Endocrine emergencies

34 Endocrine emergencies

Canine Primary Hypoadrenocorticism (Addison’s Disease)

Theory refresher

The adrenal cortex produces corticosteroid hormones, including mineralocorticoids (primarily aldosterone) and glucocorticoids (primarily cortisol). Naturally occurring primary hypoadrenocorticism in dogs and cats is thought to be the result of immune-mediated destruction of both adrenal cortices and is the focus of this discussion. Secondary adrenocortical failure may also occur, either naturally due to diseases of the brain or as a result of chronic exogenous corticosteroid administration (i.e. iatrogenic causes).

Primary hypoadrenocorticism classically manifests with signs of both mineralocorticoid and glucocorticoid deficiency. Lack of aldosterone results in hyponatraemia (and hypochloraemia) with concurrent extracellular fluid volume depletion. Reduced cardiac output, systemic hypoperfusion and hypotension may ensue as a result of chronic renal fluid loss, acute gastrointestinal fluid loss and inadequate dietary intake. Reduced glomerular filtration rate (GFR) results in prerenal azotaemia. The aetiology of hyperkalaemia in primary hypoadrenocorticism is multifactorial and the most deleterious effects occur on cardiac function.

Cortisol affects almost every tissue in the body, and is significantly involved in haemodynamics and the cardiovascular system, metabolism, inflammation and immunological function, and gastrointestinal integrity. Its production increases during times of physiological stress. Lack of secretion may result in gastrointestinal signs, reduced mentation and activity levels, reduced energy metabolism and fasting hypoglycaemia, and especially impaired tolerance to stress.

Some dogs have atypical primary hypoadrenocorticism with only glucocorticoid insufficiency.

Clinical signs

Clinical signs are nonspecific and variable in both nature and severity. Most dogs are chronically affected. However, owners may not have noticed more subtle abnormalities or may not have considered them significant. Thus some dogs are only presented for veterinary attention when they suffer an acute Addisonian crisis. Clinical signs reported in primary hypoadrenocorticism are listed in Box 34.1. These signs are vague and nonspecific and may also occur in a large number of other disorders. It is therefore essential to keep primary hypoadrenocorticism on the differential diagnosis list for all dogs presenting with any of these signs until a definitive diagnosis is made.

Case example 1

Presenting Signs and Case History

A 4-year-old female neutered bearded collie dog presented with a 3-day history of lethargy that had progressed to noticeable weakness, and occasional vomiting. Her owners reported that her appetite had been variable over the preceding 3 months and that she had had occasional episodes of diarrhoea. No other significant history was reported.

Clinical Tip

• Primary hypoadrenocorticism is diagnosed most commonly in young to middle-age female dogs and breeds at increased risk include Poodle breeds, the Great Dane, the West Highland White terrier (and other terrier breeds), the bearded collie and the Rottweiler. Mixed breed dogs are most commonly affected.

Major body system examination

On presentation the dog was ambulatory but depressed. Cardiovascular examination revealed a heart rate of 80 beats per minute with mildly weak femoral pulses and even weaker dorsal pedal pulses. Mucous membranes were pink with a capillary refill time of 2 seconds, and the dog’s extremities were cool to the touch. Respiratory examination and abdominal palpation were unremarkable. Rectal temperature was mildly reduced (37.3°C). Electrocardiography was performed and the dog was found to be in sinus rhythm.

Assessment

The dog’s cardiovascular examination was suggestive of moderate hypovolaemia and her apparently normal heart rate was therefore considered to be an inappropriate bradycardia. Together with her signalment and history, this finding prompted a very high index of suspicion for hypoadrenocorticism (Addison’s disease) with the bradycardia thought to be the result of hyperkalaemia and impaired response to endogenous catecholamines due to glucocorticoid deficiency.

Emergency database

An intravenous catheter was placed in a cephalic vein and blood obtained via the catheter for an emergency database. This revealed remarkable findings of moderate to severe hyponatraemia (128.5 mmol/l, reference range 140.0–153.0 mmol/l), moderate hyperkalaemia (7.0 mmol/l, reference range 3.6–4.6 mmol/l), mild hypoglycaemia (4.0 mmol/l, reference range 4.2–6.6 mmol/l), mild azotaemia (blood urea nitrogen 20 mmol/l, reference range 3–10 mmol/l; creatinine 250 µmol/l, reference range 50–140 µmol/l) and mild hyperphosphataemia (2.90 mmol/l, reference range 0.94–2.13 mmol/l). The sodium to potassium ratio was markedly reduced (18.4 : 1, normal range 27 : 1–40 : 1). Peripheral blood smear examination was considered remarkable due to an absence of a neutrophilia and lack of an obvious lymphopenia (i.e. absence of a stress leucogram); a subjective eosinophilia was not noted.

Clinical Tip

• Serum sodium to potassium ratio is often, but not always, reduced in primary hypoadrenocorticism. The majority of dogs presenting in an acute crisis will have electrolyte abnormalities but electrolytes are normal in a small percentage (atypical primary hypoadrenocorticism). Other causes of hyperkalaemia and/or hyponatraemia should also be considered as appropriate (see Ch. 3)

• Hypercalcaemia (typically mild) and hypoalbuminaemia are also reported in some cases.

Clinical Tip

• Many dogs with primary hypoadrenocorticism have isosthenuric urine (specific gravity 1.007–1.015). Increased urine specific gravity is usually expected in the face of prerenal azotaemia; however, chronic urinary sodium loss disturbs the normal medullary concentration gradient (renal medullary washout) and therefore impairs water reabsorption.

Although not identified in this case, bone marrow suppression due to hypocortisolism can result in anaemia that may be mild to moderate in severity. A normocytic normochromic non- or minimally regenerative anaemia is identified. However, manual packed cell volume (PCV) at presentation may also be affected by both haemoconcentration (increases PCV) and potentially also gastrointestinal blood loss (decreases PCV).

Case management

Clinical Tip

• An acute Addisonian crisis is one of the true canine emergencies with a very real risk of rapid deterioration and death. Death as a result of an acute Addisonian crisis is more likely to be due to hypovolaemia and cardiovascular collapse than the effects of hyperkalaemia. While hyperkalaemia may be common in dogs with Addison’s disease, in the author’s experience specific intervention beyond fluid therapy (causes dilution and promotes kaliuresis) is rarely indicated.

• Isotonic crystalloid fluid therapy for hypovolaemia is therefore the most important intervention. There is ongoing debate regarding the relative merits of 0.9% sodium chloride (normal, physiological saline) versus buffered lactated Ringer’s solution (Hartmann’s solution, compound sodium lactate). Ultimately which of these is chosen is likely to be inconsequential in the vast majority of cases and starting fluid therapy is the priority.

The findings of the emergency database strongly supported the suspected diagnosis of classic hypoadrenocorticism. The dog was started on intravenous 0.9% sodium chloride (normal, physiological saline). A conservative bolus of 20 ml/kg was administered over 20 minutes and a constant infusion of 6 ml/kg/hr was then provided. As the dog was clinically stable, an adrenocorticotrophic hormone (ACTH) stimulation test was performed over 1 hour prior to the administration of dexamethasone (0.5 mg/kg i.v. q 6). As hypoglycaemia was only mild, supplementation was not provided.

Tags: Saunders Solutions in Veterinary Practice Small Animal Emergency

Sep 3, 2016 | Posted by admin in SMALL ANIMAL | Comments Off

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