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The Case: Troubled Endocrine Treatment

Clinician's Brief

Endocrinology & Metabolic Diseases

|October 2012|Web-Exclusive

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Presentation

  • 10-year-old, spayed female mixed-breed dog is presented for progressive polyuria/polydipsia of 2 weeks’ duration. Side/belly are often wet with urine after reclining. No stranguria/pollakiuria described.
  • Client recounts recent significant weight loss (formerly 80 lb)
  • New client, so limited history to this point. Vaccination and heartworm preventive are up to date.

Physical Examination

  • Vital Signs
    • Temperature: 101.2⁰F
    • Pulse: 100 bpm
    • Respiration: 60 bpm (Excessive panting but normal bronchovesicular sounds in all lung     fields)
  • Bright, alert, responsive; mucous membranes pink/moist; CRT: <2 sec (estimated hydration adequate)   
  • Obese: BCS 9/9 (58 lb)
  • Grade 2 periodontal disease
  • Abdominal  palpation: abdomen distended/round, soft/pain free; moderate hepatomegaly
  • Integument: Flaky/dry skin with hyperpigmentation of ventral abdomen

Diagnostic Procedures

  • Serum biochemical profile
    • ALP:  1724 U/L (range, 10–150)
    • Glucose: 447 mg/dL (range, 60–125)
    • Anion gap: 32 mEq/L (range, 12–24)
    • Bicarbonate: 10 mEq/L (range, 17–24)
  • CBC
    • Platelets: 538 × 103/μL) (range, 164–510)
    • WBCs: 25.0 × 103/μL (range, 5.7–16.3)
    • Absolute monocytes: 1500/μL (range, 150–1350)
    • Absolute neutrophils: 21.25 × 103/μL) (range, 3–11.5); neutrophils slightly toxic
  • Urinalysis (urine collected free-catch)
    • Glucose:  3+
    • Ketones: 3+
    • Specific gravity: 1.021
    • pH: 5.0
  • ACTH Stimulation Test (Performed day after blood analysis at request of  owner)
    • Pre-ACTH resting cortisol: 9.9 μg/dL (range, 2–6)
    • Post-ACTH: 27.2 μg/dL (>22 consistent with hyperadrenocorticism)

Treatment

  • Continue high-fiber diet (Already feeding a dry commercial weight-management food)
  • Initiated NPH insulin (6 U q12h) with instructions to check blood glucose curve in 1 week
    • Client scheduled glucose curve 4 days after starting insulin. Client checked blood glucose with in-home  glucometer; administered 6 U NPH insulin prior to presentation: 
      • Initial value: 563
        • Hour 2: 371    
        • Hour 4: 621    
        • Hour 6: 654    
        • Hour 8: 596
  • Recalculated starting dose of insulin; recommended 12 U q12h
  • Discussed with client concurrent Cushing’s disease/challenge of adequately controlling diabetes mellitus. Because dog was clinically stable/not showing clinical signs of diabetic ketoacidosis, recommended increasing dose of insulin; then initiating treatment for Cushing’s disease after several days. Due to cost of trilostane, client opted for mitotane. Strict instructions were given to client on multiple occasions during visit to wait several days (until after the weekend) to initiate treatment for Cushing’s disease to enable daily communication regarding the dog’s status.
    • Mitotane (750 mg q24h; divided into 500 mg AM/250 mg PM) for induction phase
    • Prednisolone (5 mg) also prescribed for use in case of emergency.  Client instructed about signs to monitor, when to give prednisolone if unable to reach anyone at the hospital, and to continue giving insulin if, and only if, the dog is eating.  

Presentation 2
Patient was presented on Monday AM (when mitotane should have been started) recumbent/unable to stand.  For last 2 days, patient had not been eating; was dribbling urine, trembling in rear legs, breathing heavily/panting excessively, lethargic/acting drunk, drinking excessively. Vomited this morning. Currently on 9 U NPH insulin; owners gave “a few doses” of aspirin at some point over the weekend and had elected against medical advice to start mitotane (250 mg in first dose) 4 days ago “to get a jump-start on Cushing’s.”  Aforementioned clinical signs appeared on days 3 and 4 after initiating mitotane.  Owners then proceeded to give prednisolone, insulin, and mitotane (250 mg in AM/500 mg in PM) q12h through the weekend.

Physical Examination

  • Patient in lateral recumbency/minimally responsive/nonambulatory
  • Blood glucose (by glucometer): 640
  • Hydration: severely tacky, pink mucous membrances; CRT 3 sec (estimated 10% to 12% dehydration)
  • Tachycardic (HR: 145)/tachypneic (RR: 42) at rest; panting when manipulated
  • Temperature: 103.1⁰F
  • Weight: 51 lb

Diagnostic Procedures

  • Serum biochemistry panel
    • ALP: >2000 U/L (range, 23–212)
    • Glucose: 630 mg/dL (range, 70–143)
    • BUN: 49 mg/dL (range, 7–27)
    • Lipase: 5670 U/L (range, 200–1800)
    • Electrolytes
      • K: 5.7 mmol/L (range, 3.5–5.8)
      • HCO3: 6.3 mmol/L (range, 20–29)
      • pCO2: 20 mmHg (range, 32–49)
    • pH: 7.14 (range, 7.31–7.42)
    • tCO2: 7 mmol/L (range, 21–31)
  • CBC
    • HCT: 28.3%
    • RBCs: 4.85 × 103/μL (range, 5.5–8.5)
    • HGB: 8.9 g/dL (range, 12–18)
    • MCV: 58.4 fL (range, 60–77),
    • Reticulocytes: 0.8%
    • WBCs: 55.29 × 103/μL (range, 5.5–16.9)
    • Neutrophils: 44.67 × 103/μL (range, 2–12)
    • Monocytes: 8.43 × 103/μL (range, 0.3–2)
    • PLTs: 564 × 103/μL (range, 175–500)
  • Urinalysis
    • Glucose: 100 mg/dL
    • Ketones: 15 mg/dL
    • Protein: 30 mg/dL
    • Erythrocytes: 250/μL
    • pH: 7.0

Treatment/Progress

  • 0.9% NaCL bolus (400 mL over 90 minutes IV)
  • For diabetic ketoacidosis: 0.9% NaCl + 20 mEq/L KCl + 29 mEq HCO3 (in 600 mL) over next 6 hr at 100–150 mL/hr
  • Glucose measurements by glucometer:
    • Initial value: 607; administered 5 U regular insulin IM
      • Hour 1: 538; administered 2.5 U regular insulin IM. Blood pressure: 165; Temperature: 102.8⁰F
      • Hour 2: 448, administered 2.5 U regular insulin IM. Dog more responsive when stimulated, wagging tail, breathing more easily and steadily. Rectal exam: darker, possibly tarry stools. Administered cefazolin (500 mg IV)
      • Hour 3: 354; no additional insulin
      • Hour 4: 304; no additional insulin
      • Hour 5: 311; administered 9 U NPH insulin SC
  • Abdominal ultrasound: homogenous, hyperechoic region noted in area of pancreas; consistent with pancreatitis. Both adrenal glands enlarged but normal in shape; caudal pole of left = 0.7 cm; caudal pole of right = 0.8 cm.  No other abnormalities noted.
  • Electrolytes 6 hours after starting treatment: HCO3 improved but still low.
  • Administered maropitant IV, sucralfate (1 gm slurry PO), famotidine (10 mg IV)
  • Hour 6: Respirations increased/dog less responsive. Continued IV fluids with KCl additive only  (75 mL/hr)

Outcome
During the day, owners were advised of severity of diabetic ketoacidosis. Recommended continued treatment/hospitalization overnight at Emergency Clinic for continued close observation. Owners could   not afford financially; patient remained in-house on IV fluid pump overnight.  Late in the day,  owners had been informed that pet appeared to be declining despite treatment; prognosis now guarded to poor. Patient died overnight.


The Specialist’s Opinion
Gretchen Statz, DVM, DACVECC

Typically in cases of diabetic ketoacidosis (DKA), aggressive therapy including IV fluids and short-acting (regular) insulin is warranted. Clinical signs of illness can occur quickly once ketonemia, ketonuria, and metabolic acidosis occur.  Animals that are eating normally, not acting sick, and not acidotic can sometimes do well with outpatient therapy; however, more aggressive treatment in a 24-hour ICU environment is often necessary.  This patient was ketotic and acidotic on initial presentation so a more aggressive approach was warranted. 

When presented, the dog had an elevated white blood cell count with toxic changes. This factor, in combination with the DKA, should prompt further investigation to look for other underlying disease processes such as pyelonephritis (diabetic patients are prone to urinary tract infections) or pancreatitis. A urine culture and abdominal ultrasound were also indicated. 

It is not recommended to test or treat for hyperadrenocorticism in a newly diagnosed diabetic patient, as the metabolic stress of the concurrent illness can cause adrenal hypersensitivity and a falsely elevated posttest result. It is best to stabilize the diabetes prior to adrenal testing, which is especially true with DKA as there may be other disease processes present and the metabolic derangements are more severe.  An ACTH-stimulation test is the test of choice when looking for hyperadrenocorticism in a diabetic dog, but it should be reserved for those that are nonketotic, nonacidotic, and  stable.

The clinical signs that were present when the dog re-presented may have been related to the DKA and/or adrenal suppression from mitotane. An ACTH-stimulation test would have been ideal at this point to help determine whether steroid therapy was indicated. A physiologic dose of steroids may have been helpful pending the test results as adrenal suppression may have been contributing to the patient’s status.  

This case was complicated by a lack of owner compliance and possibly a lack of owner understanding of the underlying disease processes and treatments. It is important to educate owners properly about the various diseases and the reasoning behind and side effects of their treatments. Proper client education and printed discharge instructions can sometimes help decrease compliance issues. 

Diabetic Ketoacidosis Treatment
DKA requires aggressive monitoring and treatment, including hourly or every-other-hour glucose monitoring and short-acting insulin, which can be administered via continuous rate infusion (CRI) or intermittent intramuscular (IM) injection to slowly bring the glucose down. The electrolytes, acid–base status, and fluid balance must be monitored closely. The IM regular insulin in this case was switched to a subcutaneous injection after 3 doses. A more aggressive approach (ie, CRI or continued IM injections) is generally indicated until the patient has normal hydration and the glucose is consistently below 250 mg/dL. Short-acting insulin should be used to maintain the glucose at this level until the patient is eating and ketones are not present. Because animals with DKA require fairly aggressive micromanagement of their glucose, electrolytes, and hydration status, they are difficult to treat successfully outside a 24-hour care facility. In this case 24-hour care was offered but declined. 

Hyperadrenocorticism Diagnosis & Treatment
As discussed previously, hyperadrenocorticism treatment is typically reserved for stable patients that are not currently ill from other disease processes.  In cases of DKA, the ketosis and acidosis should be stabilized before diagnostics are performed. Hyperadrenocorticism treatment is rarely, if ever, an emergency need and should be initiated after other disease processes have been stabilized. 

Gretchen Statz, DVM, DACVECC, is an internal medicine consultant for Antech Diagnostics and a VIN consultant on the internal medicine boards. A graduate of University of Wisconsin – Madison, Dr. Statz interned at VCA West Los Angeles and then worked for several years at two emergency/referral hospitals in the Boston area. After completing a residency at VCA Veterinary Referral Associates in Gaithersburg, Maryland, she became boarded in emergency and critical care and practiced in that area for some time. Having a strong interest in internal medicine, she has been practicing in that field for the past several years. 

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

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