oxygen distribution should be matched regionally when at rest, during exercise, and in different disease states. Finally, oxygen should pass efficiently across the extravascular tissue matrix. The mechanisms that control oxygen distribution are complex and not completely understood. In the critically ill patient, these mechanisms may have an important role in determining the clinical outcome. The relationship between oxygen delivery and consumption has not been clearly established despite considerable investigation during the last decade. However, these variables are often measured to define a population of critically ill patients in whom oxygen consumption is limited by oxygen delivery, the state of so-called delivery-dependent oxygen consumption or pathologic supply dependency. The recent literature in critical care and many leading intensive care units has emphasized the importance of raising oxygen delivery to "supranormal" levels in an attempt to satisfy the increased metabolic demands of these patients. This practice has been justified by the observation that increasing oxygen delivery improves oxygen debt and outcome in postoperative surgical patients requiring intensive care. In the severely hypovolemic patient, most physicians would agree that volume replacement to improve oxygen delivery must be beneficial. However, in patients with more complex problems, including sepsis, cardiovascular collapse, and hypoxic hypoxemia, controlled trials to examine the influence of such strategies on clinical outcome have produced conflicting data. Several methodologic factors may have contributed to these contradictory and often controversial results. These factors include failure to define the disease and patient population adequately, the relationship between the time of investigation and the evolution of the disease process, and the accuracy and frequency of measurement.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The relationship between oxygen delivery and consumption. 802 Mar 86

We studied the efficacy of low-dose nitric oxide inhalation in nine consecutive patients with severe persistent pulmonary hypertension of the newborn (PPHN) who were candidates for extracorporeal membrane oxygenation (ECMO). All patients had marked hypoxemia despite aggressive ventilator management and echocardiographic evidence of pulmonary hypertension. Associated diagnoses included meconium aspiration syndrome (3 patients), sepsis (3 patients), and congenital diaphragmatic hernia (2 patients). Infants were initially treated with inhaled nitric oxide at 20 ppm for 4 hours and then at 6 ppm for 20 hours. In all infants, oxygenation promptly improved (arterial/alveolar oxygen ratio, 0.077 +/- 0.016 at baseline vs 0.193 +/- 0.030 at 4 hours; p < 0.001) without a decrease in systemic blood pressure. Sustained improvement in oxygenation was achieved in eight patients treated with inhaled nitric oxide for 24 hours at 6 ppm (arterial/alveolar oxygen ratio, 0.270 +/- 0.053 at 24 hours; p < 0.001 vs baseline). One patient with overwhelming sepsis had an initial improvement of oxygenation with nitric oxide but required ECMO for multiorgan and cardiac dysfunction. We conclude that low doses of nitric oxide cause sustained clinical improvement in severe PPHN and may reduce the need for ECMO. However, immediate availability of ECMO is important in selected cases of PPHN complicated by severe systemic hemodynamic collapse.
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PMID:Clinical responses to prolonged treatment of persistent pulmonary hypertension of the newborn with low doses of inhaled nitric oxide. 832 Jun 29

Cardiac tamponade, a potentially lethal complication following cardiac surgery, may present either early or late postoperatively and may be difficult to diagnose due to atypical clinical, hemodynamic, or echocardiographic findings. To determine the frequency and clinical features of postoperative cardiac tamponade, we performed a review of 510 consecutive patients who underwent cardiac surgery. The incidence of postoperative cardiac tamponade was 2.0 percent (10/510 patients) and occurred following valvular, bypass, and aortic surgery. Nine of ten patients had either atypical clinical, hemodynamic, and/or echocardiographic findings. The diagnosis of tamponade was made 1 to 30 days (mean = 8.5 days) postoperatively. Presenting symptoms were often mild and nonspecific. Classic signs including hypotension, pulsus paradoxus greater than 12 mm Hg, and elevated jugular venous pressure were present in 7, 6, and 5 patients, respectively. Right heart hemodynamics revealed elevated and equalized diastolic pressures in three of six patients. Two-dimensional echocardiography revealed selective compression of the left ventricle (LV) (four patients), right ventricle (RV) (one patient), left atrium (LA)/RV (one patient), LA/LV (one patient), LA/LV/RV (one patient), all four chambers (one patient), and no diastolic collapse of any chamber (one patient). There was often an absence of anterior pericardial fluid (six patients) with tethering of a portion of the RV to the chest wall anteriorly (five patients). Coagulation parameters were "supratherapeutic" in only three of eight patients who were receiving systemic anticoagulants at the time of diagnosis. The initial diagnosis was confused with congestive heart failure in one patient, pulmonary embolism in three patients, acute myocardial infarction in two patients, and sepsis in one patient. Eight of ten patients survived; all of these patients underwent surgical removal of fluid and/or hematoma in the operating room. We conclude that postoperative tamponade after cardiac surgery may have varied clinical and hemodynamic presentations, often due to selective chamber compression by loculated fluid or clot. Due to its frequently atypical features and presentation that may simulate other disorders, the diagnosis of tamponade should be considered whenever hemodynamic deterioration or signs of low output failure occur in the postcardiotomy patient.
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PMID:Atypical presentations and echocardiographic findings in patients with cardiac tamponade occurring early and late after cardiac surgery. 832 20

Post-extubation atelectasis (PEA) constitutes the commonest cause of lung collapse in ventilated neonates. The clinical and radiological features of 47 ventilated infants who developed PEA within 24 h of extubation are reported. Three main radiographic patterns of atelectasis were identified: (1) transient unilobar collapse resolving within 12 h of extubation (19 cases), (2) multilobar atelectasis developing over a 48-h period (18 cases), and (3) progressive atelectasis resulting in complete collapse of a whole lung. A similar number of ventilated infants without PEA served as controls. We found a significant association between the incidence of PEA and multiple intubation (P < 0.02), presence of patent ductus arteriosus (P < 0.001) and neonatal sepsis (P < 0.05). Prophylactic physiotherapy is recommended for ventilated infants, particularly those with the above risk factors.
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PMID:Post-extubation atelectasis in ventilated newborn infants. 833 4


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