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===Pathophysiology===
===Pathophysiology===
The glucococorticoid hormone '''cortisol''' enables animals to cope with stress while the minerlaocorticoid '''aldosterone''' plays a critical role in the regulation of sodium and potassium concentrations and of extracellular fluid volume. Aldosterone normally acts to increase sodium excretion and potassium reabsorption in the kidney so deficient aldosterone secretion will result in '''hyponatraemia''', '''hypochloraemia''' and '''hyperkalaemia'''. Since they are unable to regulate their body sodium concentration, Addisonian animals become severely dehydrated and hypovolaemic, reducing the perfusion of peripheral tissues. During an Addisonian crisis, this can result in gastro-intestinal haemorrhage and allow translocation of bacteria across the gut barrier.
The glucococorticoid hormone '''cortisol''' enables animals to cope with stress while the minerlaocorticoid '''aldosterone''' plays a critical role in the regulation of sodium and potassium concentrations and of extracellular fluid volume. Aldosterone normally acts to increase sodium reabsorption and potassium excretion in the kidney so deficient aldosterone secretion will result in '''hyponatraemia''', '''hypochloraemia''' and '''hyperkalaemia'''. Since they are unable to regulate their body sodium concentration, Addisonian animals become severely dehydrated and hypovolaemic, reducing the perfusion of peripheral tissues. During an Addisonian crisis, this can result in gastro-intestinal haemorrhage and allow translocation of bacteria across the gut barrier.
Deficiency of cortisol results in '''hypoglycaemia''' (as cortisol usually antagonises the action of insulin), increased circulating levels of [[Lymphocytosis|lymphocytes]] and [[Eosinophilia|eosinophils]] and increased skin pigmentation. This latter syndrome occurs as low levels of glucocorticoids allow increased ACTH production as negative feedback on the pituitary is removed or decreased. As ACTH is released, so is MSH (Melanocyte Stimulating Hormone), increasing the pigmentation of the skin in chronic cases of hypoadrenocorticism.
Deficiency of cortisol results in '''hypoglycaemia''' (as cortisol usually antagonises the action of insulin), increased circulating levels of [[Lymphocytosis|lymphocytes]] and [[Eosinophilia|eosinophils]] and increased skin pigmentation. This latter syndrome occurs as low levels of glucocorticoids allow increased ACTH production as negative feedback on the pituitary is removed or decreased. As ACTH is released, so is MSH (Melanocyte Stimulating Hormone), increasing the pigmentation of the skin in chronic cases of hypoadrenocorticism.
==Treatment==
==Treatment==
===Stabilisation===
===Stabilisation===
It is important to get as much information during initial triage of a collapsed animal as possible. Some differentials include anaphylaxis, HGE, Parvo, arrythmias, pericardial effusion, any cause of hyperkalemia, hemoabdomen. A FAST ultrasound exam can be used to investigate anaphylaxis (gall bladder edema), pericardial effusion, and hemoabdomen. ECG can evaluate for heart block and bradycardias as well as typical hyperkalemia induced changes (prolonged S-T interval, enlarged T waves). Electrolytes, PCV, blood gas, lactate can all help with initial work up and diagnosis.
The classic Addisonian is ~ 3 years old and as such anaphylaxis and HGE are the most common differentials. Differentiating anaphylaxis from Addison's early on is critical to saving these patients.
Since collapsed, bradycardic animals are unlikely to survive for long, urgent intervention is required to stabilise these patients. '''Intra-venous 0.9% sodium chloride (saline) solution''' should be provided at shock rates to restore normovolaemia and begin to correct the electrolyte imbalances. Additional '''glucose''' can be added to fluids in hypoglycaemic animals but blood glucose levels should be monitored closely if this is undertaken.
Since collapsed, bradycardic animals are unlikely to survive for long, urgent intervention is required to stabilise these patients. '''Intra-venous 0.9% sodium chloride (saline) solution''' should be provided at shock rates to restore normovolaemia and begin to correct the electrolyte imbalances. Additional '''glucose''' can be added to fluids in hypoglycaemic animals but blood glucose levels should be monitored closely if this is undertaken.
Hypothermia must be corrected slowly so as not to cause cell shrinkage in the brain. Hyperkalemia will improve with [[Fluid therapy|IV fluid therapy]], but in the case of life threatening arrhythmias 10% CaGluconate can be given to protect the heart (1ml/kg @ 1ml/minute to effect). Insulin and Dextrose can be used to drive potassium into the cells and sodium bicarbonate can be used to correct acidosis.
When the diagnosis has been made with some certainty, '''intra-venous glucocorticoid replacement therapy''' can be initiated together with a '''mineralocorticoid'''. Hydrocortisone sodium succinate is the steroid of choice as it is short acting and provides equal glucocorticoid and mineralocorticoid activity. Although there is an intra-muscular injectable mineralocorticoid (desoxycorticosterone acetate) available in the USA, this is not usually required for stabilisation.
When the diagnosis has been made with some certainty, '''intra-venous glucocorticoid replacement therapy''' can be initiated together with a '''mineralocorticoid'''. Hydrocortisone sodium succinate is the steroid of choice as it is short acting and provides equal glucocorticoid and mineralocorticoid activity. Although there is an intra-muscular injectable mineralocorticoid (desoxycorticosterone acetate) available in the USA, this is not usually required for stabilisation.
Avoid giving prednisone or prednisolone as it will alter the results of ACTH stim test. Dexamethasone or Dex-SP are accetable pre-test steroids.
[[Gastroprotective Drugs|'''Gastro-protectant drugs''']] (such as sucralfate, ranitidine or omeprazole) may be administered to vomiting animals and '''antibiotics''' should be provided to any animals that develop pyrexia.
[[Gastroprotective Drugs|'''Gastro-protectant drugs''']] (such as sucralfate, ranitidine or omeprazole) may be administered to vomiting animals and '''antibiotics''' should be provided to any animals that develop pyrexia.