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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the 27 years, 1951--1977, 4315 babies weighing over 1 kg were born alive in Newcastle suffering from haemolytic disease of the newborn due to Rhesus isoimmunization; 197 (4.5 per cent) died within four weeks of delivery. Many babies with severe anaemia (cord Hb less than or equal to 8 g/dl) died of cerebral and/or pulmonary haemorrhage as a result of coagulation failure; others with hydrops had a chance of recovery with intensive care as long as there was no associated pulmonary hypoplasia. Hyaline membrane disease was no more common in babies with haemolytic disease than in other preterm babies of comparable birthweight, but incorrect assessment of gestational age prior to the induction of labour increased the risk of death from hyaline membrane disease. The introduction of closed chest cardiac massage virtually eliminated the risk of sudden unexpected death during exchange transfusion but there was still a 1.5 per cent chance of sudden circulatory collapse during exchange transfusion. Affected babies of less than 36 weeks gestation with respiratory problems face a substantial risk of kernicterus when the indirect serum bilirubin level exceeds 270 mumol/l (15 mg/100 ml). The establishment of a single referral centre for Rhesus isoimmunization reduced neonatal mortality in the area to half the national average in the early 1950's and this superiority was maintained throughout the next decade.
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PMID:Neonatal death in babies with rhesus isoimmunization. 11

Magnesium-deficient fetuses exhibited malformations (44%), anemia, and edema. Maternal plasma magnesium levels at day 21 of pregnancy reflected the level of dietary magnesium (2.43 +/- 0.09 mg Mg/100 ml, control; 0.74 +/- 0.02 mg Mg/100 ml, deficient). Plasma magnesium levels of deficient fetuses showed similar decreases although all fetal magnesium values at term were hihger than maternal values from the same group (3.29 +/- 0.22 mg Mg/100 ml, control; 1.78 +/- 0.07 mg Mg/100 ml, deficient). Magnesium deficiency did not appear to affect the maternal blood parameters. However, when fetal blood was examined, all of the parameters measured were altered in magnesum-deficient fetuses (Table 2). No abnormalities in hemoglobin bands or plasma proteins were seen between any groups by electrophoresis. Measurement of total protein contents showed no differences between maternal blood protein contents, but total plasma protein from magnesium-deficient fetuses was significantly lower than controls (2.00 +/- 0.14 versus 2.62 +/- 0.13 g/100 ml), thus establishing a factor in fetal edema production. Morphologic data showed that in magnesium-deficient fetuses, fetal erythropoiesis was significantly greater in liver, adrenal glands, and spleen than in controls and that maturation was normoblastic. Stained and unstained peripheral blood smears of magnesium-deficient fetuses showed and obvious macrocytosis and at least 50% of the red cells stained abnormally, exhibiting pale areas. Erythrocytic morphology seen in fetal magnesium deficiency is consistent with inadequate filling of the cell by hemoglobin as suggested by Cohlan et al. (5), a probable cause of membrane collapse. The inadequate filling of magnesium-deficient red blood cells (RBC) with hemoglobin might be explained by a reduction in hemoglobin synthesis which is consistent with the reduced mean corpuscular hemoglobin (MCH) and MCH concentration (MCHC) of the deficient fetal red cells. The role of magnesium in protein synthesis is also compatible with a reduction in hemoglobin synthesis, yet may not completely explain the abnormalities and resultant shortened lifespan of the red cells.
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PMID:Magnesium deficiency anemia in the rat fetus. 86 20

The long term administration of dimethylhydrazine to mice induces severe hepatotoxic damage. Parenchymal cell pleomorphism and necrosis were later associated with reticulin collapse and bile duct proliferation. Withdrawing the drug after 17 weeks was followed by some improvement in the parenchymal cells but there was a chronic proliferative response tending towards early cirrhotic changes. The rats appeared relatively resistant to the hepatotoxic effects but unlike the mice the colon tumors arising in these animals bled frequently and could result in profound anemia.
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PMID:Chronic hepatotoxicity and intestinal bleeding in 1,2-dimethylhydrazine carcinogenesis in rats and mice. 108 70

Epidural hematomas in infancy, meaning up until the closing of the cranial sutures, have special clinical manifestations and courses; four cases will be demonstrated here. Following an often mild cranio-cerebral trauma a characteristical subperiosteal hematoma lacking primary consciousness disturbance and free interval can develop. The considerable loss of blood coming from the epidural hemorrhage, of mainly venous origin, leads to an often extreme anemia and shock syndrome. Due to the combination of shock and increasing brain compression a fulminant course with sudden coma, respiratory failure and irreversible circulatory collapse can terminally occur. Thus one should always think of an epidural hematoma in cases of increasing anemia, shock syndrome and an extending cranial hematoma following a brain trauma in infancy. Rapid trepanation with shock therapy and accompaning blood transfusion allows the prognosis of the epidural hemorrhage in infancy to be essentially better than in adulthood.
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PMID:[Special features of epidural hematoma in neonates and infants (author's transl)]. 123 59

The authors report a series of 33 hematomas of the recti-abdominis muscles from a surgery department: 15 occurred under anticoagulants 6 were spontaneous, 5 followed trauma and 6 a surgical procedure. The clinical picture was subacute in 24 cases, combining an abdominal pain (32 cases) a mass (10 cases) and an extensive ecchymosis (6 cases). The picture was acute in 6 extensive hematomas with collapse and anemia. In 3 cases an isolated mass was the first symptom. Echography has represented, since 1977, a decisive advance in the diagnosis, which was found to be accurate in 5 out of 10 cases before its introduction, and in 19 out of 20 when it was resorted to in the 23 cases recorded later. TDM is useful only in few cases. 23 patients were have been operated on: 6 for cardiovascular collapse, 3 because the diagnosis had not been made, 8 on order to confirm the diagnosis, 3 because of an increase in size of the hematoma and 3 owing to infection. In the 10 cases not submitted to surgery, the evolution was favourable. The therapeutic approach must be lanced according to the patient's condition, the size, side effect and evolution of hematoma. The aim of the operation is to evacuate the hematoma, to drain it and sometimes to tie up the bleeding vessel.
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PMID:[33 cases of hematoma of the rectus abdominis muscle in a surgical department]. 215 12

It is sometimes necessary for the practitioner to transfuse the ruminant with whole blood or plasma. These techniques are often difficult to perform in practice and are time-consuming, expensive, and stressful to the animal. Acute loss of 20-25% of the blood volume will result in marked clinical signs of anemia, including tachycardia and maniacal behavior. The PCV is only a useful tool with which to monitor acute blood loss after intravascular equilibration with other fluid compartments has occurred. An acutely developing PCV of 15% or less may require transfusion. Chronic anemia with PCV of 7-12% can be tolerated without transfusion if the animal is not stressed and no further decline in erythrocyte mass occurs. Seventy-five per cent of transfused bovine erythrocytes are destroyed within 48 hours of transfusion. A transfusion rate of 10-20 ml/kg, recipient weight, is necessary to result in any appreciable increase in PCV. A nonpregnant donor can contribute 10-15 ml of blood/kg body weight at 2-4 week intervals. Sodium citrate is an effective anticoagulant, but acid citrate dextrose should be used if blood is to be stored for more than a few hours. Blood should not be stored more than 2 weeks prior to administration. Heparin is an unsuitable anticoagulant because the quantity of heparin required for clot-free blood collection will lead to coagulation defects in the recipient. Blood crossmatching is only rarely performed in the ruminant. In field situations, it is advisable to inject 200 ml of donor blood into the adult recipient and wait 10 minutes. If no reaction occurs, the rest of the blood can probably be safely administered as long as volume overload problems do not develop. Adverse reactions are most commonly seen in very young animals or pregnant cattle. Signs of blood or plasma transfusion reaction include hiccoughing, tachycardia, tachypnea, sweating, muscle tremors, pruritus, salivation, cough, dyspnea, fever, lacrimation, hematuria, hemoglobinuria, collapse, apnea, and opisthotonos. Intravenous epinephrine HCl 1:1000 can be administered (0.2 to 0.5 ml) intravenously or (4 to 5 ml) intramuscularly if clinical signs are severe. Pretreatment with antipyretics and slowing the administration rate may decrease the febrile response. Blood or plasma administered too rapidly will also result in signs of cardiovascular overload, acute heart failure, and pulmonary hypertension and edema. Furosemide and slower administration of blood or plasma should alleviate this problem.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Use of blood and blood products. 217 38

Primary hypoadrenocorticism was diagnosed in ten young to middle-aged cats of mixed breeding. Five of the cats were male, and five were female. Historic signs included lethargy (n = 10), anorexia (n = 10), weight loss (n = 9), vomiting (n = 4), and polyuria (n = 3). Dehydration (n = 9), hypothermia (n = 8), prolonged capillary refill time (n = 5), weak pulse (n = 5), collapse (n = 3), and sinus bradycardia (n = 2) were found on physical examination. Results of initial laboratory tests revealed anemia (n = 3), absolute lymphocytosis (n = 2), absolute eosinophilia (n = 1), and azotemia and hyperphosphatemia (n = 10). Serum electrolyte changes included hyponatremia (n = 10), hyperkalemia (n = 9), hypochloremia (n = 9), and hypercalcemia (n = 1). The diagnosis of primary adrenocortical insufficiency was established on the basis of results of adrenocorticotropic hormone (ACTH) stimulation tests (n = 10) and endogenous plasma ACTH determinations (n = 7). Initial therapy for hypoadrenocorticism included intravenous administration of 0.9% saline and dexamethasone and intramuscular administration of desoxycorticosterone acetate in oil. Three cats were euthanatized shortly after diagnosis because of poor clinical response. Results of necropsy examination were unremarkable except for complete destruction of both adrenal cortices. Seven cats were treated chronically with oral prednisone or intramuscular methylprednisolone acetate for glucocorticoid supplementation and with oral fludrocortisone acetate or intramuscular injections of repository desoxycorticosterone pivalate for mineralocorticoid replacement. One cat died after 47 days of therapy from unknown causes; the other six cats are still alive and well after 3 to 70 months of treatment.
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PMID:Primary hypoadrenocorticism in ten cats. 246 93

In the treatment of severe Plasmodium falciparum infection antimalarial drugs should, ideally, be given by controlled rate intravenous infusion until the patient is able to swallow tablets. In cases where infection has been acquired in a chloroquine resistant area, and where it has broken through chloroquine prophylaxis or where the geographical origin or species are uncertain, quinine is the treatment of choice. When access to parenteral quinine is likely to be delayed, parenteral quinidine is an effective alternative. A loading dose of quinine is recommended in order to achieve therapeutic plasma concentrations as quickly as possible. In the case of chloroquine sensitive P. falciparum infection, chloroquine, which can be given safely by slow intravenous infusion, may be more rapidly effective and has fewer toxic effects than quinine. There is limited experience with parenteral administration of pyrimethamine sulphonamide combinations such as Fansidar, and resistance to these drugs has developed in South East Asia and elsewhere. Mefloquine and halofantrine cannot be given parenterally. Qinghaosu derivatives are not readily available and have not been adequately tested outside China. Supportive treatment includes the prevention or early detection and treatment of complications, strict attention to fluid balance, provision of adequate nursing for unconscious patients and avoidance of harmful ancillary treatments. Anaemia is inevitable and out of proportion to detectable parasitaemia. Hypotension and shock ('algid malaria') are often attributable to secondary gram-negative septicaemia requiring appropriate antimicrobial therapy and haemodynamic resuscitation. Many patients with severe falciparum malaria are hypovolaemic on admission to hospital and require cautious fluid replacement. Failure to rehydrate these patients may lead to circulatory collapse, lactic acidosis, renal failure and severe hyponatraemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of severe malaria. 269 26

The authors have followed 140 patients with sickle cell disease anemia (101 cases) or related hemoglobinopathies (39 cases). Among them hip involvement was noted in 55 (104 hips). Forty three times the hip involvement occurred in childhood and twelve times in adult life. When the necrosis appeared in childhood (84 hips) the average age was twelve. The deformity involved the femoral head (coxa plana, coxa magna) as well as the neck (short neck, coxa vara). After an average follow-up of nineteen years, clinical and radiological examinations evidenced 64 functional impairments and 25 arthrosis, 10 of which have already been operated on. The necrosis appearing during adult life (20 hips) had the same outcome as idiopathic necroses, leading rapidly to arthrosis after collapse of the sequestrum. It seems that the etiology of the necroses is linked to rheologic disorders, the deformity of the red cells causing arteriolar thromboses. In this series the hip disease was correlated with sickle cell retinopathy as defined after angiography. On the contrary there was no correlation with the severity of anemia, its treatment, the ethnical origin of the patient.
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PMID:[Natural history of hip necrosis in sickle cell disease. Apropos of 104 necroses]. 269 46

Pathophysiological significance of hypoxia in malarial infection was investigated in mice infected with Plasmodium berghei NK65. Intraperitoneal inoculation of mice with 1 X 10(7) parasitized red blood cells resulted in death of the hosts 6-7 days later. Anaemia of infected animals developed on day 4 after inoculation and oxygen affinity of whole blood, measured as P50 act pH, increased simultaneously. This change may be a physiological adaptive response to a reduction in oxygen delivery to the tissues to day 5. However, the blood oxygen supply on day 6 appeared to be deteriorating and this is thought to be an important factor contributing to the death of the host. The value of adenylate energy charge in red cells during malarial infection, however, was comparatively well-maintained. Allopurinol stimulated the multiplication of malaria parasites and seems to have induced collapse in host-parasite balance more rapidly. Decrease in blood pH and in blood oxygen transport may be important factors for the pathogenesis of the allopurinol-treated hosts.
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PMID:Pathophysiology of hypoxia in mice infected with Plasmodium berghei. 330 17


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