RESUMO
La rabdomiólisis como complicación de un síndrome compartimental agudo es algo habitual, pero lo contrario es infrecuente. Presentamos el caso de un hombre de 74 años con una infección aguda por virus Coxsakie B que desarrolló una rabdomiólisis con un nivel de creatinfosfocinasa (CPK) máximo de 161.757 UI/l. Se complicó con un fracaso renal agudo y con un síndrome compartimental de la pierna derecha. La función renal se normalizó en unas semanas, pero a consecuencia del síndrome compartimental desarrolló un pie equino, a pesar de la realización de fasciotomías, precisando una ortesis para deambular. El síndrome compartimental es una complicación a tener en cuenta en rabdomiólisis graves, porque puede pasar desapercibida con facilidad, y se puede asociar a secuelas
Rhabdomyolysis as a complication of an acute compartimental syndrome is somewhat common, but on the contrary, is rare. We present the case of a 74 year man with acute infection by Coxsackie B virus who developed a rhabdomyolysis with a maximum CPK of 161, 757 IU/l. It became complicated with acute renal failure and compartment syndrome of the right leg. Renal function normalized in a few weeks, however, due to the compartment syndrome, he developed an equinus foot in spite of the performance of fasciotomies and required an orthesis to walk. Compartment syndrome is a complication to be considered in serious rhabdomyolysis because it may go unnoticed easily and can be associated to sequels
Assuntos
Masculino , Idoso , Humanos , Infecções por Coxsackievirus/complicações , Rabdomiólise/microbiologia , Síndromes Compartimentais/complicações , Creatina Quinase/análise , Injúria Renal Aguda/etiologia , Miosite/virologiaRESUMO
In 21 patients from the out-patient clinic of the Internal Medicine Department of our hospital with chronic hepatitis (HC) due to B virus (HBV) and anti-HBC (IgG) serology but not HBsAg, a study was made of the possible correlation between viral replication levels (RV) --as expressed by DNA polymerase values (DNAp)-- and, respectively, histologic changes and serum enzyme movements (GPT, GOT). Our study parted from the diverse criteria cited in the literature concerning the role assigned to viral replication per se and/or immune response per se in the genesis of histologic damage (DH). All patients exhibited signs of moderate clinical and enzymatic activity. The levels of viral replication in the group studies were significant (compared to a control group), which supports the thesis that a certain degree of viral replication, although very attenuated, persists in these patients and is the basis of the continued histological damage that eventually leads to liver cirrhosis (CH) and its derivatives, often with little clinical translation. As regards histologic damage, the correlation with DNAp is reciprocal and of moderate significance, supporting the criterion that the multiform expression of histologic damage in liver cirrhosis due to HBV (HCB) (cellular necrosis, intracellular degenerative phenomena, inflammatory cellular infiltrate, fibrosis) is, at the very least, unproportional to the degree of viral replication and can even be reciprocal. Only the severity of the overall hepatic process remains a function of immune response.(ABSTRACT TRUNCATED AT 250 WORDS)
