The incidence of cysts in pregnancy was established with ultrasound. In 3,330 pregnant patients who underwent sonography, 38 adnexal cystic lesions (1.14%) were found. All but two cysts were discovered before 16 weeks. Follow-up showed that the majority of the cystic lesions resolved spontaneously; these were presumed to represent corpus luteum cysts. Five patients underwent surgery because of persistent cystic lesions; a mucinous cystadenoma, a benign cystic teratoma, a paraovarian cyst, an inclusion cyst, and a tuboovarian abscess were found. Septations and echogenic material were seen within the cystic teratoma and the tuboovarian abscess but the sonographic features of the other operated lesions were identical to those seen in the corpus luteum cysts.
Two dogs developed delayed neurological deterioration after rapid correction of severe hyponatremia. Sequential magnetic resonance imaging showed the development of lesions in the thalamus. One dog was necropsied, and the lesions were characterized by myelinolysis with sparing of axons and neurons. The second dog gradually recovered n humans, rapid correction of chronic hyponatremia by I upward shifts in serum sodium concentrations exceeding 12 mmol/L in 24 hours commonly leads to delayed neurological deterioration. This deterioration is associated with lesions of well-demarcated myelin loss, affecting the pons and other sites in the brain (central pontine myelinolysis).',' Neither the genesis of the lesions nor the reason for their peculiar neuroanatomic distribution is ~nderstood,~ but recent advances in identifying antemortem lesions by magnetic resonance imaging (MRI) suggest that the condition is more common in humans than once believed'~~ and is not uniformly fatal.'-* Similar clinical signs and lesions occur after rapid correction of experimental hyponatremia in a variety of animal species,'-" including dogs." We report the delayed development of neurological signs and extrapontine (predominantly thalamic) lesions after rapid correction of spontaneous hyponatremia in 2 dogs. In 1 patient, postmortem examination confirmed the focal loss of myelin and degeneration of glia in the central thalamic nuclei and rostra1 commissure, with preservation of neurons and axons. The other dog recovered with no residual neurological deficits. Our experience with these patients highlights the need for gradual correction of profound hyponatremia in the clinical setting. Case Reports Dug OneA 4-year-old female English Setter dog developed lethargy after a history of weight loss of several weeks' duration. At physical examination, the 12-kg dog had a temperature of 97°F (36.1°C), a pulse of48 beats per minute, and a respiratory rate of 20 breaths per minute. She was thin and depressed, had pale mucous membranes and labored breathing, and was approximately 5% dehydrated. A complete blood count (CBC) showed neutrophilia with a left shift. Se- (0 'Brien, Kroll, Covert) rum biochemical abnormalities included profound hyponatremia, hypochloremia, hypo-osmolality, hyperkalemia, hyperglycemia, and azotemia (Table 1). An electrocardiogram (EKG) showed no P waves and a T wave deflection of greater than 1/4 of the R wave in lead 11. A tentative diagnosis of hypoadrenocorticism was reached, and an adrenocorticotropic hormone (ACTH) challenge test was performed. From the Departments of Veterinary Medicine and SurgeryThe dog was treated with amoxicillin (250 mg PO BID), dexamethasone ( 1 mg/kg intravenously), and intravenous 0.9% sodium chloride (NaCI) at a rate of 6 1 mL/h. During the first day of hospitalization, the dog's attitude improved dramatically. Her body temperature and heart rate returned to normal; however, watery diarrhea was noted. On day two, the dexamethasone dose was decreased to 0.25 mg/kg, amoxicillin was continued, an...
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