{"id":11516,"date":"2016-08-31T11:25:13","date_gmt":"2016-08-31T11:25:13","guid":{"rendered":"http:\/\/phosdev.com\/todaysveterinarypractice\/?p=11516"},"modified":"2022-02-17T21:16:13","modified_gmt":"2022-02-17T21:16:13","slug":"consider-this-casethe-adr-aint-doing-right-dog-endocrine-emergencies","status":"publish","type":"post","link":"https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/endocrinology\/consider-this-casethe-adr-aint-doing-right-dog-endocrine-emergencies\/","title":{"rendered":"The ADR (Ain\u2019t Doing Right) Dog: Endocrine Emergencies"},"content":{"rendered":"

Lucky, a 6-year-old, 20-kg, female spayed, mixed-breed dog was presented due to a 1-week history of progressive \u201cADR\u201d (ain\u2019t doing right).<\/p>\n

History<\/strong><\/h2>\n

Lucky was presented to the emergency referral veterinary clinic because her primary care veterinarian was closed for the evening.<\/p>\n

The owner reported that Lucky vomited in the car a week earlier when coming home from the groomer. Over the past week, Lucky\u2019s appetite diminished but she seemed thirstier. Lucky had become progressively more lethargic and anorectic over the past 2 days.<\/p>\n

\n

Note:<\/strong> The first annual Today\u2019s Veterinary Practice<\/em> symposium\u2014Insights from Experts<\/strong>\u2014took place at the NAVC Conference 2016 in Orlando, Florida. This article reviews the information provided by Dr. Justine Lee and Dr. Garret Pachtinger in the session, Emergency Management of Hypoadrenocorticism<\/strong>.<\/p>\n

\n

Lucky was up-to-date on vaccines, receiving seasonal flea and tick medication and heartworm preventative, and healthy until a week ago.<\/p>\n

Physical Examination<\/strong><\/h2>\n

The physical examination findings for Lucky upon presentation to the referral facility are listed in Table 1<\/strong>. Doppler blood pressure measurement revealed that Lucky\u2019s systolic blood pressure was 80 mm Hg.<\/p>\n

\"T1609C08Table01\"<\/p>\n

Initial Diagnostics<\/strong><\/h2>\n

Due to the combination of Lucky\u2019s dehydration and hypovolemia (based on poor pulse quality), a peripheral 18-gauge, 6-cm cephalic IV catheter was placed. A small amount of blood from the catheter hub was obtained for analysis of packed cell volume, total solids, blood urea nitrogen (Azostix, usa.healthcare.siemens.com), blood glucose, and venous blood gas\/electrolytes. Laboratory results are listed in Table 2<\/strong>.<\/p>\n

\"T1609C08Table02\"<\/p>\n

Due to the severe hyperkalemia (see INITIAL DIAGNOSIS, Electrolyte Abnormalities<\/strong>), an electrocardiogram (ECG) was obtained immediately. A sinoventricular rhythm was observed, with absent P waves and widened QRS complexes (Figure 1<\/strong>). Typical ECG findings in hyperkalemic patients include bradycardia; tall, tented T waves; prolonged QRS intervals; prolonged PR intervals; absent P waves; and deviation of the ST segment.<\/p>\n

\"FIGURE<\/a>

FIGURE 1. Electrocardiogram showing sinoventricular rhythm, with absent P waves and widened QRS complexes. Courtesy Gordon Peddle, VMD, Diplomate ACVIM (Cardiology)<\/em><\/p><\/div>\n

\n

Severe hyperkalemia<\/strong><\/h2>\n

is a potentially life-threatening complication in a variety of conditions and, thus, emphasizes the importance of rapid evaluation and treatment.<\/p>\n<\/div>\n

Initial Diagnosis<\/strong><\/h2>\n

Electrolyte Abnormalities<\/strong><\/h3>\n

Lucky\u2019s sodium:potassium ratio was 16:1, which is most often seen in veterinary patients as a result of hypoadrenocorticism and mineralocorticoid deficiency. The hyperkalemia can potentially be life-threatening, resulting in severe arrhythmias. The hypoglycemia can result in clinical signs of weakness, tremors, vomiting, seizures, collapse, and death. Prompt treatment of the electrolyte abnormalities and hypoglycemia in this patient was imperative.<\/p>\n

Dehydration & Hypovolemic Shock<\/strong><\/h3>\n

This patient had both dehydration and hypovolemic shock. While the patient was only mildly bradycardiac, this was likely an inappropriate response to hypovolemia secondary to a life-threatening hyperkalemia. The presence of both dehydration and hypovolemia are likely due to both glucocorticoid and mineralocorticoid deficiencies.<\/p>\n

Differential Diagnosis<\/strong><\/h3>\n

Differential diagnosis\u2014in addition to glucocorticoid\/mineralocorticoid deficiencies\u2014includes underlying metabolic conditions (eg, ascites, pericardial effusion, severe metabolic acidosis), gastrointestinal disease (eg, whipworm infection), acute kidney injury (AKI), neoplasia, trauma (eg, uroabdomen, rhabdomyolysis), and sepsis.1-6<\/sup><\/p>\n

Initial Therapy<\/strong><\/h2>\n

Therapy for Electrolyte Abnormalities<\/strong><\/h3>\n

Hyperkalemia decreases resting potential, which makes it less negative and initially results in more hyperexcitable cells.7<\/sup> To increase the normal threshold membrane potential, thereby normalizing the difference between the 2 potentials, a bolus of 50 mg\/kg 10% calcium gluconate, delivered slowly over 15 minutes, was administered to Lucky.7<\/sup><\/p>\n

Alternatively, use of sodium bicarbonate or insulin:dextrose can be considered. Although calcium gluconate has the most rapid stabilizing effect in hyperkalemic patients, it does not address the hyperkalemia itself. Both sodium bicarbonate and insulin therapy result in a transient lowering of serum potassium, promoting its translocation from the extracellular to the intracellular fluid compartment (Figure 2<\/strong>).<\/p>\n

\"FIGURE<\/a>

FIGURE 2. The effects of potassium and calcium on the action potential. Reprinted with permission from DiBartola SP (ed). Disorders of potassium. Fluid Therapy in Small Animal Practice, 2nd ed. Philadelphia: WB Saunders, 2000.<\/p><\/div>\n

Lucky received continuous ECG monitoring during calcium gluconate administration and until she was more cardiovascularly stable. It is important to remember that calcium gluconate does not directly affect potassium levels.<\/p>\n

Therapy for Dehydration & Hypovolemic Shock<\/strong><\/h3>\n

Lucky received an initial IV bolus of 0.5 g\/kg dextrose (10 mL of 50% dextrose diluted in 20 mL of 0.9% saline) over 2 to 3 minutes to address the hypoglycemia. An additional bolus of 400 mL (20 mL\/kg) of warmed lactated Ringer\u2019s solution was administered over 15 minutes.<\/p>\n

Ongoing Fluid Therapy<\/strong><\/h3>\n

1. Replacement fluids: <\/strong>Lucky\u2019s estimated dehydration was 5%. To correct this deficit over the next 8 hours, Lucky needed to receive fluids at a rate of 125 mL\/H:<\/p>\n

1000 mL (deficit)\/8 H = <\/em>125 mL\/H
\n<\/em><\/strong>20 kg (body weight) \u00d7 0.05 (dehydration) = 1000 mL fluid deficit<\/em><\/p>\n

2. Maintenance fluids<\/strong>: Lucky also needed to concurrently receive maintenance fluids at a rate of 42 mL\/H:<\/p>\n

20 kg (body weight) \u00d7 50 mL Q 24 H = 1000 mL Q 24 H
\n<\/i>1000 mL \/24 H = <\/em>42 mL\/H<\/em><\/strong><\/p>\n

More information on the dosage of 50 mL Q 24 H can be found at aaha.org\/public_documents\/professional\/guidelines\/fluidtherapy_guidlines_toolkit.pdf.<\/p>\n

3. Ongoing losses<\/strong>: Ongoing losses (eg, vomiting, urinary losses) were estimated at 30 mL\/H.<\/p>\n

4. Crystalloid fluid therapy<\/strong>: Crystalloid fluid rate for the first 8 hours\u2014after the initial fluid bolus\u2014was calculated:<\/p>\n

Replacement (125 mL\/H) + maintenance (42 mL\/H) + ongoing losses (30 mL\/H)
\n= approximately 200 mL\/H
\n<\/i><\/p>\n

Once the dehydration deficit had been replaced, the fluid rate was adjusted to reflect maintenance and ongoing losses. Based on blood glucose monitoring results, glucose supplementation (2.5%\u20135% dextrose supplementation) was adjusted to maintain normoglycemia.<\/p>\n

Patient Monitoring<\/strong><\/p>\n

Reassessment of perfusion parameters showed improvement after the initial crystalloid and dextrose bolus, and Lucky was carefully and frequently assessed while receiving fluid therapy (Table 3<\/strong>). Blood glucose was measured Q 8 H in order to guide glucose supplementation.<\/p>\n

\"T1609C08Table03\"<\/p>\n

Additional Diagnostics<\/strong><\/h2>\n

While the patient was stabilized, further diagnostics were pursued, including a complete blood count (CBC), serum biochemical profile, urinalysis (Table 4<\/strong>), and baseline and resting cortisol levels.<\/p>\n

\"T1609C08Table04\"<\/p>\n

CBC results revealed:<\/p>\n

    \n
  • Eosinophilia and lymphocytosis: May be due to glucocorticoid deficiency (eg, lack of a stress leukogram)1<\/sup><\/li>\n
  • Mild anemia: In the face of dehydration, may be due to gastrointestinal bleeding or anemia of chronic disease.<\/li>\n<\/ul>\n

    Biochemistry revealed:<\/p>\n

      \n
    • Hypoglycemia: Rarely seen in adult dogs secondary to anorexia; may be due to glucocorticoid deficiency, insulinoma, iatrogenic insulin administration, hunting dog hypoglycemia, neoplasia, or sepsis<\/li>\n
    • Electrolyte abnormalities, with a sodium:potassium ratio of 16:1<\/li>\n
    • Azotemia: May be due to prerenal or primary AKI<\/li>\n
    • Hypercalcemia: May be due to underlying metabolic disease (eg, hypoadrenocorticism, hyperparathyroidism), toxicosis (eg, cholecalciferol, calcipotriene), or neoplasia<\/li>\n
    • Isosthenuria: May be due to medullary washout secondary to excessive sodium loss into the urine or underlying renal disease.<\/li>\n<\/ul>\n

      Lucky\u2019s baseline cortisol (< 2 mcg\/dL) was consistent with hypoadrenocorticism. Due to concern regarding the low baseline cortisol, a complete adrenocorticotropic hormone (ACTH) stimulation test was submitted. Both pre-ACTH (< 2 mcg\/dL) and post-ACTH (< 2 mcg\/dL) stimulation test results were consistent with hypoadrenocorticism.<\/p>\n

      Definitive Diagnosis<\/strong><\/h2>\n

      Based on the baseline cortisol and ACTH stimulation tests, all the clinicopathologic tests were consistent with a diagnosis of hypoadrenocorticism. Additional diagnostics may include fecal testing (to rule out whipworms) and advanced diagnostic imaging, such as ultrasound (to rule out signs and disease, such as gastrointestinal bleeding, ascites, and neoplasia).<\/p>\n

      Therapy for Hypoadrenocorticism<\/h2>\n

      Typical supportive therapies for the patient with hypoadrenocorticism include:8,9<\/sup><\/p>\n

        \n
      • Crystalloid fluids<\/strong>, along with dextrose<\/strong> supplementation as needed<\/li>\n
      • Steroids<\/strong>, such as dexamethasone, due to lack of adequate glucocorticoid levels; other types of steroids (eg, prednisone, prednisolone, hydrocortisone) should not be used before diagnostic testing (eg, ACTH stimulation, baseline cortisol) because they interfere with the radioimmunoassay for glucocorticoid measurement<\/li>\n
      • Gastric protectants<\/strong>, such as famotidine or pantoprazole, if gastric ulceration is suspected<\/li>\n
      • Antiemetics<\/strong>, such as maropitant, dolasetron, ondansetron, or metoclopramide, if vomiting is present<\/li>\n
      • Mineralocorticoids<\/strong>, such as desoxycorticosterone pivalate (DOCP) or fludrocortisone acetate (Florinef, bms.com), to help normalize electrolytes; they should be administered once the patient is stable, with life-threatening electrolyte abnormalities corrected, and can tolerate oral medication.<\/li>\n<\/ul>\n

        Lucky\u2019s therapeutic approach included:<\/p>\n

          \n
        1. Initial therapy for electrolyte abnormalities and arrhythmias (calcium gluconate), with continuous ECG monitoring<\/li>\n
        2. Initial therapy for dehydration and hypovolemia (dextrose and fluid boluses, then fluid therapy)<\/li>\n
        3. Rapid diagnosis of, and therapy for (Table 5<\/strong>), hypoadrenocorticism.<\/li>\n<\/ol>\n

          \"T1609C08Table05\"<\/p>\n

          Lucky\u2019s hydration and hypovolemic state improved with fluid therapy and her blood pressure returned to normal after 2 crystalloid boluses. Within 12 hours, Lucky was eating and drinking, and her electrolyte abnormalities had resolved.<\/p>\n

          Prognosis & Follow-Up Care<\/h2>\n

          Lucky was discharged the day after presentation\u2014once she was appropriately hydrated, her electrolytes were corrected, and she was eating and drinking voluntarily.<\/p>\n

          Lucky\u2019s owner was instructed on the long-term management of hypoadrenocorticism, taught how to administer medications (including extra dosing during stressful events), and counseled to follow up with the veterinarian for long-term mineralocorticoid management (eg, DOCP).<\/p>\n

          The primary care veterinarian performed a recheck examination 3 days after discharge and noted that the physical examination and electrolyte findings were normal; follow-up was scheduled for 3 weeks later to recheck electrolytes and administer DOCP (Table 6<\/strong>).<\/p>\n

          \"T1609C08Table06\"<\/p>\n

          The owner was pleased with the outcome and rapid improvement in Lucky\u2019s condition.<\/p>\n

          \n

          Overview of Hypoadrenocorticism<\/strong><\/h2>\n

          Pathophysiology<\/strong><\/h3>\n

          The adrenal gland is composed of an outer cortex and the inner medulla: The adrenal medulla, which is not affected in hypoadrenocorticism, secretes catecholamines, such as epinephrine and norepinephrine. Hypoadrenocorticism results from atrophy or destruction of the adrenal cortex, which is subdivided into 3 layers:<\/p>\n

            \n
          • The outer layer\u2014zona glomerulosa<\/strong>\u2014is involved with synthesis and secretion of the mineralocorticoid hormone, aldosterone.<\/li>\n
          • The middle layer\u2014zona fasciculata<\/strong>\u2014synthesizes glucocorticoids.<\/li>\n
          • The inner layer\u2014zona reticularis\u2014produces adrenal sex steroids.<\/strong><\/li>\n<\/ul>\n

            Primary versus Secondary Disease<\/strong><\/h3>\n

            Hypoadrenocorticism may be classified as primary or secondary8<\/span><\/sup>: Primary hypoadrenocorticism<\/strong> results from bilateral destruction of the adrenal cortices, presumed in most cases to result from immune-mediated destruction of the adrenal gland. Less common causes of primary hypoadrenocorticism include trauma (eg, surgical versus other), infections (eg, fungal or bacterial), neoplasia, or medical therapy (eg, mitotane, trilostane, ketoconazole, megestrol acetate).<\/p>\n

             <\/p>\n

            Secondary hypoadrenocorticism<\/b> results from lack of adrenal gland stimulation due to hypothalamic\u2013pituitary\u2013adrenal axis dysfunction, which most commonly results from inflammation, tumors, or trauma. Exogenous steroid administration may also suppress ACTH release, resulting in adrenal atrophy.<\/p>\n

            Signalment<\/strong><\/h3>\n

            With hypoadrenocorticism, certain breeds of dogs are over-represented, including standard poodles, Great Danes, Rottweilers, West Highland white terriers, Wheaten terriers, Leonbergers, Portuguese water dogs, Labrador retrievers, bearded collies, Old English sheepdogs, and standard schnauzers. Hypoadrenocorticism is also seen more often in young to middle-aged female dogs.11-18<\/sup><\/p>\n

            Clinical Signs<\/b>\u00a0<\/strong><\/h3>\n

            Pathophysiologic changes seen with hypoadrenocorticism are directly a result of glucocorticoid and mineralocorticoid deficiencies. Common clinical signs typically include lethargy, inappetence, vomiting, diarrhea, bradycardia, hypotension, weight loss, and, rarely, death.11<\/span><\/sup><\/p>\n

            Clinical Findings<\/b><\/h3>\n

            Clinicopathologic findings seen with hypoadrenocorticism include the failure to mount a stress leukogram (resulting in eosinophilia, lymphocytosis, and normal overall white blood cell and neutrophil count) and electrolyte abnormalities secondary to direct aldosterone effects (eg, hyperkalemia, hyponatremia, hypochloremia, metabolic acidosis).<\/p>\n

            Other common laboratory abnormalities include azotemia, isosthenuria (from osmotic diuresis secondary to sodium losses), hypoglycemia (due to impaired gluconeogenesis), hypercalcemia (due to altered renal excretion, reduced gastrointestinal absorption, and decreased resorption of calcium from bone), hypoalbuminemia, and hypocholesterolemia.11,12<\/sup><\/p>\n

            Therapeutic Approach<\/strong><\/h3>\n

            Without treatment, hypoadrenocorticism can be life-threatening due to dehydration, hypovolemia, severe electrolyte derangements, and ongoing fluid losses. To ensure the best outcome, the hypoadrenocorticism state should be rapidly identified.<\/p>\n

            Treatment for the critically ill patient with hypoadrenocorticism should include symptomatic supportive care, aggressive fluid therapy, correction of electrolyte abnormalities and hypoglycemia, antiarrhythmic therapy (if needed), steroid administration, and mineralocorticoid supplementation, if needed. Appropriate use of steroids needs to be weighed so as not to impair diagnostic testing for baseline cortisol levels or for future ACTH stimulation tests.<\/p>\n<\/div>\n

            In Summary<\/strong><\/h2>\n

            Clinicians should be able to rapidly recognize hypoadrenocorticism on the basis of history, signalment, clinical signs, and classic clinicopathologic testing. Rapid and appropriate diagnostic workup should be performed (eg, baseline cortisol, ACTH cortisol evaluation) to rule out other \u201clook-alike\u201d diseases, such as metabolic disorders (eg, renal disease, pancreatitis), toxicosis (eg, from ingestion of grapes, cholecalciferol), and infectious disease (eg, Leptospira<\/em> infection, urinary tract infection, pyelonephritis).<\/p>\n

            While long-term management may be cumulatively expensive (eg, prednisone, periodic electrolyte monitoring, and mineralocorticoid supplementation), with medical management, the prognosis for hypoadrenocorticism is good to excellent.<\/p>\n

            ACTH = adrenocorticotropic hormone; AKI = acute kidney injury; CBC = complete blood count; ECG = electrocardiogram<\/p>\n","protected":false},"excerpt":{"rendered":"

            This article reviews the information provided by Dr.<\/p>\n","protected":false},"author":15,"featured_media":11519,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"iawp_total_views":443,"footnotes":""},"categories":[363],"tags":[13],"class_list":["post-11516","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-september-october-2016","tag-peer-reviewed","clinical_topics-emergency-medicine-critical-care","clinical_topics-endocrinology"],"acf":{"hide_sidebar":false,"hide_sidebar_ad":false,"hide_all_ads":false},"yoast_head":"\nThe ADR (Ain\u2019t Doing Right) Dog: Endocrine Emergencies | Today's Veterinary Practice<\/title>\n<meta name=\"robots\" content=\"noindex, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta 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