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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The first pyrethroid pesticide, allethrin, was identified in 1949. Allethrin and other pyrethroids with a basic cyclopropane carboxylic ester structure are type I pyrethroids. The insecticidal activity of these synthetic pyrethroids was enhanced further by the addition of a cyano group to give alpha-cyano (type II) pyrethroids, such as cypermethrin. The finding of insecticidal activity in a group of phenylacetic 3-phenoxybenzyl esters, which lacked the cyclopropane ring but contained the alpha-cyano group (and hence were type II pyrethroids) led to the development of fenvalerate and related compounds. All pyrethroids can exist as at least four stereoisomers, each with different biological activities. They are marketed as racemic mixtures or as single isomers. In commercial formulations, the activity of pyrethroids is usually enhanced by the addition of a synergist such as piperonyl butoxide, which inhibits metabolic degradation of the active ingredient. Pyrethroids are used widely as insecticides both in the home and commercially, and in medicine for the topical treatment of scabies and headlice. In tropical countries mosquito nets are commonly soaked in solutions of deltamethrin as part of antimalarial strategies. Pyrethroids are some 2250 times more toxic to insects than mammals because insects have increased sodium channel sensitivity, smaller body size and lower body temperature. In addition, mammals are protected by poor dermal absorption and rapid metabolism to non-toxic metabolites. The mechanisms by which pyrethroids alone are toxic are complex and become more complicated when they are co-formulated with either piperonyl butoxide or an organophosphorus insecticide, or both, as these compounds inhibit pyrethroid metabolism. The main effects of pyrethroids are on sodium and chloride channels. Pyrethroids modify the gating characteristics of voltage-sensitive sodium channels to delay their closure. A protracted sodium influx (referred to as a sodium 'tail current') ensues which, if it is sufficiently large and/or long, lowers the action potential threshold and causes repetitive firing; this may be the mechanism causing paraesthesiae. At high pyrethroid concentrations, the sodium tail current may be sufficiently great to prevent further action potential generation and 'conduction block' ensues. Only low pyrethroid concentrations are necessary to modify sensory neurone function. Type II pyrethroids also decrease chloride currents through voltage-dependent chloride channels and this action probably contributes the most to the features of poisoning with type II pyrethroids. At relatively high concentrations, pyrethroids can also act on GABA-gated chloride channels, which may be responsible for the seizures seen with severe type II poisoning. Despite their extensive world-wide use, there are relatively few reports of human pyrethroid poisoning. Less than ten deaths have been reported from ingestion or following occupational exposure. Occupationally, the main route of pyrethroid absorption is through the skin. Inhalation is much less important but increases when pyrethroids are used in confined spaces. The main adverse effect of dermal exposure is paraesthesiae, presumably due to hyperactivity of cutaneous sensory nerve fibres. The face is affected most commonly and the paraesthesiae are exacerbated by sensory stimulation such as heat, sunlight, scratching, sweating or the application of water. Pyrethroid ingestion gives rise within minutes to a sore throat, nausea, vomiting and abdominal pain. There may be mouth ulceration, increased secretions and/or dysphagia. Systemic effects occur 4-48 hours after exposure. Dizziness, headache and fatigue are common, and palpitations, chest tightness and blurred vision less frequent. Coma and convulsions are the principal life-threatening features. Most patients recover within 6 days, although there were seven fatalities among 573 cases in one series and one among 48 cases in another. Management is supportive. As paraesthesiae usually resolve in 12-24 hours, specific treatment is not generally required, although topical application of dl-alpha tocopherol acetate (vitamin E) may reduce their severity.
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PMID:Poisoning due to pyrethroids. 1618 Sep 29

Reactions after bee or wasp sting are similar to anaphylaxis. Symptoms such as weakness, fatigue, vomiting, diarrhea, urticaria, and hypotension may occur. Serious toxic reactions usually occur after numerous stings. Massive bee envenomations can result in immediate onset of shock, hemolysis, rhabdomyolysis, disseminated intravascular coagulation (DIC), coma, and renal failure. In milder cases, patients may only have isolated prolonged activated partial thromboplastin time (aPTT) and normal prothrombin time (PT), clinically without a tendency to bleed. As a rule, they recover spontaneously without any complication. We report three cases of wasp stings; they all manifested prolongation of aPTT and finally recovered completely. Isolated prolongation of aPTT in cases of wasp stings may be related to an extract from the venom inhibiting the coagulation pathway.
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PMID:Isolated prolongation of activated partial thromboplastin time following wasp sting. 1623 65

Nonketotic hyperosmolar coma (NHC) is characterized by severe hyperglycemia; absence of, or only slight ketosis; nonketotic acidosis; severe dehydration; depressed sensorium or frank coma; and various neurologic signs. This condition is uncommon in type 1 diabetes. Because of little or no osmotic diuresis in patients with diabetic nephropathy, increases in plasma osmolality and therefore the likelihood of neurologic symptoms are limited. A 20-year-old male patient with type 1 diabetes with chronic kidney disease on conservative treatment (glomerular filtration rate [GFR], 18 mL/dk) presented with acute nonketotic hyperosmolar syndrome. The patient was admitted presenting with thirst, fatigue, and drowsiness. Blood biochemistry levels were urea 87 mg/dL, creatinine 5.09 mg/dL, glucose 830 mg/dL, glycosylated hemoglobin (HbA1c) 8%, C peptide <0.3 ng/mL, sodium 131 mmol/L, chloride 93 mmol/L, potassium 5.2 mmol/L, and calculated serum osmolality 385 mOsm/kg. The presumptive diagnosis on admission was nonketotic hyperosmolar syndrome precipitated by urinary infection. This is the first case report of hyperosmolar coma in a patient with type 1 diabetes with chronic kidney disease.
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PMID:Nonketotic hyperosmolar coma in a patient with type 1 diabetes-related diabetic nephropathy: case report. 1641 50

A case of acute intoxication involving lidocaine and chlorpheniramine (an antihistamine) in a 13-month-old child after ingestion of a commercial topical agent is presented. The major toxic reaction consisted of convulsion, coma, tachycardia, fever, and fatigue. This report shows that parents and physicians should be made aware of the hazards of lidocaine and overdose of other topical agents in infants and children.
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PMID:Acute intoxication of lidocaine and chlorpheniramine: report of one case. 1664 43

Hyponatremia is often associated with arginine vasopressin (AVP) dysregulation that is regulated by the hypothalamo-neurohypophyseal tract in response to changes in plasma osmolality, commonly in patients with the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Potentially lethal complications of hyponatremia most frequently involve the central nervous system and include anorexia, fatigue, lethargy, delirium, seizures, hypothermia and coma, and require prompt treatment. Chronic hyponatremia also complicates patient care and is associated with increased morbidity and mortality, particularly among patients with congestive heart failure. Conventional treatments for hyponatremia (e.g. fluid restriction, diuretic treatment, and sodium replacement) may not be effective in all patients and can lead to significant adverse events. Preclinical and clinical trial results have shown that AVP receptor antagonism is a promising approach to the treatment of hyponatremia that directly addresses the effects of increased AVP and consequent decreased aquaresis, the electrolyte-sparing excretion of free water. Agents that antagonize V(2) receptors promote aquaresis and can lead to increased serum sodium. Dual-receptor antagonism, in which both V(2) and V(1A) receptors are blocked, may provide additional benefits in patients with hyponatremia.
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PMID:Hyponatremia, arginine vasopressin dysregulation, and vasopressin receptor antagonism. 1717 May 24

Encephalopathy is a potentially fatal toxicity of ifosfamide. Clinical manifestations of encephalopathy range from fatigue and confusion to coma and death. Early identification of this toxicity and prompt cessation of ifosfamide are the essential elements in the management of ifosfamide encephalopathy. Accurate prediction of this toxicity is often difficult. Based on the limited available evidence, methylene blue, an electron acceptor, may have a role in the treatment and the prevention of neurotoxicity. This paper reviews the current understanding of ifosfamide encephalopathy.
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PMID:Ifosfamide encephalopathy. 1735 5

Primary HIV infection (PHI) is symptomatic in 50-90% of patients. The diagnosis, however, is seldom made at first presentation. This is probably because of the multifaceted and unspecific manifestations, the omission to perform adequate diagnostic testing and the failure to assess risks for PHI. Meningoencephalitis has been described as a fairly common presenting condition in PHI, with nuchal rigidity, fatigue, photophobia and headache; therefore, PHI should be considered in the differential diagnosis of aseptic meningitis. We present the case of a man with acute coma and a presumptive diagnosis of viral encephalitis in whom serological testing showed HIV encephalitis during PHI.
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PMID:Coma as a presenting symptom of primary HIV infection. 1743 51

Traumatic penetrations of foreign objects into the craniocerebral cavity are often encountered in the department of emergency and traumatology. A 5-year-old child was brought to the department of pediatric neurosurgery with a severe headache and fatigue. On admission, the patient had initial neurologic examinations and radiologic scans. The consciousness assessment by Glasgow Coma Scale was 13. Neuroradiologic studies revealed a long hyperdense object extending from the extracranial cavity into the middle cranial fossa. A thorough history was obtained with attention to how and when the injury was sustained. Two weeks before the incident, the child had a blunt trauma of mandibular fractures with dislocation of the temporomandibular joint. Maxillomandibular surgery was performed with a Kirschner's knitting needle to fixate the temporomandibular articulation and simple interdental ligatures for mandibular fracture stabilization. The present radiologic film suggested that the mandibular fracture was not properly fixated allowing the mobilization of Kirschner's needle moving either externally or internally. A standard pterional access with frontotemporosphenoidal approach was performed according to the method of Yasargil and Oikawa-Miyazawa followed by an extradural approach method of Dolenc to the middle cranial structure at the skull base. Several stages of hemostasis were carried out with electrohemocoagulation on the penetrated Kirschner's needle during the needle extracting process at the extradural space of the middle cranial fossa. Two weeks postoperatively, computed tomography scan revealed the supratentorial and middle craniocerebral structures were in symmetric localization. The patient was free of neurologic deficits with no signs of excessive cerebrospinal fluid volume formation. In conclusion, the method of fixation requires appropriate application techniques to ensure adequate fracture fixation during the healing cascade. The neurosurgical approach also requires a specific measure on its management and rehabilitation for the maintenance of such a patient.
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PMID:Iatrogenic traumatic brain injury: penetration of Kirschner's knitting needle into the middle cranial cavity. 1753 37

The rosuvastatin inducing rhabdomyolysis in McArdle disease (MD) has not been reported to date. A 35-years-old man had exercise intolerance, muscular fatigue and cramps during physical activity since infancy. He presented severe rhabdomyolysis episode with seizure and coma after use of rosuvastatin. The investigation showed increased serum creatine-kinase levels and the forearm ischemic exercise did not increase venous lactate. The muscle biopsy showed subsarcolemmal and central accumulation of glycogen and absence of the myophosphorylase enzyme. The statin induced myopathy is discussed and the danger of its use in MD is emphasized.
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PMID:McArdle disease with rhabdomyolysis induced by rosuvastatin: case report. 1795 91

In 1892 Osler described 'rapid loss of flesh' in prolonged sepsis. Thereafter, for years, limb weakness was attributed to cachectic myopathy, and difficulty weaning from mechanical ventilation was attributed to diaphragmatic fatigue. In 1961 Mertens described 'coma-polyneuropathies', and in 1971 Henderson and colleagues described polyneuropathy in patients with burns. In 1984 Bolton and colleagues, in a series of reports, defined the clinical, electrophysiological and morphological features of septic encephalopathy and critical illness polyneuropathy. Evidence suggested that polyneuropathy was due to the 'toxic' effects of sepsis. Polyneuropathy was a common cause of difficulty in weaning when lung and cardiac cause had been excluded. Since 1984, cases of critical illness polyneuropathy have been reported from several countries. Moreover, a number of investigators reported instances of critical illness myopathy. Comprehensive studies by Latronico and colleagues indicated that polyneuropathy and myopathy often occurred together in the same patient. With successful treatment of sepsis, improvement often occurred in encephalopathy, polyneuropathy and myopathy, except in very severe cases.
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PMID:The discovery of critical illness polyneuropathy. 1828 19


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