Anaphylactic shock following intravenous administration of lignocaine

1997 ◽  
Vol 41 (8) ◽  
pp. 1071-1072 ◽  
Author(s):  
K. ISMAIL ◽  
P. J. SIMPSON
2002 ◽  
Vol 13 (3) ◽  
pp. 480-481 ◽  
Author(s):  
M. Benchalal ◽  
E. Yahchouchy-Chouillard ◽  
S. Fouere ◽  
A. Fingerhut

1936 ◽  
Vol 64 (5) ◽  
pp. 717-721 ◽  
Author(s):  
K. Landsteiner ◽  
John Jacobs

Experiments are described which show that with a given treatment guinea pigs can be sensitized to arsphenamine, so that a considerable percentage die in anaphylactic shock on intravenous administration of the substance.


1957 ◽  
Vol 190 (2) ◽  
pp. 310-316 ◽  
Author(s):  
William M. Manger ◽  
Jesse L. Bollman ◽  
Frank T. Maher ◽  
Joseph Berkson

A fluorometric method was used to quantitate plasma epinephrine and norepinephrine during hemorrhagic and anaphylactic shock in healthy adult dogs anesthetized with pentobarbital. Arterial plasma was analyzed before and after hemorrhage in four dogs. Loss of approximately 18% of blood volume through rapid arterial bleeding caused no remarkable change in pressor amines. Loss of approximately one-third of the total blood volume decreased the mean arterial pressure by a range of 56–81% and invariably caused increased concentration of plasma pressor amines. The average concentration of epinephrine increased from 1.0 to 7.8 µg/1. of plasma, and that of norepinephrine increased from 2.5 to 3.6 µg. Additional bleeding caused further increase of plasma pressor amines. Seven dogs were given egg white intravenously to sensitize them. Subsequently, whenever a severe reaction (hypotension, bradycardia and respiratory depression) resulted from intravenous administration of egg white, venous plasma pressor amines increased. The average concentration of epinephrine increased from 0.7 to 7.7 µg/1. of plasma; norepinephrine increased in three dogs but remained unchanged or decreased in the remaining animals. Without a preceding ‘shock’ reaction, change in concentration of epinephrine-like substance was unremarkable. Intravenous administration of 1 mg of histamine base produced hypotension and usually slight increase of plasma pressor amines.


Author(s):  
Hyun Ho Seong ◽  
Nam Yung Kim ◽  
Yun Ho Yang ◽  
Ju Youn Kim ◽  
Seongsik Kang

Anaphylactic reactions during anesthesia can have a high mortality. The most common cause of anaphylaxis during anesthesia is neuromuscular blocking agents and, even though considered intermediate risk, rocuronium is frequently involved, probably due to its greater use. We present the case of a woman with anaphylactic shock secondary to the intravenous administration of rocuronium and recovered without complications by early aggressive management combination with conventional methods and sugammadex.


1996 ◽  
Vol 12 (5) ◽  
pp. 214-216 ◽  
Author(s):  
Noorizan Abdul Aziz ◽  
Zaitun Kamaruddin ◽  
Yahaya Hassan ◽  
Kamarudin Jaalam

Objective: To report a case of anaphylactic shock induced by the rapid intravenous administration of vitamin K1 in a patient in the intensive care unit (ICU). Case Summary: A 9-year-old Malay girl was admitted to the ICU and was diagnosed with Guillain-Barré syndrome. She developed an allergy to atropine that was manifested by a symmetric generalized transient macular rash over the trunk; it subsided 10 minutes after the drug was stopped. About 7 hours later, vitamin K1 10 mg iv was administered over 3 minutes due to the slight prolongation of prothrombin time and activated partial thromboplastin time. Immediately after the drug was administered, the patient developed a generalized transient macular rash, cyanosis, and shock. Her blood pressure and heart rate could not be detected. She responded well, however, after resuscitation. Discussion: Anaphylactic shock in this patient was most probably caused by the intravenous administration of vitamin K1, because this event occurred immediately after its administration. There have also been a few reported cases of severe reaction and death associated with intravenous administration of vitamin K1. The likelihood that the incident was drug-related could be classified as “probable” based on Naranjo's causal relationship algorithm. Conclusions: Rapid intravenous administration of vitamin K1 may induce anaphylactic shock in a critically ill patient with hemodynamic instability. If vitamin K1 is required, oral administration is preferred because it is rarely associated with severe reactions. Intravenous administration of vitamin K1 should be considered only in an emergency situation and the rate of administration should not exceed 1 mg/min.


JAMA ◽  
1967 ◽  
Vol 200 (10) ◽  
pp. 824-829 ◽  
Author(s):  
M. Davidov

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