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 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hereditary galactosemia is a biochemical genetic disease due to a deficiency of galactose-1-phosphate uridyltransferase (GALT) enzyme activity (OMIM 606999). Acute manifestations occur in the neonatal period and are, with rare exceptions, related to lactose ingestion. They include poor feeding and growth, emesis, jaundice, liver disease, bleeding diathesis, anemia, renal tubulopathy, cataracts, encephalopathy and death from E. coli sepsis. Chronic manifestations, which also develop in prospectively treated patients, involve (a) the brain, resulting in delayed language acquisition, speech defects, and learning problems, and (b) the ovary, in the majority of females, producing hypergonadotropic hypogonadism. The serum FSH level is elevated in infancy/early childhood in many, but not all patients with a severe phenotype. There are few reports of patients with classic galactosemia having undergone pregnancy, labor, and delivery. The pathologic findings in the ovary, including a persistence of primordial follicles and streak gonads, have been variable. The etiology of primary ovarian insufficiency (POI) in galactosemia is unknown. Clinical surveillance includes screening for abnormalities in ovarian function at an early age. Treatment consists of estrogen/progesterone supplementation at the appropriate age. Reduced BMD has been reported. Future research is needed (1) to delineate the mechanisms behind reduced ovarian function in these young women; (2) to determine the timing of the lesion: prenatal, postnatal, and both pre- and postnatal; (3) to determine whether elevated galactose-1-phosphate is both necessary and sufficient to induce primary ovarian insufficiency; and (4) to understand the mechanism(s) behind the reduced BMD seen in children and adolescents with galactosemia.
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PMID:Galactosemia and amenorrhea in the adolescent. 1857 15

In the last 20 years, in developed countries, maternal mortality rates have fallen such that analysis of cases of severe maternal morbidity is necessary to provide sufficient numbers to give a clinically relevant assessment of the standard of maternal care. Different approaches to the audit of severe maternal morbidity exist, and include need for intensive care, organ system dysfunction and clinically defined morbidities. In both developed and developing countries, the dominant causes of severe morbidity are obstetric haemorrhage and hypertensive disorders. In some low-resource regions, obstructed labour and sepsis remain significant causes of severe maternal morbidity. The death to severe morbidity ratio may reflect the standard of maternal care. Audits of severe maternal morbidity should be complementary to maternal mortality reviews.
Best Pract Res Clin Obstet Gynaecol 2008 Oct
PMID:Epidemiology of obstetric critical care. 1866 64

Infections in critically ill obstetric patients are observed worldwide, although the incidence, aetiology and patient outcome vary between geographic locations. This chapter focuses on sepsis, with emphasis on the pathophysiology, outcome and specific management issues.
Best Pract Res Clin Obstet Gynaecol 2008 Oct
PMID:Infection in obstetric critical care. 1869 41

Nosocomial hyperthermia (fever) occurs in about 30% of all medical patients at some time during their hospital stay. In patients admitted to the intensive care unit with severe sepsis the incidence of hyperthermia is greater than 90%, while in a specialized neurological critical care unit the incidence is reported as 47%. In contrast, hyperthermia during anaesthesia is rare owing to the impairment of thermoregulation by anaesthetic agents. This article is designed to give an overview on the various causes of hyperthermia with special emphasis on fever during general and regional anaesthesia in general and neurological critical care patients.
Best Pract Res Clin Anaesthesiol 2008 Dec
PMID:Hyperthermia during anaesthesia and intensive care unit stay. 1913 10

Disseminated intravascular coagulation (DIC) is a syndrome that may complicate a variety of diseases, including malignant disease. DIC is characterized by widespread, intravascular activation of coagulation (leading to intravascular fibrin deposition) and simultaneous consumption of coagulation factors and platelets (potentially resulting in bleeding). Clinically, DIC in cancer has, in general, a less fulminant presentation than the types of DIC complicating sepsis and trauma. A more gradual, but also more chronic, systemic activation of coagulation can proceed subclinically. Eventually, this process may lead to exhaustion of platelets and coagulation factors, and bleeding (e.g. at the site of the tumour) may be the first clinical symptom indicating the presence of DIC. In some cases, the clinical presentation of DIC in cancer may be reminiscent of thrombotic microangiopathies, which is understandable in view of the role of the endothelium in both conditions. The therapeutic cornerstone of DIC is treatment of the underlying disorder, but supportive treatment specifically aimed at the haemostatic system may be required.
Best Pract Res Clin Haematol 2009 Mar
PMID:Disseminated intravascular coagulation in cancer patients. 1928 79

Sepsis and/or acute blood loss can be encoutered as an emergency condition in gynaecology, especially in women with ectopic pregnancy/miscarriage, acute pelvic inflammatory disease (PID)/tuboovarian abscesses, post-puerperal sepsis/haemorrhage and even in postoperative scenarios. If underestimated or suboptimally treated, both can lead to an inadequate tissue perfusion (defined as shock) and the development of multi-organ failure. Morbidity and mortality after development of one of the shock syndromes (septic or haemorrhagic) correlates directly with the duration and severity of the malperfusion. The patient's prognosis depends on a prompt diagnosis of the presence of shock and immediate resuscitation to predefined physiological end-points, often before the cause of the shock has been identified. In septic shock, hypotension is primarily treated with fluid administration and eventually vasopressors, if required, in order to improve the circulation. Timely administration of antibiotics, control of infectious foci, appropriate use of corticoids and recombinant human activated protein C, tight glucose control, prophylaxis of deep vein thrombosis and stress ulcer prevention complete the therapy of septic shock. In haemorrhagic shock, the treatment primarily involves controlling haemorrhage, reversal of possible coagulopathy and administration of sufficient volumes of fluids and blood products to restore normal tissue perfusion.
Best Pract Res Clin Obstet Gynaecol 2009 Oct
PMID:Urgent care in gynaecology: resuscitation and management of sepsis and acute blood loss. 1959 11

Platelets are active metabolising cells that are evolved for the tasks of haemostasis, inflammatory reactions and wound healing. When platelet products are stored in the blood bank a complex series of changes occur, leading to partial activation, up-regulation of inflammatory mediators, cellular morphology changes, loss of cell membrane lipids and micro-particle formation, as well as apoptosis. The resultant coagulation transfusion product has a number of potential expected side effects including fever, alloimmunisation, sepsis, thrombosis and transfusion-related acute lung injury. Of course, these events are occasional side effects yet they are some of the most common potential disasters of transfusion. Platelet transfusions in patients bleeding from thrombocytopaenia or severe platelet suppression will most likely benefit from a platelet transfusion. However, outcome data (controversial) have shown in some populations that platelet transfusions are associated with worse patient outcomes. Such associations may be due to the biologic changes that have occurred during storage, lack of HLA matching as well as other causes or it could be a mismatch of the platelet products to patient's needs (over-use). Platelets are administered in the surgical arena often due to 'clinical judgement', which errs on the side of, perhaps, too frequent use.
Best Pract Res Clin Anaesthesiol 2010 Mar
PMID:Platelet transfusions: the science behind safety, risks and appropriate applications. 2040 71

Premature infants have immature respiratory control that predisposes them to apnoea, haemoglobin oxygen desaturation and bradycardia. Apnoeas are loosely classified, according to the presence or absence of respiratory effort, into central, obstructive or mixed. There are a variety of conditions, in the perioperative period, that predispose an infant to apnoea, including: central nervous system (CNS) lesions, infections and sepsis, ambient temperature fluctuations, cardiac abnormalities, metabolic derangements, anaemia, upper airway structural abnormalities, necrotising enterocolitis, drug administration (including opiates and general anaesthetics) and possibly gastro-oesophageal reflux. Various monitoring techniques are discussed; the mainstay are pulse oximetry and abdominal-pressure transduction. There is some evidence of both short- and long-term complications of repeated apnoeas in the neonatal period, but the causal relationship is difficult to establish. Continuous positive airway pressure and caffeine therapy (up to 10 mg kg(-1)) are the most common treatments of neonatal apnoea. The less soluble volatile agents and regional anaesthetic techniques (without concurrent sedation) are associated with a lower incident of postoperative apnoea.
Best Pract Res Clin Anaesthesiol 2010 Sep
PMID:Neonatal apnoea. 2103 10

Sepsis, a potentially life-threatening infection, is a common complication related to the use of central venous catheters (CVCs) in the preterm infant population. Best practice guidelines include successful strategies to prevent infections. Central venous catheter use is a fairly recent intervention in Finnish neonatal intensive care units (NICUs). As part of a quality improvement project to evaluate catheter-related care practices, 4 NICUs collaborated in a multicenter, multiprofessional study aimed at decreasing the incidence of catheter-related sepsis among a population of preterm infants. This article describes the initial phase that evaluated current protocols and practices. The findings were that current protocols need revision to include more detailed and accurately focused instructions on infection prevention associated with CVC. Many challenges in performing certain procedures with catheters were found. Precis CVC protocols and practices in 4 Finnish NICUs were reviewed for infection control measures.
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PMID:A multicentred clinical improvement project among preterm population evaluation of current practices. 2104 13

A central feature of the endocrine pathophysiology of septic shock is thought to be the existence of adrenal dysfunction. Based on changes in glucocorticoid secretion and responsiveness, protein binding, and activity. These changes have been described by the terms "Relative Adrenal Insufficiency" (RAI), or "Critical Illness Related Corticosteroid Insufficiency" (CIRCI), and form part of the rationale for trials of glucocorticoid treatment in septic shock. Diagnostic criteria for these conditions have been based on plasma cortisol profiles and have proven notoriously difficult to establish. The uncertainty in this area arises from the inability of current tests to clearly identify who is truly glucocorticoid "deficient" at a cellular level, and hence who requires supplemental glucocorticoid administration. Emerging data suggest that there may be abnormalities in the tissue activity of glucocorticoids in patients with severe sepsis and plasma profiles may not be reliable indicators of tissue glucocorticoid activity, We put forward an alternative point of view, that is the spectrum of adrenocortical dysfunction in sepsis - plasma and tissue, can be grouped under the umbrella of a "sick euadrenal syndrome" rather than an adrenocortical insufficiency.
Best Pract Res Clin Endocrinol Metab 2011 Oct
PMID:Adrenocortical (dys)function in septic shock - a sick euadrenal state. 2192 73


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