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 .
2016 JULY 13
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
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