RESUMEN
AIMS: To investigate the relationship of unawareness of hypoglycemia with spectral analysis of heart rate variability (HRV) and clinical variables in type 1 diabetes (T1D) individuals. METHODS: Participants with type 1 diabetes mellitus (type 1 diabetes) were prospectively assessed for hypoglycemia awareness using the Pedersen-Bjergaard method and were classified as normal hypoglycemia awareness, impaired hypoglycemia awareness and hypoglycemia unawareness. Indices of HRV in frequency domain were evaluated and Ewing tests were used for the diagnosis of cardiovascular autonomic neuropathy (CAN). RESULTS: Ninety-eight participants with T1D (mean age 26â¯years, average diabetes duration 13â¯years, and mean HbA1c 8.4%) were included in this study. The prevalence of hypoglycemia unawareness was 28%. No significant difference was observed on the prevalence of CAN among groups of different hypoglycemia awareness (pâ¯=â¯0.740). On regression analyses, abnormal results of HRV in frequency domain were not associated with unawareness of hypoglycemia. On univariable regression analysis, age, diabetes duration and estimated creatinine clearance were associated with unawareness of hypoglycemia. CONCLUSION: CAN as assessed by Ewing tests and spectral analysis of HRV is not associated with unawareness of hypoglycemia. There is association of age, diabetes duration and renal deficit with unawareness of hypoglycemia.
Asunto(s)
Enfermedades del Sistema Nervioso Autónomo/diagnóstico , Concienciación , Diabetes Mellitus Tipo 1/complicaciones , Neuropatías Diabéticas/diagnóstico , Frecuencia Cardíaca/fisiología , Hipoglucemia/psicología , Adolescente , Adulto , Enfermedades del Sistema Nervioso Autónomo/etiología , Enfermedades del Sistema Nervioso Autónomo/psicología , Diabetes Mellitus Tipo 1/fisiopatología , Diabetes Mellitus Tipo 1/psicología , Neuropatías Diabéticas/etiología , Neuropatías Diabéticas/psicología , Femenino , Humanos , Hipoglucemia/diagnóstico , Hipoglucemia/etiología , Masculino , Persona de Mediana Edad , Estudios Prospectivos , Adulto JovenRESUMEN
JUSTIFICATIVA E OBJETIVOS: O infarto hepático é definido como necrose isquêmica do parênquima hepático envolvendo pelo menos dois ácinos. Trata-se de evento considerado raro devido ao duplo suprimento sangüíneo, arterial e venoso. O objetivo deste estudo foi relatar um caso de paciente não sabidamente diabética que desenvolveu extensas áreas isquêmicas de infarto hepático, após quadro de descompensação aguda da diabete. RELATO DO CASO: Paciente do sexo feminino, 67 anos, hipertensa, procurou o Pronto Socorro com queixas de polidipsia, poliúria, turvação visual, náuseas e vômitos, dificuldade para deambular, havia aproximadamente 10 dias. Ao exame físico foi observado desidratação, palidez cutânea, cianose periférica, hipotermia, taquicardia, hipotensão, dor abdominal leve e difusa. Exames laboratoriais mostraram: leucócitos: 16800, creatinina (Cr): 3,7, uréia (Ur): 167, Na: 133, K: 6.9, glicose: 561; gasometria arterial (cateter de oxigênio: 2 L/min): pH: 6.93, pCO2: 12.1, pO2: 107, BE: -28,8, HCO3: 2,4, Sat 91,3 por cento, lact: 79; urina I: pH: 6,0; leucócitos: 13; densidade: 1015; eritrócitos: 19; proteína: ++; glicose: +++; bilirrubina: negativa; corpos cetônicos: + denotando cetonemia. Eletrocardiograma com onda T apiculada, bloqueio de ramo direito. A paciente foi tratada com insulina, hidratação, bicarbonato de sódio e introduzido antibioticoterapia. Após o tratamento inicial, os exames laboratoriais mostraram: Cr: 2,2, Ur: 122, Na: 162, K: 4,3, Ca: 6,4, glicose: 504, pH: 7,01, HCO3: 7.1, BE: - 22. Um dia após, a paciente apresentou importante dor abdominal acompanhada de irritação peritoneal, além de sonolência e dificuldade para falar; exames laboratoriais mostraram: pH: 7,4, pCO2 : 31, pO2: 68, BE: -4,4, HCO3: 19, Sat.O2: 93,5 por cento; Ur: 95; Cr: 1,4, albumina: 2,4, Ca: 0,95, Na: 166, K:4, bilirrubina: 0,5, bilirrubina D/I: 0,2/0,3, amilase: 1157, Gama-GT: 56, AST 7.210, ALT: 2.470, VHS: 15, lipase: 84. Ultrasonografia abdominal...
BACKGROUND AND OBJECTIVES: Hepatic infarction is characterized by parenchyma ischemic necrosis involving at least two acinis. It is extremely uncommon due to the arterial and portal venous blood supply. We report a case of a patient not know to have diabetes who developed massive areas of ischemic infarcts of the liver after episode of acutely diabetes decompensated. CASE REPORT: A 67 year-old hypertensive female who has been presenting, for the last 10 days, polydipsia, high urinary volume, visual and gait impairment, nausea and vomiting was admitted to the emergency room (ER). During the physical examination it was observed dehydration, skin discoloration, peripheral cyanosis, hypothermia, tachycardia, hypotension and mild diffuse abdominal pain. Admissional laboratory exams demonstrated total leukocytes: 16.800, Cr: 3.7, Ur: 167, Na: 133, K: 6.9, glucose: 561; arterial gasometry (O2 catheter: 2 L/min): pH: 6.93, pCO2: 12.1, pO2: 107, B.E.: -28.8, HCO3: 2.4, Sat 91.3 percent, lactato: 79; urinalysis: pH: 6; leukocytes: 13; density: 1015; erythrocytes: 19; protein: ++; glucose: +++; bilirubin: negative; ketonic bodies: + denote ketonemia. EKG: sharp T wave, right branch block. Patient was treated with intravenous insulin, hydration, sodium bicarbonate and ceftriaxone. After initial treatment, the laboratory exams showed Cr: 2.2, Ur: 122, Na: 162, K: 4.3, Ca: 6.4, glucose: 504, pH: 7.01, HCO3: 7.1, B.E.: -22. One day after admission the patient presented with important abdominal pain and peritoneal irritation, followed by difficulty for talking and somnolence; routine laboratory exams showed arterial gasometry: pH: 7.4, pCO2: 31, pO2: 68, BE: -4.4, HCO3: 19, SatO2: 93.5 percent; Ur: 95,Cr: 1.4, albumin: 2.4, Ca: 0.95, Na: 166, K:4, bilirubin: 0.5, bilirubin D/I: 0.2/0.3, Amylase: 1157, Gamma-GT: 56, AST 7.210, ALT: 2.470, SR (sedimentation rate): 15, Lipase: 84. Abdominal ultrasound was unremarkable. Patient respiratory function and conscience...
Asunto(s)
Humanos , Femenino , Anciano , Diabetes Mellitus , Necrosis Hepática Masiva , Vena Porta/anomalíasRESUMEN
BACKGROUND AND OBJECTIVES: Hepatic infarction is characterized by parenchyma ischemic necrosis involving at least two acinis. It is extremely uncommon due to the arterial and portal venous blood supply. We report a case of a patient not know to have diabetes who developed massive areas of ischemic infarcts of the liver after episode of acutely diabetes decompensated. CASE REPORT: A 67 year-old hypertensive female who has been presenting, for the last 10 days, polydipsia, high urinary volume, visual and gait impairment, nausea and vomiting was admitted to the emergency room (ER). During the physical examination it was observed dehydration, skin discoloration, peripheral cyanosis, hypothermia, tachycardia, hypotension and mild diffuse abdominal pain. Admissional laboratory exams demonstrated total leukocytes: 16.800, Cr: 3.7, Ur: 167, Na: 133, K: 6.9, glucose: 561; arterial gasometry (O2 catheter: 2 L/min): pH: 6.93, pCO2: 12.1, pO2: 107, B.E.: -28.8, HCO3: 2.4, Sat 91.3%, lactato: 79; urinalysis: pH: 6; leukocytes: 13; density: 1015; erythrocytes: 19; protein: ++; glucose: +++; bilirubin: negative; ketonic bodies: + denote ketonemia. EKG: sharp T wave, right branch block. Patient was treated with intravenous insulin, hydration, sodium bicarbonate and ceftriaxone. After initial treatment, the laboratory exams showed Cr: 2.2, Ur: 122, Na: 162, K: 4.3, Ca: 6.4, glucose: 504, pH: 7.01, HCO3: 7.1, B.E.: -22. One day after admission the patient presented with important abdominal pain and peritoneal irritation, followed by difficulty for talking and somnolence; routine laboratory exams showed arterial gasometry: pH: 7.4, pCO2: 31, pO2: 68, BE: -4.4, HCO3: 19, SatO2: 93.5%; Ur: 95,Cr: 1.4, albumin: 2.4, Ca: 0.95, Na: 166, K:4, bilirubin: 0.5, bilirubin D/I: 0.2/0.3, Amylase: 1157, Gamma-GT: 56, AST 7.210, ALT: 2.470, SR (sedimentation rate): 15, Lipase: 84. Abdominal ultrasound was unremarkable. Patient respiratory function and conscience level worsened, requiring intubation. Despite all resuscitation efforts, she died. Necropsy showed multiple ischemic infarcts of the liver with vascular thrombosis, splenic infarcts, generalized visceral congestion and atherosclerosis of aorta and its branches. Pancreas was normal. CONCLUSIONS: The mechanisms of hepatic and splenic infarctions in this case were unclear. The following factors may have contributed to necrosis: vomiting and fever should be considered to induce dehydration and hypotension, which further decreased portal and hepatic arterial inflows; elevated level of catecholamine in hyperglycemic states might induce vasoconstriction effects; widespread atherosclerosis is commonly seen in diabetic and hypertensive patients. This case underlies the importance of searching for hepatic necrosis or infarction in any diabetic patient with elevated liver enzymes. Anticoagulation therapy should be instituted promptly upon recognition of vascular thromboses.