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Acute peripheral circulatory failure caused by acute venous thrombosis
444
AMEKICAN
Wilson, M. G.: Immunologic and Special Reference to Rheumatic Pediatrics 2:239 (Sept.), 1918.
H'XRT
Biochemical Fever.
JOURNAL
I.
Studies in Infants and The Role of Genetic
Children With Susceptibility.
In rheumatic fever, susceptibility of the host is the important factor in the pathogenesis of the disease, and from epidemiologic and genetic studies it is concludq~’ that this susceptibility , is on a genetic and age basis. It is postulated that among families ot’ know;, hereditary background there are children who are susceptible and not susceptible to the acquisition of rheumatic fever. The nature of the hereditary factors is obscure, but there are recent biochemical observations which demonstrate that such biochemical reactions as enzyme and protein specificities are gene determined. Perhaps in a susceptible child abnormal physiologic, chemical, immunologic, or hormonal responses may be present. If such endogenous factors were known, the role of possible exogenous agents might be clarified. Studies have been completed on complement tilers and electrophoretic patterns in an attempt to evaluate immunologic response and possible differences in serum protein patterns among normal, susceptible, and rheumatic children. Other studies are in progress and it is hoped that information will be obtained as to the nature of the hereditable factors responsible for susceptibility to rheumatic fever. JOHNSON. Moore,
Treatment R. L.: Pediatrics 2:266 (Sept.),
of 1948.
an
Infant
With
Paroxysmal
huricular
Tachycardja,,
A case of an infant with paroxysmal auricular tachycardia is described. At 20 days of age there were definite signs of heart failure and marked distress. He was digitalized by mouth with . the tincture of digitalis, the dose being calculated as 0.2 C.C. per kilogram. After 0.6 C.C. was given, there was rapid improvement, and the greatly enlarged heart returned to a normal size. He was maintained on 0.1 C.C. daily, but within two to three weeks, symptoms recurred, and paroxysmal auricular tachycardia, confirmed by electrocardiogram, was diagnosed. Increased dosage of digitalis was without effect, and 0.5 mg. of acetyl-beta-methylcholine (Mecholyl chloride) was given intramuscularly. Within thirty seconds the baby became pale and cold, salivated profusely, and developed labored respirations. The heart rate suddenly slowed from 270 per minute to 40 to 50 per minute. The infant’s condition improved in a few minutes with administration of 0.065 mg. atropine, intravenously. The pulse rose subsequently to 140 per minute and stayed there. The infant was maintained on 0.2 C.C. of the tincture of digitalis daily. rlt 3 months of age another parosysm occurred. Increased digitalization was not effective and 2.0 mg. of Mecholyl were required to stop the attack, with the alarming side effects just described. Three weeks later, another episode occurred and quinidine was tried orally, starting with a dogi“ of 20 mg. and with an increase of 20 mg. each two hours until, with a dose of 120 mg., the attac subsided. Further attacks required up to 180 milligrams. At the age of 5 months he had hi. last episode, which required 200 mg. quinidine for its control. From that time to the time of re:,, porting at the age of 25 months he has been well, without evidence of cardiovascular abnormalit).. JOHMOX. Morgan, E. H., Allen, E. V., and MacCarty, C. S.: Acute Peripheral Circulatory Failure Caused by Acute Venous Thrombosis. Proc. Staff Meet., Mayo Clin. 23:425 (Sept. 15), 1948. Acute peripheral circulatory failure is a rare systemic effect of acute venous thrombosis. Manifestations include cold, pale, moist skin, tachycardia, hypotension, and the loss of peripheral This condition differs from the transient pulses. Anemia and azotemia are additional features. arteriospastic disappearance of pulsations in a limb following extensive acute venous thrombosis. ‘Three cases of the more severe and generalized complication are described. Although objective determinations of circulating blood volume and of limb volume were not made, it is the impression of these authors that a considerable quantity of blood, the equivalent of an extensive hemorrhage, had been trapped in the involved limbs as the result of acute venous thrombosis and that this caused peripheral circulatory failure in each of the three instances reviewed. ARKLESS
AMEKICAN
Wilson, M. G.: Immunologic and Special Reference to Rheumatic Pediatrics 2:239 (Sept.), 1918.
H'XRT
Biochemical Fever.
JOURNAL
I.
Studies in Infants and The Role of Genetic
Children With Susceptibility.
In rheumatic fever, susceptibility of the host is the important factor in the pathogenesis of the disease, and from epidemiologic and genetic studies it is concludq~’ that this susceptibility , is on a genetic and age basis. It is postulated that among families ot’ know;, hereditary background there are children who are susceptible and not susceptible to the acquisition of rheumatic fever. The nature of the hereditary factors is obscure, but there are recent biochemical observations which demonstrate that such biochemical reactions as enzyme and protein specificities are gene determined. Perhaps in a susceptible child abnormal physiologic, chemical, immunologic, or hormonal responses may be present. If such endogenous factors were known, the role of possible exogenous agents might be clarified. Studies have been completed on complement tilers and electrophoretic patterns in an attempt to evaluate immunologic response and possible differences in serum protein patterns among normal, susceptible, and rheumatic children. Other studies are in progress and it is hoped that information will be obtained as to the nature of the hereditable factors responsible for susceptibility to rheumatic fever. JOHNSON. Moore,
Treatment R. L.: Pediatrics 2:266 (Sept.),
of 1948.
an
Infant
With
Paroxysmal
huricular
Tachycardja,,
A case of an infant with paroxysmal auricular tachycardia is described. At 20 days of age there were definite signs of heart failure and marked distress. He was digitalized by mouth with . the tincture of digitalis, the dose being calculated as 0.2 C.C. per kilogram. After 0.6 C.C. was given, there was rapid improvement, and the greatly enlarged heart returned to a normal size. He was maintained on 0.1 C.C. daily, but within two to three weeks, symptoms recurred, and paroxysmal auricular tachycardia, confirmed by electrocardiogram, was diagnosed. Increased dosage of digitalis was without effect, and 0.5 mg. of acetyl-beta-methylcholine (Mecholyl chloride) was given intramuscularly. Within thirty seconds the baby became pale and cold, salivated profusely, and developed labored respirations. The heart rate suddenly slowed from 270 per minute to 40 to 50 per minute. The infant’s condition improved in a few minutes with administration of 0.065 mg. atropine, intravenously. The pulse rose subsequently to 140 per minute and stayed there. The infant was maintained on 0.2 C.C. of the tincture of digitalis daily. rlt 3 months of age another parosysm occurred. Increased digitalization was not effective and 2.0 mg. of Mecholyl were required to stop the attack, with the alarming side effects just described. Three weeks later, another episode occurred and quinidine was tried orally, starting with a dogi“ of 20 mg. and with an increase of 20 mg. each two hours until, with a dose of 120 mg., the attac subsided. Further attacks required up to 180 milligrams. At the age of 5 months he had hi. last episode, which required 200 mg. quinidine for its control. From that time to the time of re:,, porting at the age of 25 months he has been well, without evidence of cardiovascular abnormalit).. JOHMOX. Morgan, E. H., Allen, E. V., and MacCarty, C. S.: Acute Peripheral Circulatory Failure Caused by Acute Venous Thrombosis. Proc. Staff Meet., Mayo Clin. 23:425 (Sept. 15), 1948. Acute peripheral circulatory failure is a rare systemic effect of acute venous thrombosis. Manifestations include cold, pale, moist skin, tachycardia, hypotension, and the loss of peripheral This condition differs from the transient pulses. Anemia and azotemia are additional features. arteriospastic disappearance of pulsations in a limb following extensive acute venous thrombosis. ‘Three cases of the more severe and generalized complication are described. Although objective determinations of circulating blood volume and of limb volume were not made, it is the impression of these authors that a considerable quantity of blood, the equivalent of an extensive hemorrhage, had been trapped in the involved limbs as the result of acute venous thrombosis and that this caused peripheral circulatory failure in each of the three instances reviewed. ARKLESS