High-output heart failure in mitochondrial myopathy: a fulminant form with severe lactic acidosis and rhabdomyolysis.
A 17-year-old male with mitochondrial myopathy was transferred to our hospital because of respiratory distress and a rapidly deteriorating level of consciousness. He had a markedly increased cardiac output with low systemic vascular resistance and decreased arteriovenous oxygen difference. Severe lactic acidosis, rhabdomyolysis and acute renal failure were also present. He was treated in the intensive care unit with continuous hemofiltration and hemodialysis. This case demonstrates that cardiac failure in mitochondrial encephalomyopathy may be caused by myocardial abnormalities as well as by reduced systemic vascular resistance secondary to disturbed oxidative metabolism.
Critical Care Medical Center, Niigata City General Hospital.
Y
Y
Hirose
T
T
Miida
K
K
Yoshida
H
H
Kimura
H
H
Oda
T
T
Toeda
N
N
Higuma
D000140:Acidosis, Lactic / Q000150:complications* / Q000628:therapy; D058186:Acute Kidney Injury / Q000150:complications / Q000628:therapy; D000293:Adolescent; D016534:Cardiac Output, High / Q000150:complications*; D017583:Hemodiafiltration; D006801:Humans; D008297:Male; D017240:Mitochondrial Myopathies / Q000150:complications* / Q000503:physiopathology / Q000628:therapy; D010084:Oxidation-Reduction; D012206:Rhabdomyolysis / Q000150:complications* / Q000628:therapy; D014655:Vascular Resistance