Disfunción neuroendócrina secundaria a hemorragia subaracnoidea por ruptura de aneurisma. Revisión

La disfunción neuroendócrina es una complicación secundaria a lesión cerebral aguda que cursa con alteración del eje hipotálamo-hipofisario, por daño directo de origen vascular. Se caracteriza por la alteración de uno o varios de los sistemas hormonales regulados por la glándula pituitaria, llegando en casos graves al hipopituitarismo franco. Una de las causas más importantes de esta patología es la hemorragia subaracnoidea. El déficit hormonal aparece poco tiempo después de ocurrido el sangrado y puede persisitir a largo plazo, causando síntomas secundarios al nivel bajo de ciertas hormonas, y trastornos neuropsicológicos alterando en gran medida la calidad de vida de aquellos pacientes cuyo pronóstico funcional ya se encontraba alterado por la hemorragia en sí. El tratamiento con sustitución hormonal está indicado tanto en la fase aguda, como en la deficiencia permanente de cada hormona. A continuación se ofrece una actualización sobre el tema, con el fin de conocer mejor la enfermedad, cómo sospecharla, cuándo identificarla, y brindar el manejo adecuado

Disfunción neuroendócrina secundaria a hemorragia subaracnoidea por ruptura de aneurisma: Revisión

La disfunción neuroendócrina es una complicación secundaria a lesión cerebral aguda que cursa con alteración del eje hipotálamo-hipofisario, por daño directo de origen vascular. Se caracteriza por la alteración de uno o varios de los sistemas hormonales regulados por la glándula pituitaria, llegando en casos graves al hipopituitarismo franco. Una de las causas más importantes de esta patología es la hemorragia subaracnoidea. El déficit hormonal aparece poco tiempo después de ocurrido el sangrado y puede persisitir a largo plazo, causando síntomas secundarios al nivel bajo de ciertas hormonas, y trastornos neuropsicológicos alterando en gran medida la calidad de vida de aquellos pacientes cuyo pronóstico funcional ya se encontraba alterado por la hemorragia en sí. El tratamiento con sustitución hormonal está indicado tanto en la fase aguda, como en la deficiencia permanente de cada hormona. A continuación se ofrece una actualización sobre el tema, con el fin de conocer mejor la enfermedad, cómo sospecharla, cuándo identificarla, y brindar el manejo adecuado

Coagulation abnormalities in the cirrhotic patient

The clotting process is a dynamic array of multiple processes which can be described in four phases: platelet plug initiation and formation, clotting process propagation by the coagulation cascade, clotting termination by antithrombotic mechanisms and clot removal by fibrinolysis. The liver plays a central role in each of these phases of clotting process, as it synthesizes the majority of coagulation factors and proteins involved in fibrinolysis as well as thrombopoeitin, which is responsible for platelet production from megakaryocytes. Many pathological processes associated with cirrhosis, such as portal hypertension and endothelial dysfunction, as well as co-morbid conditions, may also alter the coagulation process. Consequently, patients with liver disease have a disturbed balance of procoagulant and anti-coagulant factors which deviates from the normal coagulation cascade. This situation poses an additional problem in the diagnostic and therapeutic approach to this group of patients, since traditional coagulation test may not be reliable for assessing bleeding or thrombotic risk and traditional transfusional strategies may not be applicable in cirrhotic patients. In this article, we review the pathophysiological bases of coagulation abnormalities, in cirrhotic patients, the diagnostic therapeutic strategies to be followed and its impact on the clinical outcome in the cirrhotic patient

Acute kidney injury in critically ill cirrhotic patients: a review

Acute kidney injury (AKI) is an important marker of morbidity and mortality in critically ill cirrhotic patients. The most common causes of AKI in cirrhotic patients include prerenal or hepatorenal syndrome (HRS). Diagnosis of AKI may be delayed by the lack of clinical, biochemical, and radiological markers with proven sensitivity and specificity in cirrhotic patients. In this review, we discuss the epidemiology, patho-physiology, diagnosis, and therapies for AKI in cirrhotic patients admitted to an intensive care unit (ICU)

Thrombosis and hemorrhage in the critically ill cirrhotic patients: five years retrospective prevalence study

Background. Cirrhotic patients present a complex interaction between deficient synthetic liver function, hemodynamic abnormalities and superimposed conditions that alter coagulation system. This alters both coagulation and fibrinolytic processes,increasing bleeding and thrombosis risks. Particularly, critically ill cirrhotic patients represent a diagnostic challenge since they have multiple comorbidities making the thrombotic and bleeding risks unpredictable. The prevalence of bleeding and thrombosis in this subset of patients remains poorly described. The main aim of this article is to describe the prevalence of thrombotic and hemorrhagic complications in cirrhotic patients admitted between 2007 and 2012 at Médica Sur Clinic and Foundation ICU.Material and methods. We performed a five years retrospective study including every cirrhotic patient admitted to ICU between January 2007 and December 2012.Results. The incidence of hemorrhage was 48.5%, the overall incidence of thrombotic complications was 13.66%. Variceal bleeding was the most prevalent hemorrhagic event and portal vein thrombosis the most common thrombotic event. Factors associated with presenting a bleeding episode included kidney injury, infection an thrombosis. Factors associated with increased thrombotic risk included ascitis,infection and bleeding.Conclusion. Critically ill cirrhotic patients have an high risk for both thrombotic and bleeding episodes. The association between the presence of bleeding and thrombotic events was statistically significant

Interstitial pneumonitis associated with pegylated interferon α-2b therapy for chronic hepatitis C: Case report

Since 2004, pegylated interferon (P-IFN) in combination with ribavirin has become the optimal choice of therapy for chronic hepatitis C virus (HCV) infection. IFN α-2b suppresses HCV replication and restores elevated serum aminotransferase levels, leading to improvements in the histological changes in the livers of patients with chronic hepatitis C.1 Unfortunately, P-IFN has several adverse effects, including pneumonitis. This complication has been reported in the treatment of malignant diseases and CHC.2 We report a patient with interstitial pneumonitis thought to be caused by an IFN-based treatment in an unusual scenario of a patient with HCV-related Child-Pugh stage A cirrhosis, who experienced dyspnea, fever, and cough after 12 months of treatment with P-IFN α-2b. Her lung injury and pulmonary symptoms did not disappear despite discontinuation of IFN and the administration of corticosteroid. We concluded that the patient developed a fatal interstitial pneumonitis associated with P-INF α-2b therapy

Liver involvement in severe human influenza A H1N1

Influenza A is a disease caused by a RNA virus, member of the orthomyxoviridae family. The influenza infection is characterized primarily by pulmonary affection that may advance to an acute pulmonary respiratory failure course. Hepatic involvement is not frequent and accounts for < 3% of all cases. We describe two patients with acute Influenza A H1N1 infection who developed hepatic involvement. Needle core liver biopsy of one of the patients revealed only micro and macrovesicular steatosis