oedema and emphysema are the outstanding gross lesions . In dogs on the other hand , where the major shock organ is the liver , severe hepatic congestion with widespread visceral hemorrhage are the most common findings .
In humans there is now a body of evidence to support a primary role of heart mast cells in inducing acute myocardial anaphylaxis . With this background one could expect that there may well also be variation in clinical signs and pathology among different wildlife species .
• Cardiovascular signs of anaphylaxis = hypotension and sinus tachycardia .
• Respiratory signs of anaphylaxis = bronchospasm , laryngeal oedema and dyspnea .
• Cutaneous signs of anaphylaxis = pruritis , erythema and angioedema .
Following mast cell degranulation there is release of cell mediators which drives the acute phase of the anaphylactic reaction ( occurring within minutes ) characterized by increased vascular permeability with oedema and hemorrhage plus smooth muscle contraction . The late phase response ( developing over a period of hours ) is dominated by inflammatory cell infiltrates in particular eosinophils , which accompany the fluid phases of the inflammatory reaction ( oedema and hemorrhage ).
and therefore inflammatory cell infiltrates in particular mast cells and eosinophils do not for part of the histopathological picture .
Disseminated intravascular coagulation ( DIC ) is a form of “ consumptive coagulopathy ” or “ defibrination syndrome ”, where consumption coagulation occurs throughout the vasculature ( micro and macrovasculature ). It is initiated by massive activation of coagulation and platelets and maybe acute / chronic , compensated / uncompensated . Protein components of some injectable agents are capable of initiating DIC through direct activation of the common coagulation pathway .
Gross Pathology Indicators of an Acute Adverse Drug Reaction Generalized congestion and blood pooling are common and consistent lesions of shock . Pulmonary congestion , oedema , haemorrhage and emphysema ( Figures 1 and 2 ) are often outspoken and frequently accompanied by extensive epi and endocardial haemorrhages ( Figure 3 ). As mentioned previously in domestic dog ’ s severe hepatic congestion , congestion of the duodenum and widespread haemorrhage are also commonly documented . Similar variations might be expected in different wildlife species . Histopathology Indicators of an Acute Adverse Drug
Therefore , in animals developing type I hypersensitivities or anaphylactoid reactions which are fatal in < 30 minutes following drug application , there is unlikely to be any significant eosinophil infiltrates into target shock organs on histological examination , pathology being dominated by the fluid phases of acute inflammation .
Cardiogenic shock develops following the failure of the heart to adequately pump blood . In acute drug reactions ventricular tachycardia , fibrillation , other arrhythmias or myocardial infarction are the most common causes of cardiac failure . Central in the pathogenesis of cardiogenic shock is a decrease in both stroke volume and cardiac output . This response to injected agents is not mediated by IgE
Figure 1 : Jaguar lung – acute anaphylactoid reaction with severe pulmonary oedema , note the accentuation of lobulation due to interlobular oedema . Thick foamy oedema fluid fills the entire length of the trachea .
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