Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A subject is conscious when he is awake and with an adequate awareness of him and the environment. The term alteration of consciousness requires specification as to whether it defines alteration of arousal--when the patient might be confused, in a stupor or in some degree of coma (light, deep)--or alteration of awareness--that is, confused (spatio-temporally disoriented, with difficulty in maintaining his attention), with or without delirious ideation. The coma, in the strict sense, originates from structural (neurological) or functional (metabolic) dysfunction of the ascending reticular activator system, but it is accepted that it can derive also from diffuse bi-hemispheric cortical-subcortical damage. In the emergency department the starting point is the triad of situations that requires immediate treatment applying the normal protocol (ABC); next, pathologies involving risk to life, which might cause cerebral hypoxia, are ruled out: diminished cardiac output, shock and respiratory failure. Subsequently, a neurological evaluation is made, bearing in mind two situations of potential gravity: endocranial hypertension and diseases that might cause respiratory failure due to muscular fatigue. Neurological exploration will specify the respiratory, pupil and ocular patterns and motor responses. The depth of the coma is established through scales; a simplification of Jouvet's scale is proposed. The etiological diagnosis will on occasion require image tests and lumbar puncture.
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PMID:[Patients with alteration of consciousness in the emergency department]. 1852 46

Carbon monoxide (CO) is a colorless, odorless, nonirritating gas that is produced through the incomplete combustion of hydrocarbons. Sources of CO include combustion devices (e.g., boilers and furnaces), motor-vehicle exhaust, generators and other gasoline or diesel-powered engines, gas space heaters, woodstoves, gas stoves, fireplaces, tobacco smoke, and various occupational sources. CO poisoning is a leading cause of unintentional poisoning deaths in the United States; it was responsible for approximately 450 deaths each year during 1999-2004 and an estimated 15,200 emergency department (ED) visits each year during 2001-2003. Health effects of CO exposure can range from viral-like symptoms (e.g., fatigue, dizziness, headache, confusion, and nausea) to more severe conditions (e.g., disorientation, unconsciousness, long-term neurologic disabilities, coma, cardiorespiratory failure, and death). CO poisoning often is misdiagnosed and underdetected because of the nonspecific nature of symptoms. To update a previously published report and provide national estimates of CO-related ED visits during 2004-2006, CDC analyzed data from the National Electronic Injury Surveillance System--All Injury Program (NEISS-AIP) database. During 2004-2006, an estimated average of 20,636 ED visits for nonfatal, unintentional, non-fire-related CO exposures occurred each year. Approximately 73% of these exposures occurred in homes, and 41% occurred during winter months (December-February). Prevention efforts targeting residential and seasonal CO exposures can substantially reduce CO-related morbidity.
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PMID:Nonfatal, unintentional, non--fire-related carbon monoxide exposures--United States, 2004-2006. 1871 81

Tiagabine hydrochloride (TGB) is a selective gamma-aminobutyric acid (GABA) reuptake inhibitor. TGB is effective as an add-on medication in adults and children 12 years and older in the treatment of partial seizures. Results of nonrandomized add-on trials with TGB show treatment success with seizure reduction of at least 50% in 33% to 46% of patients. In newly diagnosed patients with partial epilepsy, TGB monotherapy was as effective as carbamazepine. Comedication with TGB elevates the risk of nonconvulsive status (7.8% vs 2.7% without TGB). The most common side effects include dizziness/lightheadedness, asthenia/lack of energy and somnolence. TGB has no negative effects on cognition; it does not increase the risk of fractures or rash. TGB may interfere with color perception. TGB presents an intermediate risk for depression in patients with epilepsy (approximately 4%). Regarding the risk of overdose, 96-680 mg TGB (mean 224 mg) caused seizures or coma. TGB is an antiepileptic drug exhibiting a specific anticonvulsive mechanism of action, the efficacy of which is relatively low when used in comedication. Critical side effects, such as the induction of nonconvulsive status epilepticus, further limit its use.
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PMID:Tiagabine: efficacy and safety in partial seizures - current status. 1904 17

The precise definition of a severe asthmatic exacerbation is an issue that presents difficulties. The term 'status asthmaticus' relates severity to outcome and has been used to define a severe asthmatic exacerbation that does not respond to and/or perilously delays the repetitive or continuous administration of short-acting inhaled beta(2)-adrenergic receptor agonists (SABA) in the emergency setting. However, a number of limitations exist concerning the quantification of unresponsiveness. Therefore, the term 'acute severe asthma' is widely used, relating severity mostly to a combination of the presenting signs and symptoms and the severity of the cardiorespiratory abnormalities observed, although it is well known that presentation does not foretell outcome. In an acute severe asthma episode, close observation plus aggressive administration of bronchodilators (SABAs plus ipratropium bromide via a nebulizer driven by oxygen) and oral or intravenous corticosteroids are necessary to arrest the progression to severe hypercapnic respiratory failure leading to a decrease in consciousness that requires intensive care unit (ICU) admission and, eventually, ventilatory support. Adjunctive therapies (intravenous magnesium sulfate and/or others) should be considered in order to avoid intubation. Management after admission to the hospital ward because of an incomplete response is similar. The decision to intubate is essentially based on clinical judgement. Although cardiac or respiratory arrest represents an absolute indication for intubation, the usual picture is that of a conscious patient struggling to breathe. Factors associated with the increased likelihood of intubation include exhaustion and fatigue despite maximal therapy, deteriorating mental status, refractory hypoxaemia, increasing hypercapnia, haemodynamic instability and impending coma or apnoea. To intubate, sedation is indicated in order to improve comfort, safety and patient-ventilator synchrony, while at the same time decrease oxygen consumption and carbon dioxide production. Benzodiazepines can be safely used for sedation of the asthmatic patient, but time to awakening after discontinuation is prolonged and difficult to predict. The most common alternative is propofol, which is attractive in patients with sudden-onset (near-fatal) asthma who may be eligible for extubation within a few hours, because it can be titrated rapidly to a deep sedation level and has rapid reversal after discontinuation; in addition, it possesses bronchodilatory properties. The addition of an opioid (fentanyl or remifentanil) administered by continuous infusion to benzodiazepines or propofol is often desirable in order to provide amnesia, sedation, analgesia and respiratory drive suppression. Acute severe asthma is characterized by severe pulmonary hyperinflation due to marked limitation of the expiratory flow. Therefore, the main objective of the initial ventilator management is 2-fold: to ensure adequate gas exchange and to prevent further hyperinflation and ventilator-associated lung injury. This may require hypoventilation of the patient and higher arterial carbon dioxide (PaCO(2)) levels and a more acidic pH. This does not apply to asthmatic patients intubated for cardiac or respiratory arrest. In this setting the post-anoxic brain oedema might demand more careful management of PaCO(2) levels to prevent further elevation of intracranial pressure and subsequent complications. Monitoring lung mechanics is of paramount importance for the safe ventilation of patients with status asthmaticus. The first line of specific pharmacological therapy in ventilated asthmatic patients remains bronchodilation with a SABA, typically salbutamol (albuterol). Administration techniques include nebulizers or metered-dose inhalers with spacers. Systemic corticosteroids are critical components of therapy and should be administered to all ventilated patients, although the dose of systemic corticosteroids in mechanically ventilated asthmatic patients remains controversial. Anticholinergics, inhaled corticosteroids, leukotriene receptor antagonists and methylxanthines offer little benefit, and clinical data favouring their use are lacking. In conclusion, expertise, perseverance, judicious decisions and practice of evidence-based medicine are of paramount importance for successful outcomes for patients with acute severe asthma.
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PMID:Acute severe asthma: new approaches to assessment and treatment. 1991 54

This study describes the profile of 100 cases of diabetic ketoacidosis (DKA) at a teaching hospital in 1 Benghazi, Libyan Arab Jamahiriya. DKA was more frequent in young women with type 1 diabetes and mostly due to preventable causes, e.g., disrupted insulin treatment and/or infection. DKA also occurred in type 2 diabetics, with a higher mortality rate, as they were older patients with co-morbidity. Polyurea, fatigue, abdominal pain and vomiting were the most common clinical features, while coma was rarer. A high number of cases were first presentations of type 1 diabetes; hence this diagnosis should be considered in all patients with acute abdomen or decreased level of consciousness. The reasons for high mortality rate in this study (10%) were multifactorial.
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PMID:Profile of diabetic ketoacidosis at a teaching hospital in Benghazi, Libyan Arab Jamahiriya. 2079 43

We report a case of a 46-year-old female demonstrating general fatigue and visual disturbances with retinal bleeding. She had a white blood cell count of 419,300/mm. Thereafter, she developed vomiting associated with vertigo caused by cerebellar hemorrhage, deteriorating to acute hydrocephalus secondary to obstruction of the cerebral aqueduct. Emergency procedures for cerebral protection, such as hyperventilation, administration of mannitol, and barbiturate coma, were performed. Bone marrow examination showed a positive BCR-ABL/t(9;22)(q34;q11) chromosomal translocation detected by FISH and RT-PCR (masked Ph) and she was diagnosed as having chronic myeloid leukemia (CML) in the chronic phase (CP). She was administered Ara-C, together with imatinib 600 mg/d through a nasogastric tube. Eight days later, she underwent successful extubation and recovered without any neurological defect. She was maintained on imatinib 400 mg/d and demonstrated a major molecular response at 15 months. Physicians need to be aware that brain hemorrhage may develop as an initial symptom of CML patients in CP.
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PMID:[Chronic myeloid leukemia complicated with cerebellar hemorrhage and acute hydrocephalus successfully treated with imatinib and intensive supportive care]. 2125 87

Central nervous system (CNS) toxicity has been reported in approximately 10-30% of patients receiving intravenous infusions of ifosfamide. Encephalopathy is a rare but serious CNS adverse reaction in these patients, and although usually transient and reversible, may cause persistent neurological dysfunction or death. Clinical features range from fatigue and confusion to coma and death. Although methylene blue can be used to treat ifosfamide-induced neurotoxicity, including encephalopathy, its mechanism of action remains poorly defined. We describe here two patients with recurrent epithelial ovarian cancer who experienced fatal encephalopathy following ifosfamide/mesna treatment.
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PMID:Fatal Ifosfamide-induced metabolic encephalopathy in patients with recurrent epithelial ovarian cancer: report of two cases. 2224 13

Hyponatremia can be defined like the low sodium concentration, lower that 135 mmol/l. It becomes really serious when the concentration is lower than 120 mmol/l. The most frequent causes of hyponatremia are: the extrarenal loss (GIT, skin, bleeding, sequestration), the renal loss (diuretics, nephritis with the salt loss, osmotical diuresis, the Addison disease), hypothyroidism, the lack of glucocorticoids, emotional stress, pain, pseudohyponatremia (incorrect taking, dyslipoproteinemia). There is fatigue, exhaustion, headache and vertigoes dominating in the clinical record file. By the deficit increasing a patient becomes delirious, comatose even with the shock development. It is necessary to separate sufficient supply of sodium from much more often reason, which is loss of sodium which can be caused by: excessive sweating, vomitting with the metabolical alkalosis development, diarrhoea with the metabolical acidosis development, renal losses (a phase of renal failure). Treatment of hyponatremia: intensive treatment starts at the level of plasmatic concentration of sodium under 120 mmol/l or when neurological symptoms of brain oedema are present. In the therapy it is necessary to avoid fast infusions of hypertonic saline solutions (3-5% NaCl solutions) because of the danger of the development of serious CNS complications (intracranial bleeding, etc.). It is recommended to adjust the plasmatic concentration of sodium up to 120 mmol/l during the first four hours and a subsequent correction should not be higher than 2 mmol per an hour. Treatment of the basic illness is very important. We present 2 case histories: a 74-year old female patient and a 69-year old female patient both with the hyponatremia caused by taking of carbamazepine. We want to inform and warn about not only a well known side effect during long-term treatment but about hyponatremia that arose within 48 hours after the start of taking medicine as well.
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PMID:[Hyponatremia - carbamazepine medication complications]. 2244 5

We report two patients having hyperammonemic encephalopathy while being treated with chemotherapy for colorectal cancer. The first patient was a 69-year-old man with sigmoid colon cancer, having a massive invasion to the urinary bladder. He received SOX therapy following a pelvic exenteration operation. After the third course of SOX therapy, he presented with general fatigue and repeated seizures, and blood examination showed a high level of serum ammonium. He was diagnosed as hyperammonemic encephalopathy. The second patients was a 60-year-old woman with ascending colon cancer and liver metastasis having portal vein tumor thrombosis, who was given a palliative resection of ascending colon, and then underwent modified FOLFOX6 therapy. At the second course, she fell into a deep coma, and blood examination revealed a high level of serum ammonium. In both patients, treatment with infusion of branched-chain amino acid solutions resolved the symptoms of encephalopathy. Acute neurotoxicity caused by hyperammonemic encephalopathy during chemotherapy for colorectal cancer is rare and not well recognized, but it is a clinically important complication. We should pay more attention to hyperammonemic encephalopathy of patients receiving chemotherapy for colorectal cancer.
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PMID:[Two cases of hyperammonemic patients treated by chemotherapy for colorectal cancer]. 2258 45

Sheehan's syndrome, first described in 1937, is characterised by postpartum haemorrhage, pituitary necrosis, lactational failure and hypopitutarism. Presentation is variable and late presentations are not unusual due to partial ischaemic injury of the pituitary and gradual loss of endocrine function. A history of postpartum haemorrhage is usual but in some cases it is not elicited. Presentations such as malaise, fatigue, hypoglycaemia, decline in cognition, hyponatraemia, pancytopoenia, osteoporosis, secondary infertility, confusion and coma have all been reported. Two interesting cases of Sheehan's syndrome are presented that were diagnosed in the eighth decade; one due to atypical presentation of recurrent hyponatraemia and confusion, another from hypoglycaemic coma and symptoms of malaise and lethargy.
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PMID:Practice of symptomatic treatment in the era of evidence-based medicine: report of 2 cases of diagnosis of Sheehan's syndrome delayed till eighth decade. 2273 28


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