atuais
Hyperglycemic crises in diabetes mellitus – Current aspects
Resumo
A cetoacidose diabética e o estado hiperglicêmico hiperosmolar são as duas
complicações agudas mais graves que observamos durante a evolução do
diabetes melito. Em centros de excelência, a taxa de mortalidade para a
cetoacidose diabética é < 5% enquanto que, para o estado hiperglicêmico
hiperosmolar ainda continua elevada, em torno de 15%. Entre os fatores
precipitantes, os estados infecciosos são as causas mais comuns,
predominando as do trato respiratório alto, as de vias urinárias e as
pneumonias. A fisiopatologia da descompensação metabólica da cetoacidose
diabética é mais entendida do que a do estado hiperglicêmico hiperosmolar.
Fundamentalmente, na cetoacidose diabética o que ocorre é a redução da
concentração efetiva de insulina circulante associada à liberação excessiva de
hormônios contra-reguladores, entre eles, o glucagon, as catecolaminas, o
cortisol e o hormônio de crescimento. Esta combinação libera grandes
quantidades de ácidos graxos livres na circulação. No fígado, estes ácidos
graxos livres são oxidados em corpos cetônicos, resultando assim em
cetonemia e acidose metabólica. Os principais critérios diagnósticos utilizados
para a cetoacidose diabética são, a glicemia ≥250mg/dL, o pH arterial ≤7.3, o
bicarbonato sérico ≤15mEq/L e graus variáveis de cetonemia e cetonúria. Para
o estado hiperglicêmico hiperosmolar são, a glicemia em geral >600mg/dL, a
osmolalidade sérica >320mOsm/Kg, e o bicarbonato sérico ≥15mEq/L com
discreta cetonemia. As metas terapêuticas para as crises hiperglicêmicas
agudas são, a liberação das vias aéreas superiores, a correção da
desidratação com solução salina, a correção dos distúrbios eletrolíticos e da
acidose, a redução da hiperglicemia com insulina em baixas doses e a
identificação e o tratamento dos fatores precipitantes.
Descritores
Diabetes melito: cetoacidose diabética; estado hiperglicêmico hiperosmolar
Abstract
Diabetic ketoacidosis and the hyperosmolar hyperglycemic state are the two
most severe acute complications that are observed in diabetes mellitus.
Managed properly, the mortality rate for diabetic ketoacidosis is less than 5% in
experienced centers, whereas for the hyperosmolar hyperglycemic state it still
remains high, about 15%. Among precipitating factors, infeccious diseases are
the most common, mainly of the upper respiratory and urinary tracts and
pneumonia. The pathophysiology of diabetic ketoacidosis is better understood
than that of the hyperosmolar hyperglycemic state. Fundamentally, in diabetic
ketoacidosis the basic underlying mechanism is a reduction in the net effective
action of circulating insulin associate with a concomitant elevation of counter-
regulatory hormones, such as glucagon, catecholamines, cortisol and growth
hormone. This combination releases great amounts of free fatty acids into the
circulation from adipose tissues (lipolysis) that are tranformed by oxidation to
ketones bodies, causing ketonemia ad metabolic acidosis. The main criteria
used to diagnoses diabetic ketoacidosis are plasma glucose ≥250mg/dL, pH
≤7.3 and serum bicarbonate ≤15mEq/L and variable degrees of ketonemia and
ketonuria. To diagnose hyperosmolar hyperglycemic state, the criteria are
plasma glucose greater than 600mg/dL, serum osmolality >320mOsm/kg and
serum bicarbonate ≥15mEq/L with mild ketonemia. The main therapeutical
purpose of treating acute hyperglycemic crises require care of the upper
airways, correction of dehydration with fluid therapy (saline solution), correction
of eletrolyte imbalance and acidosis, reduction of hyperglycemia with low-dose
insulin therapy, and identification as well as the treatment of comorbid
precipitating events.
Keywords
Diabetes mellitus; diabetic ketoacidosis; hyperosmolar hyperglycemic state.
Introdução
Fatores precipitantes
Achados laboratoriais
A avaliação laboratorial inicial de pacientes com CAD e com EHH deve
incluir a determinação de glicose plasmática, fósforo, uréia, creatinina,
cetonemia, eletrólitos inclusive com o cálculo de anion gap, análise urinária,
cetonúria, gasometria, hemograma e eletrocardiograma. Quando necessário,
solicitar RX de tórax e culturas de sangue e urina.
Cálculos bioquímicos:
Diagnóstico diferencial
A cetose de jejum, cetoacidose alcoólica, acidose lática pelo uso
inadequado de fármacos como salicilatos e metformina e outras causas de
acidose com anion gap elevado, como a insuficiência renal crônica. Essas
situações são facilmente diagnosticadas pela história clínica e pela avaliação
laboratorial (1, 25).
Tratamento
As metas do tratamento das crises hiperglicêmicas agudas são: a)
manutenção das vias aéreas pérvias e, em caso de vômitos, deve-se indicar
sonda nasogástrica; b) correção da desidratação; c) correção dos distúrbios
eletrolíticos e ácido-básico; d) redução da hiperglicemia e da osmolalidade; e)
identificação e tratamento do fator precipitante.
Insulinoterapia
Bicarbonato
Fosfato
Conclusões
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