Daphnie's weight problem

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  1. Ok so my fiancee and I are at our wits end. We have had Daphnie for about a year now and about 6 months ago we noticed that she was a skinny Boxer. She constently eats her food and never seems to put on any pounds. We have her on Purina One Performance Blend. We recently had to travel to North Carolina and left both of them with my parents. Because of the stress she did not eat (no fault of my parents). Both of them are free fed. When we got her back we could see all the bones in her body. We were soooo devestated because we feel like we are awful parents for having such a skinny dog. We have had her checked for worms and thyroid issues, nothing comes up. We asked our vet a month or so ago and they said that she was just a skinny boxer, but we are still worried. She is now super lethargic, but I don't know if it is because she misses my parents since she has been with them for two weeks, or if it is because she is just hungry or tired or just plain bored. We asked a breeder about this and she said that we needed to put her on wet dog food, so we went out and bought the kind she recommended. We have given her this and she loves it, but now she doesn't show very much interest in her dry food. Our little one, Hemi has a perfect body build and cannot have him eating all of her food so we have to put him in his room when we feed her the wet food. We just don't know what to do with her, which makes us more paroniod about if we are good parents or not. :crybaby:
     
  2. I know that there are naturally skinny dogs and dogs that gain weight way to easy. ;)

    Since you noticed other changes in you dog I would go to the vet for some more testing.

    And of course you are wonderful dog parents. Otherwise you wouldn't worry so much about your dogs. :smile:
     
  3. First of all, something is not right and she needs to see another vet. Have you had her tested for Addison's disease? It is something that a lot of vets do not specifically look for. This is copied and pasted from the Merck Veterinary Manual.

    Hypoadrenocorticism
    (Addison’s disease)Clinical FindingsLesionsDiagnosisTreatment
    A deficiency in adrenocortical hormones is seen most commonly in young to middle-aged dogs and occasionally in horses. The disease may be familial in Standard Poodles, Bearded Collies, and Portuguese Water Dogs. The cause of primary adrenocortical failure usually is not known, although most cases probably result from an autoimmune process. Other causes include destruction of the adrenal gland by granulomatous disease, metastatic tumor, hemorrhage, infarction, or overdose of mitotane (o,p&#8242;-DDD). Clinical Findings:Many of the functional disturbances of chronic adrenal insufficiency are not highly specific; they include recurrent episodes of gastroenteritis, a slowly progressive loss of body condition, and failure to respond appropriately to stress. Although hypoadrenocorticism occurs in dogs of any breed, sex, or age, idiopathic adrenocortical insufficiency is most common in young female adult dogs. This may be related to its suspected immune-mediated pathogenesis. A reduction in secretion of aldosterone, the principal mineralocorticoid, results in marked alterations of serum levels of potassium, sodium, and chloride. Potassium excretion by the kidneys is reduced and results in a progressive rise in serum potassium levels. Hyponatremia and hypochloremia result from renal tubular loss. Severe hyperkalemia may result in bradycardia and an irregular heart rate with alterations in the ECG. Some dogs develop a pronounced bradycardia (heart rate &#8804;50 bpm) that predisposes to weakness or circulatory collapse after minimal exertion. Although the development of clinical signs is often inapparent, acute circulatory collapse and evidence of renal failure frequently occur. A progressive decrease in blood volume contributes to hypotension, weakness, and microcardia. Increased excretion of water by the kidneys, due to decreased reabsorption of sodium and chloride, results in progressive dehydration and hemoconcentration. Emesis, diarrhea, and anorexia are common and contribute to the animal’s deterioration. Weight loss is frequently severe. Similar clinical signs are seen in cats with hypoadrenocorticism. Decreased production of glucocorticoids results in several characteristic functional disturbances. Decreased gluconeogenesis and increased sensitivity to insulin contribute to the development of moderate hypoglycemia. In some dogs, hyperpigmentation of the skin occurs due to the lack of negative feedback on the pituitary gland and increased ACTH release. Atypical Addison’s disease has been reported in dogs and is associated with hypocortisolemia with normal electrolytes. Clinical signs are similar to those seen in dogs with both glucocorticoid and mineralocorticoid insufficiency.Lesions: The most common lesion in dogs is bilateral idiopathic adrenocortical atrophy, in which all layers of the cortex are markedly reduced in thickness. The adrenal cortex is reduced to one-tenth or less of its normal thickness and consists primarily of the adrenal capsule. The adrenal medulla is relatively more prominent and, with the capsule, makes up the bulk of the remaining adrenal glands. All 3 zones of the adrenal cortex are involved, including the zona glomerulosa which is not under ACTH control; however, no obvious pituitary lesions have been seen in dogs with idiopathic adrenal cortical atrophy. A destructive pituitary lesion that decreases ACTH secretion is characterized by severe atrophy of the inner 2 cortical zones of the adrenal gland; the zona glomerulosa remains intact. a248.e.akamai.net/7/248/430/20060217203245/www.merckvetmanual.com/mvm/img/bn_btt.gifDiagnosis:A presumptive diagnosis is based on the history and supportive (although not specific) laboratory abnormalities, including hyponatremia, hyperkalemia, a sodium:Potassium ratio of <25:1, azotemia, mild acidosis, and a normocytic, normochromic anemia. Severe GI blood loss has also been reported. Occasionally, mild hypoglycemia is present. The hyperkalemia results in ECG changes: an elevation (spiking) of the T wave, a flattening or absence of the P wave, a prolonged PR interval, and a widening of the QRS complex. Ventricular fibrillation or asystole may occur with potassium levels >11 mEq/L. Differential diagnoses include primary GI disease (especially whipworm infection), renal failure, acute pancreatitis, and toxin ingestion. For definitive diagnosis, evaluation of adrenal function is required. After obtaining a baseline blood sample, ACTH (gel or synthetic) is administered IM and a second blood sample obtained 1-2 hr later. Affected dogs have low baseline cortisol levels, and there is little response to ACTH administration in classic and atypical cases. This test can be completed in most animals before replacement hormone therapy is started. a248.e.akamai.net/7/248/430/20060217203245/www.merckvetmanual.com/mvm/img/bn_btt.gifTreatment:An adrenal crisis is an acute medical emergency. An IV catheter should be inserted and a 0.9% saline infusion begun. If the dog is hypoglycemic, the saline can include 5% dextrose. The hypovolemia is corrected rapidly by administering 0.9% saline (60-70 mL/kg over the first 1-2 hr). Urine output should be assessed to determine whether the dog is anuric. Fluids should be continued, at a rate appropriate to match ongoing losses, until the clinical signs and laboratory abnormalities have resolved. Prednisolone sodium succinate (22-30 mg/kg) or dexamethasone sodium phosphate (2.2-4.4 mg/kg) may be used in the initial management of shock. Dexamethasone will not interfere with cortisol measurements during the ACTH stimulation test. Prednisolone or prednisone should be given at 1 mg/kg, bid, for the first few days of therapy and then at 0.25-0.5 mg/kg/day. Mineralocorticoid replacement therapy (see below) is also begun to help with electrolyte imbalances and hypovolemia. Electrolytes, renal function, and glucose should be monitored regularly to assess response to therapy. In cases of severe, nonresponsive hyperkalemia, 10% glucose (4.4-11 mL/kg) in 0.9% saline can be given over 30-60 min to increase potassium movement into the cells. Regular insulin (0.28-1.1 U/kg) administered IM will enhance glucose and potassium uptake, but 10% glucose (20 mL per unit of insulin) should be administered IV concurrently to avoid hypoglycemia. For longterm maintenance therapy, the mineralocorticoid fludrocortisone acetate is administered PO at 10-30 µg/kg/day. Serum electrolytes should be monitored weekly until the proper dose is determined. Alternatively, desoxycorticosterone pivalate may be administered at 2.2 mg/kg, IM or SC, every 25-28 days. Electrolytes should be measured at 3 and 4 wk after the first few injections to determine the duration of action. Sodium may be added to the diet (1-5 g/day) if hyponatremia persists despite normal serum potassium concentration. Some dogs also require daily oral glucocorticoid therapy to adequately control clinical signs. Replacement doses of prednisone (0.2-0.4 mg/kg/day) are required in ~50% of dogs. Additional glucocorticoid supplementation may be required (2-10 times maintenance) during times of illness or stress. Dogs with atypical Addison’s disease only require replacement doses of prednisone, although it is recommended that electrolytes be monitored every 3 mo for the first year after diagnosis. Dogs with chronic hypoadrenocorticism should be reexamined every 3-6 mo. Treatment of horses with hypoadrenocorticism is similar—aggressive replacement of fluids, steroids, and glucose if needed in an adrenal crisis. Supportive therapy and rest are indicated in cases of chronic Addison’s disease. a248.e.akamai.net/7/248/430/20060217203245/www.merckvetmanual.com/mvm/img/bn_btt.gifa248.e.akamai.net/7/248/430/20050616201425/www.merckvetmanual.com/mvm/img/shim.gif
    See AlsoIntroduction
     
  4. Thanks everyone here is an Update!!!!

    We have been feeding Daphnie (without Hemi) a can of wet dog food and 1/2 a bowl of dry dog food. She is back to her old puppy self. I think it was just being malnurished for a week and a half. We can no longer see her ribs, but we can still see her spine when she hunches over to play with Hemi. Hemi's attitude has also gotten better because Daphnie is more playful. We started the "BOO!!!!" game, both of them LOVE it!!! I say "BOOO!!!" and jump and they move back and them come tackle me and love on me. It's soo cute because my fiancee plays ROUGH with them and I cannot join in because they know not to play rough with mommy. I'm so relieved that Daphnie is feeling better and back to herself.