Endocrine Causes of Calcium Disorders

Endocrine diseases that may cause hypercalcemia and hypocalcemia include hyperparathyroidism, hypoparathyroidism, thyroid disorders, hyperadrenocorticism, hypoadrenocorticism, and less commonly pheochromocytoma and multiple endocrine neoplasias. The differential diagnosis of hypercalcemia may include malignancy (lymphoma, anal sac carcinoma, and squamous cell carcinoma), hyperparathyroidism, vitamin D intoxication, chronic renal disease, hypoadrenocorticism, granulomatous disorders, osteolysis, or spurious causes. Hypocalcemia may be caused by puerperal tetany, pancreatitis, intestinal malabsorption, ethlyene glycol intoxication, acute renal failure, hypopararthyroidism, hypovitaminosis D, hypomagnesemia, and low albumin. This article focuses on the endocrine causes of calcium imbalance and provides diagnostic and therapeutic guidelines for identifying the cause of hypercalcemia and hypocalcemia in veterinary patients.     

Intact Parathyroid Hormone Assay and Total Calcium Concentration in the Diagnosis of Disorders of Calcium Metabolism in Dogs

Serum samples from eight dogs with primary hyperparathyroidism, seven dogs with hypercalcemic lymphosarcoma (hypercalcemia of malignancy), and four dogs with primary hypoparathyroidism were submitted to the Animal Health Diagnostic Laboratory at Michigan State University for intact parathyroid hormone (PTH) assay. When compared with the adjusted total serum calcium concentration, the intact PTH concentration was consistent with the correct diagnosis in all cases. Two dogs with hypercalcemic lymphosarcoma were mildly azotemic. In both of these cases the intact PTH concentration was consistent with hypercalcemia of malignancy despite the presence of azotemia. These data support a significant role for intact serum PTH assay in the differential diagnosis of disorders of calcium metabolism.     

Management of Acute Gastric Dilation in Rabbits

Rabbits that have sudden onset anorexia commonly present to veterinary practices with dilated stomachs. Postmortem examination or surgical investigation often identifies the underlying etiology of the gastric dilation as small intestinal obstruction. The condition is frequently fatal if left untreated, but protocols for diagnosis and treatment have not been established. This article attempts to clarify diagnosis of the condition by clinical and radiographical signs, as well as providing a guide to the management of these difficult cases. With appropriate decision making and treatment, the prognosis for small intestinal obstruction in rabbits can be dramatically improved.     

Esophageal Disorders in 61 Horses: Results of Nonsurgical and Surgical Management

Obstructive esophageal disorders in 61 horses included feed or foreign body impaction (27 horses), strictures (18 horses), perforations (11 horses), and diverticula (5 horses). Horses with feed impaction were treated nonsurgically (25 horses) or by esophagotomy (2 horses). Survival to discharge was 78%, and 37% of these had persistent chronic obstruction at home. Long-term survival was 52%. Long-term survival of nine horses treated nonsurgically for esophageal strictures was 22%; for nine horses treated surgically it was 44%. Long-term survival of horses treated nonsurgically was significantly better in acute than chronic strictures. Surgical repair of esophageal mural strictures was more successful than repair of annular or mucosal strictures. One third of the horses with strictures were foals. Long-term survival for horses with strictures was 33%. Long-term survival was higher for the horses with perforations managed surgically (2 of 4) than nonsurgically (0 of 7). Long-term survival for this group was 18%. One esophageal diverticulum was managed nonsurgically, and four were treated surgically; all horses survived long term. Complications of obstructive esophageal disorders included aspiration pneumonia, chronic obstruction, esophageal mucosal ulceration, postoperative infection, pleuritis, laminitis, laryngeal paralysis, and Horner's syndrome.     

Clinical Update on Diagnosis and Management of Disorders of the Digestive System of Reptiles

The diagnosis and treatment of digestive system disorders in reptile species continues to provide challenges owing to the differences in anatomy and physiology in this diverse group of animals. Continued research efforts into diagnostic techniques, in particular imaging (e.g., contrast radiography and ultrasonography), of gastrointestinal tract have resulted in clinical advancements for practicing veterinarians. The aim of this article is to provide veterinarians up-to-date and clinically relevant summaries on the diagnosis and therapy of digestive system disorders of reptiles commonly maintained as companion animals.     

Current Concepts in the Management of Acute Spinal Cord Injury

Acute injury to the spinal cord initiates a sequence of vascular, biochemical, and inflammatory events that result in the development of secondary tissue damage. Experimental studies and clinical trials in humans have demonstrated that the extent of this secondary tissue damage can be limited by pharmacologic intervention at appropriate intervals after injury. High doses of methylprednisolone sodium succinate (MPSS) improve the outcome of acute spinal cord injury in humans if treatment is initiated within 8 hours of injury. Starting therapy more than 8 hours after injury is detrimental to outcome. The clinical efficacy of methylprednisolone in improving the outcome of canine spinal cord injuries has not yet been demonstrated and its use by veterinarians is controversial. Many dogs are not seen by a veterinarian within the 8-hour window after injury, and these dogs frequently are treated with nonsteroidal anti-inflammatory drugs or large doses of dexamethasone or prednisone before methylprednisolone treatment can be initiated, thus increasing the risk of severe adverse effects. Other drugs that may provide safer and more effective alternatives to methylprednisolone include thyrotropin-releasing hormone (TRH), the 21-aminosteroids, and kappa opioid agonists. Recent studies suggest that modulation of the influx of inflammatory cells and activation of endogenous microglial cells may provide another means of improving the outcome of acute spinal cord injuries. Many drugs being developed to treat acute spinal cord injury have shown promising results when evaluated experimentally. However, any proposed therapeutic strategy should be evaluated in prospective blinded clinical trials before being adopted in clinics.