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

The newborn infant, particularly when premature, has a haemostatic mechanism which may not be entirely capable of withstanding the onslaughts of trauma, infection, asphyxia or other complications of the neonatal period. He is at risk of local or diffuse haemorrhage, which may at times be serious or even life-threatening. The cause of haemorrhage during the newborn period can generally be ascertained by a careful history and brief physical examination directed toward recognition of any predisposing factors or underlying diseases. Screening laboratory tests can usually be correctly interpreted as long as certain laboratory artifacts and physiological peculiarities of the neonatal coagulation mechanism are kept in mind. Diagnosis of and therapy for vitamin K deficiency and haemophilia in the healthy-appearing neonate is generally carried out with little difficulty. The seriously ill neonate with bacterial sepsis, respiratory distress syndrome, or extreme immaturity presents greater problems, for laboratory tests may be more difficult to obtain and interpret and underlying conditions may be untreatable. DIC occurs commonly in such neonates, and transfusion therapy, with or without heparin, is often unsuccessful. A persistent dilemma are those neonates with fatal intravascular haemorrhage, in whom definable haemostatic abnormalities are few and transfusion therapy is futile.
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PMID:Neonatal coagulation: normal physiology and pathophysiology. 35 Apr 67

Disseminated intravascular coagulation (DIC) is a syndrome of deposition of platelet-fibrin thrombi in the microcirculation, with consumption of platelets and clotting factors and possible clinical features of bleeding or thrombosis or both. It may be produced by activation of coagulation, platelet aggregation or endothelial damage. It is not a primary disease, but a common and important complication of many serious illnesses, especially sepsis, carcinoma and obstetrical accidents. Shock and acidosis are frequent precipitating factors, and vitamin K deficiency is a common complicating factor. DIC usually produces no clinical features, but it may give rise to bleeding, ischemic organ damage or shock. Although its clinical contribution is often difficult to separate from that due to the underlying disease, DIC remains the commonest cause of a generalized bleeding tendency in acutely sick patients. Laboratory confirmation consists of the demonstration of thrombocytopenia, coagulation impairment, hypofibrinogenamia, raised levels of fibrin degradation products, and positive results of para-coagulation tests. The most important therapeutic measure is control of the underlying disease, but replacement therapy and heparin may be required, especially if bleeding is significant and the process is not acute and self-limited.
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PMID:Disseminated intravascular coagulation. 107 54

Factors associated with prolongation of the prothrombin time were analyzed in 94 patients with intra-abdominal sepsis. Patients were randomized prospectively to receive either the combination of tobramycin and clindamycin (TM/C) or moxalactam (MOX). This paper presents a retrospective review designed to compare the frequency of prolonged clotting times and to analyze predisposing factors. Prothrombin time (PT) prolongation occurred more frequently in patients given moxalactam (19 of 47 patients) than in patients given the combination of tobramycin and clindamycin (9 of 47 patients) (p less than 0.05). Prolongation of the partial thromboplastin time (PTT) occurred in all patients with a prolonged PT. Liver disease, upper gastrointestinal surgery, and use of cimetidine were more frequent in those patients with abnormal PT/PTT values (p less than 0.05). Two moxalactam-treated patients with subsequent PT/PTT prolongation had individual clotting factors assayed before moxalactam treatment and at the time of detection of the abnormal PT. The activity of clotting factors II, VII, VIII, IX, X, and XII was reduced during MOX therapy. Treatment with vitamin K reversed the abnormality. In view of underlying abnormalities and rapid response to parenteral vitamin K, the mechanism is probably an acute vitamin K deficiency superimposed upon chronic vitamin K deficiency. In patients with intra-abdominal infection, those treated with MOX are more likely to develop abnormal PT than those treated with TM/C. Since abnormal PT/PTT was common even in TM/C patients, supplemental vitamin K should be considered for all seriously ill, older patients with abdominal infections.
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PMID:Clinical risk factors for prolonged PT/PTT in abdominal sepsis patients treated with moxalactam or tobramycin plus clindamycin. 396 31

Although moxalactam is not, technically speaking, a cephalosporin it is chemically and microbiologically so closely related to those compounds that it can be viewed as a member of the cephalosporin family. Moxalactam has a spectrum of activity that includes both gram positive and gram negative bacteria. Its gram positive activity is less than earlier cephalosporins, but its activity against the Enterobacteriaceae is similar to that of the aminoglycoside family of antibiotics in most comparative studies. Although moxalactam is considerably less active against gram positive bacteria than cefotaxime, another third generation cephalosporin, its higher and more prolonged serum levels probably offset this disadvantage. Compared to cefoperazone, the stability of moxalactam to many types of beta lactamases produced by gram negative bacteria may be advantageous in the therapy of infections caused by hospital-acquired pathogens. Clinical studies suggest that moxalactam can be used for empiric therapy of suspected gram negative infections when Pseudomonas and other non-fermentative bacteria, such as Acinetobacter, are not suspected. Impressive improvements in the survival of patients with gram negative enteric bacillary meningitis have been reported. Although moxalactam, cefotaxime, and cefoperazone have activity against Pseudomonas aeruginosa, none of these antibiotics should be used alone as therapy for suspected or proven severe systemic infections caused by this pathogen. Cost is a major problem with all of the new cephalosporin-like antibiotics. While this high cost may be partially balanced by the use of a single agent compared to an antibiotic combination for therapy in some situations, these antibiotics are not cost effective for prophylactic use. Superinfection with fungi, such as Candida, and Streptococcus faecalis have occurred, and toxicities, such as bleeding due to vitamin K deficiency and disulfuram-like reactions, have also been reported. Reports of resistance to moxalactam and the other third generation cephalosporins are of major concern and indicate the need to closely monitor antibiotic susceptibility patterns of hospital acquired organisms if these antibiotics are to be used for empiric therapy of suspected gram negative non-pseudomonas sepsis.
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PMID:A comparative evaluation of moxalactam: antimicrobial activity, pharmacokinetics, adverse reactions, and clinical efficacy. 622 Dec 37

Latamoxef (LMOX) was used in the treatment and prophylaxis of infections in neonates and immature infants. The following results were obtained. Mean serum concentrations (bioassay) 30 minutes after a single intravenous injection of about 20 mg/kg of LMOX were 49.9 mcg/ml in neonates and 47.3 mcg/ml in immature infants aged 0--3 days, 54.1 mcg/ml in neonates and 60.6 mcg/ml in immature infants aged 4--7 days, 48.9 mcg/ml in neonates and 46.7 mcg/ml in immature infants aged 8--28 days and 62.1 mcg/ml in immature infants aged over 29 days. Six-hour values were 24.1 mcg/ml, 22.5 mcg/ml, 15.9 mcg/ml, 27.2 mcg/ml, 12.9 mcg/ml, 19.1 mcg/ml and 12.8 mcg/ml, respectively. Mean serum concentration half-lives were 6.70 hours in neonates and 8.16 hours in immature infants aged 0--3 days, 3.68 hours in neonates and 5.83 hours in immature infants aged 4--7 days, 3.06 hours in neonates and 4.47 hours in immature infants aged 8--28 days and 2.59 hours in immature infants aged over 29 days. Adequate clinical efficacy can be expected by the intravenous injection of LMOX in doses of 20 mg/kg 1--2 times daily, in neonates and immature infants aged 0--3 days, 20 mg/kg 2--3 times daily, in neonates and immature infants aged 4--7 days and 20 mg/kg 3 times daily, in neonates and immature infants aged 8--28 days. The clinical efficacy of LMOX was good in 5 cases of sepsis (including suspected cases), 5 cases of urinary tract infection, 2 cases of respiratory tract infection and 6 cases of intrauterine infection (including suspected cases). Only a case of respiratory tract infections due to P. aeruginosa was thought to be ineffective. Bleeding tendency was noted in 3 cases, which results from secondary vitamin K deficiency should be checked carefully during the administration of LMOX.
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PMID:[Experimental and clinical evaluation of latamoxef in newborn and premature infants]. 665 50

The protein C pathway has an important function in regulating and modulating blood coagulation and ensuring patency of the microcirculation. Protein C deficiency leads to macro- or microvascular thrombosis. Hereditary severe protein C deficiency is a life-threatening state with neonatal purpura fulminans. Patients with heterozygous protein C deficiency have an increased risk for thromboembolic events or coumarin-induced skin necrosis. Secondary protein C deficiency occurs during disseminated intravascular coagulation (DIC), sepsis (especially meningococcal sepsis with purpura fulminans), liver failure and vitamin K deficiency. Replacement with protein C concentrates is an established treatment for congenital protein C deficiency. The high-purity, plasma-derived protein C concentrate Ceprotin (Baxter AG, Vienna, Austria) is approved for this indication, but its use in acquired deficiency states is not approved. Several case series demonstrated beneficial effects in infectious purpura fulminans and DIC, but no controlled studies for these indications exist. Protein C concentrate may therefore be given off-label in such cases. Protein C concentrate has an excellent safety profile: no drug interactions, overdose or bloodborne infections, bleeding or prothrombotic complications have been observed. As with all protein preparations, a potential risk of hypersensitivity reactions exists.
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PMID:Human protein C concentrates for replacement therapy in congenital and acquired protein C deficiency. 1859 97

Bleeding in the neonates may be a result of thrombocytopenia, sepsis or vitamin K deficiency. Congenital bleeding disorders are a rare cause of bleeding. The umbilical cord bleed is an important clue to underlying bleeding disorders especially factor XIII deficiency and afibrinogenemia. In some laboratories, the routine workup for the bleeding neonate may not always include fibrinogen assays, which may then delay this diagnosis. We report a case of congenital afibrinogenemia in a neonate who presented with umbilical stump bleeding for its rarity and to re-emphasize the need for including fibrinogen assays while assessing a bleeding neonate.
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PMID:Congenital afibrinogenemia in a new born: a rare cause for bleeding. 2450 33