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

The injured brain may be damaged by primary impact, secondary injury from secondary damage due to initiation of destructive inflammatory and biochemical cascades by the primary injury or secondary ischemic injury following secondary insults that initiate or augment these immunological and biochemical cascades. Cerebral ischemia will arise whenever delivery of oxygen and substrates to the brain fall below metabolic needs. Many factors lead to the development of secondary insults to the injured brain during initial resuscitation, transport, surgery, and subsequent intensive care. Continuous monitoring of cerebral oxygenation (jugular oximetry, brain tissue PO2) and cerebral blood flow velocity (transcranial Doppler ultrasonography) in patients with brain trauma reveals multiple episodes of transient hypoperfusion with an adverse relationship between incidence and outcome. Secondary brain insults arise through systemic or intracranial mechanisms that reduce cerebral blood flow from compromised CPP, vascular distortion or cerebrovascular narrowing or lower oxygen delivery from hypoxemia associated with airway obstruction, pulmonary pathology, or anemia. Secondary brain ischemia remains a common pathway to secondary brain damage in most critically ill neurosurgical patients. In the future prevention of secondary brain injury may well hinge on giving a cocktail of novel agents that modify destructive biochemical and inflammatory pathways, each having a potential therapeutic window possibly in a subgroup of patients. To date, phase 3 clinical trials of several agents including PEGSOD and tyrilizad mesylate have failed to show relevant efficacy after brain trauma or subarachnoid hemorrhage. The therapeutic role of calcium channel blockers in traumatic subarachnoid hemorrhage is currently under investigation following the results of subgroup metaanalysis. Several phase 3, NMDA receptor antagonist studies are underway in brain trauma with results expected soon. Although we know that secondary insults promote excitotoxic secondary brain damage there is currently no pharmacological intervention with proven efficacy and, therefore, detection and correction of secondary insults appear to offer the best therapeutic strategy. After brain trauma, systemic hypotension, compromised CPP, raised ICP, elevated temperature, hypoxemia, and jugular bulb venous desaturation are associated with poor prognosis. Clinical trials of moderate hypothermia following brain trauma are ongoing. Following adult brain trauma maintenance of CPP above at least 65 mmHg (probably > 40 mmHg in children below 8 years) seems important to improve outcome indicating the need for continuous ICP monitoring during intensive care of brain-injured patients.
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PMID:Mechanisms and prevention of secondary brain damage during intensive care. 970 38

A 72-year-old patient presented himself with typical symptoms of coronary heart disease and was scheduled for invasive diagnostic procedures. Cardiac risk factors were smoking and arterial hypertension. The physical examination was inconspicious. In the laborchemistry a hemoglobin of 79 g/l with a mean corpuscular volume of 63 fl and a mean corpuscular hemoglobin of 20 pg was conspicuous. The serum iron was with 42 micrograms/dl in the lower norm. Transferrin, bili-rubin and lactate dehydrogenase were normal. Then in the gastrointestinal investigations he was diagnosed with a leiomyoma of the intestine that led to chronic anaemia and additionally to chest pain characteristic for angina pectoris. After the removal of the tumor and normalization of hemoglobin this patient was free from symptoms of the disease. The coronary angiography revealed a complex stenosis of the right coronary artery with collaterales and not significant stenosis both of the left coronary arteries. In patients with angina pectoris anaemia as the possible and only cause of angina ought to be verified. It is therefore necessary after normalization of hemoglobin and clarification of the cause for the anaemia to apply a test for coronary ischemia.
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PMID:[Angina pectoris in leiomyoma]. 975 77

Ballantyne syndrome is a condition in which the gravid patient essentially "mirrors" the in utero state of the hydropic fetus. The exact pathophysiological mechanism, however, is unclear. At 25 weeks gestation, a 28-year-old G3P2 presented with acute onset lower extremity edema, hyperuricemia, polyhydramnios, generalized pruritus, hemodilutional anemia, and pre-term labor. The human chorionic gonadotrophin (hCG) level was markedly elevated, at 570,020 mIU/ml. Postpartum, she developed a pre-eclampsia-like syndrome with oliguria and pulmonary effusions. Associated placental findings included a 8 x 7 x 7 cm chorangioma. Underlying placental ischemia, reflected by a hyperproliferative trophoblast, increased hCG secretion, and increased placental resistance may account for the maternal findings of Ballantyne syndrome.
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PMID:Ballantyne syndrome: is placental ischemia the etiology? 977 90

Optimal management of dyspnea in terminal cancer patients requires an understanding of the responsible pathophysiological mechanisms. This prospective study assessed visual analogue scales (VAS) of shortness of breath (SOB) and anxiety, bedside spirometry, maximum inspiratory pressure (MIP), chest radiography, arterial blood gases, hemoglobin, and electrocardiogram, if indicated, in 100 terminally ill cancer patients. Forty-nine percent of the patients had lung cancer. The median VAS scores for SOB and anxiety were 53 mm and 29 mm, respectively. Spirometry was abnormal in 93% of patients, with 5% having obstructive, 41% restrictive, and 47% mixed patterns. The median MIP was 16 cm H2O. Sixty-five percent of the patients had parenchymal or pleural involvement on chest radiograph. Twenty-nine percent had evidence of cardiac ischemia, recent or current myocardial infarction or atrial fibrillation. Patients had a median of five different abnormalities that could have contributed to their shortness of breath. Only anxiety (p = 0.001), a history of smoking (p = 0.02), and pCO2 levels were statistically significantly correlated with SOB VAS scores. The potentially correctable causes of dyspnea included hypoxia (40%), anemia (20%), and bronchospasm (52%). The finding of very low MIPs suggests severe respiratory muscle weakness may contribute significantly to dyspnea in this patient population. Further studies are needed to confirm this finding and characterize the underlying pathophysiology.
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PMID:Dyspnea in the advanced cancer patient. 1058 52

Thirty patients with neonatal acquired paraplegia without an identified cause were reviewed. The mean gestational age was 33 weeks (range, 25-40 weeks); the mean Apgar scores were 6 and 8 (range, 0-10); the mean weight at birth was 1.739 kg (range, 0.750-4.200 kg). Half of the infants needed neonatal intensive care for a mean period of 42 days. Fourteen (46%) had local or generalized infections, 12 (40%) had respiratory complications, and seven (22%) required mechanical ventilation. Seven (22%) had polycythemia, six (20%) had anemia, six (20%) underwent umbilical artery catheterization, and five (16%) received full exchange transfusion. Two clinical presentations were observed: flaccid (24 patients) and hypertonic (6 patients). The secondary deformities that were found and the orthopedic procedures to correct them are described. A vascular or intravascular change, such as thrombosis/embolism or ischemia/hypoxia by vasospasm or failure of autoregulation of spinal blood perfusion, is the final pathway of many events that may produce paraplegia in preterm and low birthweight neonates.
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PMID:Neonatal acquired paraplegia: retrospective review of 30 patients. 1021 64

A gene therapy strategy involving direct myocardial administration of an adenovirus (Ad) vector encoding the vascular endothelial growth factor 121 cDNA (Ad(GV)VEGF121.10) has been shown to be capable of "biological revascularization" of ischemic myocardium in an established porcine model [Mack, C.A. (1998). J. Thorac. Cardiovasc. Surg. 115, 168-177]. The present study evaluates the local and systemic safety of this therapy in this porcine ischemia model and in normal mice. Myocardial ischemia was induced in Yorkshire swine with an ameroid constrictor 21 days prior to vector administration. Ad(GV)VEGF121.10 (10(9) or 10(10) PFU), Ad5 wild type (10(9) PFU), AdNull (control vector with no transgene; 10(9) PFU), saline, or no injection (naive) was administered in 10 sites in the ischemic, circumflex distribution of the myocardium. Toxicity was assessed by survival, serial echocardiography, blood analyses, and myocardial and liver histology at 3 and 28 days after vector administration. All pigs survived to sacrifice, except for one animal in the Ad(GV)VEGF121.10 (10(10) PFU) group, which died as a result of oversedation. Echocardiograms of Ad(GV)VEGF121.10-treated pigs demonstrated no differences in pericardial effusion, mitral valve regurgitation, or regional wall motion compared with control pigs. Intramyocardial administration of Ad(GV)VEGF121.10 included only minimal myocardial inflammation and necrosis, and no hepatic inflammation or necrosis. Only a mild elevation of the white blood cell count was encountered on day 3, which was transient and self-limited in the Ad(GV)VEGF121.10 group as compared with the saline-treated animals. As a measure of inadvertent intravascular administration of vector, normal C57/BL6 mice received intravenous Ad(GV)VEGF121.10 (10(4), 10(6), 5 x 10(7), or 10(9) PFU), AdNull (5 x 10(7) or 10(9) PFU), or saline. Toxicity was assessed by survival, blood analyses, and organ histology at 3 and 7 days after vector administration. A separate group of C57/BL6 mice received intravenous AdmVEGF164 (Ad vector encoding the murine VEGF164 cDNA), Ad(GV)VEGF121.10, AdNull (10(8) PFU each group), or saline to assess duration of expression and safety of a homologous transgene. All mice survived to sacrifice except for 40% of the mice in the highest (10(9) PFU; a dose more than 10(3)-fold higher by body weight than the efficacious dose in pigs) Ad(GV)VEGF121.10 dose group, which died on days 5-6 after vector administration. The only differences seen in the blood analyses between treated and control mice were in the very high Ad(GV)VEGF121.10 dose group (10(9) PFU), which demonstrated an anemia as well as an increase in alkaline phosphatase when compared with all other treatment groups. Hepatic VEGF levels by ELISA in AdmVEGF164-treated mice did not persist beyond 14 days after vector administration, suggesting that persistent expression of a homologous VEGF gene transferred with an Ad vector is not a significant safety risk. Although this is not a chronic toxicity study, these data demonstrate the safety of direct myocardial administration of Ad(GV)VEGF121.10, and support the potential use of this strategy to treat human myocardial ischemia.
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PMID:Safety of direct myocardial administration of an adenovirus vector encoding vascular endothelial growth factor 121. 1036 64

Internists are frequently asked to do preoperative consultations and to manage perioperative complications. Realistic goals are to identify patient factors that increase the risk of surgery, to quantify this risk in order to make decisions about the appropriateness of and timing of the surgery, to provide recommendations on how to minimize the risk, to identify and manage coexisting medical conditions and their associated medication requirements, to monitor the patient for perioperative problems, and to make recommendations to deal with these problems when they occur. With few exceptions, nonselective imaging and laboratory screening tests have repeatedly been shown to be of little value when the history and physical do not suggest a problem. The risk associated with the planned surgery can be estimated, with the most common serious complications being cardiac events. Updated versions of Goldman's risk indices are particularly helpful for this. Clinical variables are optimally combined with selective stress testing to discern which patients will benefit from preoperative revascularization. This has been studied best in the setting of vascular surgery. A critical guiding principle is that the value of revascularization must be judged in terms of long term gains rather than just immediate perioperative benefit. Other interventions include the selective use of beta blockers, adequate analgesia for all, control of hypertension, and appropriate volume management, especially in the settings of preexisting CHF or valvular disease. It must also be recognized that perioperative ischemia and CHF often present atypically. An approach that combines aspects of both the ACC/AHA and the ACP guidelines seems optimal. A variety of noncardiac issues must also be addressed. Postoperative pulmonary complications are common, especially with preexisting pulmonary disease, thoracic and upper abdominal surgery, and obesity. PFTs and ABGs are indicated in selected patients. Stopping smoking, incentive spirometry, and selective use of bronchodilators and antibiotics are helpful. Patients with rheumatologic diseases have specific concerns based on systemic manifestations of disease including anemia, thrombocytopenia, pulmonary fibrosis, pericarditis, and hypercoagulability; medication effects particularly from steroids and nonsteroidal anti-inflammatory drugs; and specific joint problems including contractures and atlantoaxial joint instability. Diabetes increases the risk of infection and cardiac complications. Prevention of ketoacidosis and glucose control are necessary and can be achieved through a variety of approaches, depending on whether the patient suffers from Type 1 or Type 2 diabetes. The threshold for transfusion has increased in recent years, as has the use of erythropoietin and autologous blood donation. There is no longer an absolute hemoglobin that requires transfusion, although most require transfusion for hemoglobins less than 8 mg/dL, especially in the setting of cardiac disease and bloody surgery. The elderly require surgery at an increased rate and often do not do as well as younger patients. The primary issues are, however, not their age but their increased frequency of underlying disease and diminished reserve. The latter makes them prone to postoperative delirium, sensitivity to medications, and cardiac and pulmonary problems. Despite the many diseases that patients often have and the stresses of surgery itself, modern anesthetic and surgical techniques allow almost all patients to undergo necessary procedures at acceptable risk. The internist plays a critical role in minimizing this risk even further.
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PMID:Recognition and management of preoperative risk. 1046 30

Acute renal failure (ARF) can occur as a complication of cocaine abuse. We present a case of microangiopathic hemolytic anemia, ARF, and thrombocytopenia after inhalation of crack cocaine in a 38-year-old woman. Her renal failure ultimately required dialysis. She underwent renal biopsy because of persistent renal failure, hematuria, and thrombocytopenia. The biopsy findings consisted of thrombotic microangiopathy and glomerular ischemia. After treatment with fresh frozen plasma, her platelet count and bleeding resolved. The possible mechanisms involved in cocaine-induced thrombotic microangiopathy include: (1) endothelial injury, (2) vasoconstriction and/or impairment of vasodilatation, (3) procoagulant activity, and (4) antiplatelet activity. Although our patient survived after hemodialysis and transfusion of fresh frozen plasma, she continued to have residual renal insufficiency. One month later, the patient again used cocaine and presented with worsening ARF, anemia, and thrombocytopenia.
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PMID:Cocaine-induced acute renal failure, hemolysis, and thrombocytopenia mimicking thrombotic thrombocytopenic purpura. 1062 May 64

Despite the unicity of its genetic mutation, Sickle cell homozygosity presents different clinical features. Our objectives were to evaluate disease severity in Senegalese patients. Sixty (60) homozygous sickle cell patients were followed up monthly during one year and disease severity was assessed using the "severity index" (SI) which is resulting from epidemiologic, clinic and biological data. Mean age was 20.13, sex ratio was 0.87 and mean age of diagnosis was 9.8 years. 90% of patients presented vaso-occlusive crisis (2.53 per patient), 73.3% had infectious episodes (1.9 per patient), 69.3% had never been transfused and 25% of patients had presented chronic complications linked to anemia or ischemia. Mean hemoglobin value was 8.1 g/dl and mean Hb F was 8.2%. Low seric ferritin was found in 1.7% of patients. Benign form of homozygous sickle cell anemia (SI< or =6) was found in 48.3% of patients. Our data confirm the relative good tolerance of homozygous sickle cell disease in Senegal. The haplotype Senegal may play an important role but others host and environmental factors operate certainly because some severe cases were identified in our patients. The identification of all these factors might contribute to a better follow up of sickle cell disease.
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PMID:New results in clinical severity of homozygous sickle cell anemia, in Dakar, Senegal. 1065 Nov 22

Sickle cell anemia and the related hemoglobinopathies are associated with a large spectrum of renal abnormalities. The patients have impaired urinary concentrating ability, defects in urinary acidification and potassium excretion, and supranormal proximal tubular function. The latter is manifest by increased secretion of creatinine and by reabsorption of phosphorus and beta(2)-microglobulin. Young patients with sickle cell disease (SCD) have supranormal renal hemodynamics with elevations in both effective renal plasma flow (ERPF) and glomerular filtration rate (GFR). These parameters decrease with age as well as following the administration of prostaglandin inhibitors. Proteinuria, a common finding in adults with sickle cell disease, may progress to the nephrotic syndrome. Proteinuria, hypertension, and increasing anemia predict end-stage renal disease (ESRD). While ESRD can be managed by dialysis and/or renal transplantation, there may be an increased rate of complications in renal transplant recipients with SCD. Hematuria is seen in individuals with all of the SCDs as well as with sickle cell trait. In most cases the etiology of the hematuria turns out to be benign. However, there does appear to be an increased association between SCD and renal medullary carcinoma. Therefore, those SCD patients who present with hematuria should initially undergo a thorough evaluation in order to exclude this aggressive neoplasm. Papillary necrosis may occur due to medullary ischemia and infarction. Erythropoietin levels are usually lower than expected for their degree of anemia and decrease further as renal function deteriorates. An abnormal balance of renal prostaglandins may be responsible for some of the changes in sickle cell nephropathy. Acute renal failure is a component of the acute multiorgan failure syndrome (MOFS). Finally, progression of sickle cell nephropathy to ESRD may be slowed by adequate control of hypertension and proteinuria. However, the prevention of the renal complications of SCD will require a cure for this genetic disorder.
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PMID:Renal abnormalities in sickle cell disease. 1142 1


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