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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute respiratory distress syndrome (ARDS) is the result of severe injuries of different etiologies of the capillary system in patients with previously healthy lungs, resulting in noncardiogenic pulmonary edema. The authors studied 42 infants in whom the histopathologic aspects were suggestive for ARDS. The etiologic factors of this syndrome were: severe gastroenteritis with hypovolemic or endotoxic shock (13 cases), sepsis (9 cases), fulminans purpura (2 cases), severe neurological disorders (13 cases), pulmonary infections (5 cases). In such conditions, if the infant presents hyperpnea followed by generalised cyanosis, refractory to oxygen therapy, and if there are clinical and radiologic signs of acute pulmonary edema, the diagnosis of ARDS must be considered and a complete intensive care therapy is compulsory in order to alleviate the severe prognosis of this syndrome.
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PMID:Etiological, clinical and pathomorphological aspects of acute respiratory distress syndrome in children. 1075 53

Canadian Food Inspection Agency (CFIA) has adopted the term cyanosis to describe a category of condemnation for poultry that is dark but has no other condemnable lesions. Two case-control studies (n = 30 pairs; n = 65 pairs) of 18-wk-old tom turkeys were conducted. A case was defined as a carcass condemned by the veterinary inspector for cyanosis, and a control carcass was one that passed inspection. Microbiological tests were conducted on samples of Pectoralis major and Gastrocnemius lacteralis. A modified Rappaport Vassiliadis medium was used for Salmonella, and a Petrifilm method was used to assess aerobic counts, coliform counts, and Escherichia coli. The Salmonella (qualitative) test was negative for all cases and controls, and there were no significant differences between the aerobic counts, coliform counts, and E. coli counts of case and control carcasses. Two pathologists conducted a blind histopathological study: there were no lesions compatible with those of septicemia-toxemia, as defined by CFIA and the USDA, nor any significant histopathological differences between the skin, P. major, G. lateralis, kidney, liver, spleen, small intestine, pancreas, lung, and heart of cases and controls. The inter-rater agreement between pathologists ranged from good to excellent (Kappa = 0.7 to 1.0). In the absence of important lesions and microbial contamination, carcasses with this color change alone should be suitable for human consumption.
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PMID:Bacteriological and histological profile of turkeys condemned for cyanosis. 1094 91

Heart disease in infants and children may often lead to rapid decompensation. Early recognition by the primary physician is essential, since modern medicine and surgery can cure many heart defects. Main clinical signs are cyanosis, heart failure and/or abnormal auscultatory findings. Cyanosis appears shortly after birth or in small infants. In the newborn, cyanosis due to heart disease must be differentiated from pulmonary problems, sepsis or persistent pulmonary hypertension. Heart failure occurs more often in non cyanotic heart defects, mainly with left to right shunts. The main symptoms and signs of heart failure in the infant are briefly discussed. Abnormal auscultatory findings, usually murmurs, are the most common reason for referral to the paediatric cardiologist. However, most murmurs are "innocent" or "functional"; clues to their recognition are given. The present short review should help the primary physician to recognize signs of heart defects in infants and children so as to proceed with timely referral to the specialist.
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PMID:[Indications for pediatric cardiology evaluation]. 1123 52

Necrotizing cellulitis and fasciitis may be difficult to recognize. When skin necrosis is not obvious, the diagnosis must be suspected if there are signs of severe sepsis (accelerated heart or respiratory rates, oliguria, mental confusion.) and/or some of the following local symptoms or signs: severe spontaneous pain, indurated edema, bullae, cyanosis, skin pallor, absence of lymphangitis, skin hypoesthesia, crepitation, muscle weakness, foul smell of exudates. Many risk factors are suspected. A recent case-control study demonstrated that using ibuprofen increased the risk of cellulitis complicating chickenpox in children. Evidence is lower for other risk factors that are present with a high prevalence in most series: local lesion of skin or mucous membranes (acute or chronic disease, traumatism, surgery.), diabetes, arteriopathy, alcoholism, obesity, immunosuppression, NSAIDs. The risk of streptococcal necrotizing fasciitis is increased when in contact with patients infected by the same streptococcus.
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PMID:[Necrotizing fasciitis. Clinical criteria and risk factors]. 1131 68

This is a study of the venous gangrene of lower extremities and Staphylococcus aureus sepsis. We report on a premature infant who developed phlegmasia cerulea dolens (PCD) in both lower extremities in association with S. aureus sepsis, resulting in gangrene of the right foot. Non-pitting edema and cyanosis of the digits of the right lower extremity were noted 48 hours after hypotension and severe shock due to S. aureus sepsis. Intravenous antibiotics, isotonic fluids, and heparin were administered. Twenty-four hours later, edema and ischemic changes of the first and fifth left toes were also noted. Doppler flow study showed flow signals in both right and left popliteal arteries. However, there were no Doppler signals in neither right nor left popliteal vein. Emergency fasciotomies were performed on both lower limbs. The progression of the gangrene was limited to the right foot. There was complete resolution of PCD in both lower extremities. To the best of our knowledge, the association of S. aureus sepsis with PCD and venous gangrene in an infant has not been reported previously. This case illustrates the need for early recognition of PCD and aggressive intervention.
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PMID:Venous gangrene of lower extremities and Staphylococcus aureus sepsis. 1132 61

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.
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PMID:Severe lactic acidosis and thiamine administration in an HIV-infected patient on HAART. 1136 26

Transfusion-related acute lung injury (TRALI) is a second most serious complication of the blood transfusion. It is a group of symptoms and signs such as dyspnoea, hypotension, cyanosis, cough, elevated temperature, fever and lung oedema that usually develops within an hour or two after transfusion. The full stage clinical presentation is developed between 4th and 6th hours after transfusion. The syndrome is caused by leucoagglutinins or by other lymphocytotoxic antibodies specific for some antigens present on the donor's leukocytes. Alveoles of the lung are the main place of the pathological changes such as intra-alveolar oedema, haemorrhage, hyaline membrane formation, alveolar cell hypertrophy and scant interstitial inflammation. Chest X-ray showed bilateral pulmonary infiltrates but without vascular congestion and with normal cardiac silhouette comparing to the status before transfusion. The syndrome has to be distinquished from pulmonary oedema caused by acute cardial insufficiency, overhydration, trauma and sepsis.
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PMID:[Acute lung injury related to blood transfusion]. 1143 32

Health workers should assess all children with a cough or difficult breathing for pneumonia. They should refer any child with severe pneumonia to a hospital for admission. At the hospital, a distinction is usually made between severe or very severe pneumonia among children 2 months to 5 years old. Signs or symptoms unique to very severe pneumonia are cyanosis and inability to drink. If a child has these signs and has convulsions, hospital personnel should consider a lumbar puncture to check for meningitis. Chest indrawing may also be present in very severe pneumonia cases. Chest indrawing in children with no cyanosis who are able to drink constitutes severe pneumonia. Health workers need to look for a variety of nonspecific signs of severe or very severe pneumonia in babies younger than 2 months: not feeding well, convulsions, abnormally sleepy, fever (38 degrees Celsius), fast breathing (=or+ 60 breast/minute), cyanosis, grunting, or apnea. These signs are also signs for meningitis or sepsis in young infants. Treatment for all 3 conditions is benzylpenicillin plus gentamicin for at least 14 days. Oxygen treatment is also indicated for these young infants. Treatment for both severe and very severe pneumonia cases includes oxygen and an antibiotic (benzylpenicillin and chloramphenicol, respectively). Hospitals should have in stock at all times essential antibiotics (benzylpenicillin, cloxacillin, chloramphenicol, and gentamicin) and an oxygen supply (oxygen cylinder or oxygen concentrator). When the oxygen supply is limited, children with very severe pneumonia should be the priority. Oxygen needs to be delivered at a flow rate of 1-2 liters/minute via nasal prongs or a nasal catheter. Admitted pneumonia cases with fever (39 degrees Celsius) should receive paracetamol to treat the fever. Hospital workers need to keep the airway of pneumonia cases clear and to encourage them to drink and/or breast feed.
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PMID:Managing pneumonia. 1229 68

Newborn infants may be transferred to a special care nursery because of conditions such as prematurity (gestation less than 37 weeks), prolonged resuscitation, respiratory distress, cyanosis, and jaundice, and for evaluation of neonatal sepsis. Newborn infants' core temperature should be kept above 36.4 degrees C (97.5 degrees F). Nutritional requirements are usually 100 to 120 kcal per kg per day to achieve an average weight gain of 150 to 200 g (5 to 7 oz) per week. Standard infant formulas containing 20 kcal per mL and maternal breast milk may be inadequate for premature infants, who require special formulas or fortifiers that provide a higher calorie content (up to 24 kcal per mL). Intravenous fluids should be given when infants are not being fed enterally, such as those with tachypnea greater than 60 breaths per minute. Hypoglycemia can be asymptomatic in large-for-gestational-age infants and infants of mothers who have diabetes. A hyperoxia test can be used to differentiate between pulmonary and cardiac causes of hypoxemia. The potential for neonatal sepsis increases with the presence of risk factors such as prolonged rupture of membranes and maternal colonization with group B streptococcus. Jaundice, especially on the first day of life, should be evaluated and treated. If the infant does not progressively improve in the special care nursery, transfer to a tertiary care unit may be necessary.
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PMID:Common issues in the care of sick neonates. 1244 67

Cyanosis is a physical finding that can occur at any age but presents the greatest challenge when it occurs in the newborn. The cause is multiple, and it usually represents an ominous sign, especially when it occurs in association with neonatal sepsis, cyanotic congenital heart disease, and airway abnormalities. Cyanosis caused by abnormal forms of hemoglobin can also be life-threatening, and early recognition is mandatory to prevent unnecessary investigations and delay in management. Abnormal hemoglobin, such as hemoglobin M, is traditionally discovered by electrophoresis, so the newborn screen, which is mandatory in several states, is a useful tool for the diagnosis. Although acquired methemoglobinemia, caused by environmental oxidizing agents, is common, congenital deficiency of the innate reducing enzyme is so rare that only a few cases are documented in the medical literature around the world. We present a neonate with cyanosis as a result of congenital deficiency of the reduced nicotinamide adenine dinucleotide-cytochrome b5 reductase enzyme. This infant was found to be blue at a routine newborn follow-up visit. Sepsis, structural congenital heart disease, prenatal administration, and ingestion of oxidant dyes were excluded as a cause of the cyanosis by history and appropriate tests. Chocolate discoloration of arterial blood provided a clue to the diagnosis. A normal newborn screen and hemoglobin electrophoresis made the diagnosis of hemoglobin M unlikely as the cause of the methemoglobinemia (Hb A 59.4%, A2 1.8%, and F 38.8%). Red blood cell enzyme activity and DNA analysis revealed a homozygous form of the cytochrome b5 reductase enzyme deficiency. He responded very well to daily methylene blue and ascorbic acid administration, and he has normal growth and developmental parameters, although he shows an exaggerated increase in his methemoglobin level with minor oxidant stress such as diarrhea.
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PMID:Congenital methemoglobinemia: a rare cause of cyanosis in the newborn--a case report. 1289 22


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