RESUMO
Thyroid storm is a rare but well-known life-threatening complication that occurs due to acute exacerbation of thyrotoxicosis with the increased levels of circulating thyroid hormones. Reports of metabolic encephalopathy associated with thyroid storm are scarce. We describe the case of a 23-year-old male patient with no previous history of abnormal thyroid function who had consumed excessive amounts of alcohol before disease onset. The patient was found unconscious and febrile on a roadside by a passerby and was admitted to our hospital's emergency department. His primary clinical presentation included hyperthermia (40.8 °C), nodal tachycardia (180 beats/min), seizures, coma, and hypoglycemia (2.18 mmol/L). The hypoglycemia was quickly corrected after admission, but his level of consciousness showed no improvement. With aggressive screening, the patient was found to have severe thyroid dysfunction (T3 = 6.67 nmol/L, T4 = 252.00 nmol/L, free T3 = 29.20 pmol/L, free T4 = 65.30 pmol/L, and TSH = 0.001 µIU/mL). After medical treatment, plasmapheresis, hemofiltration, and hemoperfusion, the patient showed substantial improvement in thyroid hormone levels and stabilization of vital signs, but the impaired consciousness and seizures persisted. Multiple computed tomography scans revealed brain abnormalities. Magnetic resonance imaging performed after tracheal extubation revealed bilateral frontal lobe lesions. We reported a case of metabolic encephalopathy in a patient with life-threatening thyroid storm and bilateral frontal lobe lesions. Hypoglycemia may have been involved in the development of encephalopathy in our patient. Health care providers should consider thyroid storm in the differential diagnosis of hyperthermia, seizures, and coma. Early plasmapheresis, hemofiltration, and hemoperfusion can lower T4 levels and improve prognosis in patients with thyroid storm and encephalopathy.
Assuntos
Lobo Frontal , Crise Tireóidea , Humanos , Masculino , Crise Tireóidea/complicações , Adulto Jovem , Lobo Frontal/diagnóstico por imagem , Imageamento por Ressonância Magnética , Encefalopatias/etiologiaRESUMO
SUMMARY Thyroid storm is a rare but well-known life-threatening complication that occurs due to acute exacerbation of thyrotoxicosis with the increased levels of circulating thyroid hormones. Reports of metabolic encephalopathy associated with thyroid storm are scarce. We describe the case of a 23-year-old male patient with no previous history of abnormal thyroid function who had consumed excessive amounts of alcohol before disease onset. The patient was found unconscious and febrile on a roadside by a passerby and was admitted to our hospital's emergency department. His primary clinical presentation included hyperthermia (40.8 °C), nodal tachycardia (180 beats/min), seizures, coma, and hypoglycemia (2.18 mmol/L). The hypoglycemia was quickly corrected after admission, but his level of consciousness showed no improvement. With aggressive screening, the patient was found to have severe thyroid dysfunction (T3 = 6.67 nmol/L, T4 = 252.00 nmol/L, free T3 = 29.20 pmol/L, free T4 = 65.30 pmol/L, and TSH = 0.001 μIU/mL). After medical treatment, plasmapheresis, hemofiltration, and hemoperfusion, the patient showed substantial improvement in thyroid hormone levels and stabilization of vital signs, but the impaired consciousness and seizures persisted. Multiple computed tomography scans revealed brain abnormalities. Magnetic resonance imaging performed after tracheal extubation revealed bilateral frontal lobe lesions. We reported a case of metabolic encephalopathy in a patient with life-threatening thyroid storm and bilateral frontal lobe lesions. Hypoglycemia may have been involved in the development of encephalopathy in our patient. Health care providers should consider thyroid storm in the differential diagnosis of hyperthermia, seizures, and coma. Early plasmapheresis, hemofiltration, and hemoperfusion can lower T4 levels and improve prognosis in patients with thyroid storm and encephalopathy.
RESUMO
BACKGROUND: Acute pesticide poisoning is a major public health problem in the world. Most pesticides are toxic to human beings, because of diverse components resulting in different reaction. OBJECTIVE: As clinicians identify various symptoms due to pesticide poisoning, it is necessary for the diagnosis and treatment for treating such toxins. Accidents associated with acute avermectins poisoning are rarely reported, especially self-induced nystagmus. In the present study, a case of human abamectin poisoning with relevant toxic effects has been reported. CONCLUSIONS: Acute avermectins poisoning-induced nystagmus may be affected due to the vestibular cerebellar system, but the exact mechanism and pharmacological basis is still worthy of further study.
Assuntos
Ivermectina/análogos & derivados , Nistagmo Patológico/induzido quimicamente , China , Humanos , Ivermectina/intoxicação , Masculino , Pessoa de Meia-IdadeRESUMO
OBJECTIVE: To evaluate the effect of dexmedetomidine on outcomes following craniocerebral operation and provide evidence for individualized medication. METHODS: We searched the Cochrane Library, PubMed, Springer, CNKI, Wanfang Data Resource and other Chinese and foreign databases with electronic retrieval, within the period 1990-2013, for records relating to dexmedetomidine, brain pharmacokinetics and clinical randomized controlled studies. Records were assessed using the Cochrane system evaluation method for assessing the quality of research, using Revman 5.1 Meta-analysis software. RESULTS: After screening and removal of duplicate documents there were 22 English and 44 Chinese articles, among which there were eight describing clinical trials, with a total of 412 cases. Meta-analysis showed that dexmedetomidine on rate during craniocerebral operation (standardized mean difference=-8.32, 95% confidence interval [CI] -10.38 to 6.26, P<0.00001), and blood pressure (standardized mean difference=-3.37, 95% CI -5.36 to 1.38, P<0.00001). The study had good heterogeneity using random effects model analysis, and there was no publication bias. CONCLUSION: Dexmedetomidine can reduce the hemodynamic response and play a role in brain protection.
Assuntos
Analgésicos não Narcóticos/uso terapêutico , Encefalopatias/tratamento farmacológico , Dexmedetomidina/uso terapêutico , Hemodinâmica/efeitos dos fármacos , Encefalopatias/cirurgia , Humanos , Neurocirurgia/métodos , Resultado do TratamentoRESUMO
BACKGROUND: The traditional Chinese medicine Praeruptorin c (Pra-c) has many physiological and pharmacological effects, including antagonistic effects on blood pressure and calcium levels, maintenance of cellular calcium homeostasis, and improved cardiac systolic and diastolic function. It is potentially a novel and versatile drug for the treatment and prevention of cardiovascular diseases. OBJECTIVE: To explore the possible impact of Pra-c on blood pressure in SHR and its mechanism of action. MATERIALS AND METHODS: Twenty SHR were randomly divided into a Pra-c group [Pra-c was administered intragastrically, 20 mg kg(-1) d(-1), n=10] or an untreated control group (n=10), containing 10 age-matched SD rats. Each group of rats was followed for 8 weeks. Before and during the treatment, tail artery systolic blood pressure was measured using a tail-cuff every 2 weeks. After 8 weeks, the rats were sacrificed and RNA was extracted from homogenates of cardiac tissue. Tissue from the left ventricle was fixed, sectioned and H&E stained to assess possible changes in myocardial cell structure and morphology. Semi-quantitative RT-PCR was used to assess changes in phospholamban gene expression in treated and untreated rats. RESULTS: SHR treated with Pra-c for 8 weeks had a lower systolic pressure than untreated SHR (p<0.05), two measures of cardiac damage, the heart mass index and left ventricle mass index (HMI and LVMI, respectively) were improved, and the level of PLB mRNA expression was lower in the untreated SHR group (p<0.05). DISCUSSION AND CONCLUSION: With continuous hypertension, SHR gradually formed or developed cardiac hypertrophy and fibrosis. Pra-c had a clear effect on blood pressure in SHR, and reversed SHR ventricular remodeling by upregulating the gene expression of sarcoplasmic reticulum PLB.