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Biomedical subjects

C W Kohn

Publications and source records attributed to C W Kohn.

53 records · Page 3Linked to original sources
PubMed1988

Ultrastructure of junctional epidermolysis bullosa in Belgian foals.

Ultrastructural examination of a mechanobullous disease of probable hereditary nature in Belgian foals, confirmed light microscopic findings that separation of the dermo-epidermal junction occurred through the lamina lucida of the basement membrane, leaving the intact lamina densa adherent to the dermis and the plasmalemma of the basal epithelial cells intact. The location of the cleft and the presence of small hemidesmosomes in adjacent intact skin are additional characteristics which make this condition similar to junctional epidermolysis bullosa of man.

Animals↗
PubMed1987

Laboratory diagnosis and characterization of renal disease in horses.

Laboratory evaluation of renal function in horses has advanced dramatically in the last 10 years largely as a result of the interest generated by the creative approach to diagnostic indices taken by Brobst, Traver, Coffman, and others. Some methods of assessing renal function discussed here are clearly outside the scope of a practice environment but are available in referral hospitals for use in difficult or unusual cases. Other methods described, such as calculation of fractional excretions and urine to serum creatinine ratios, are accessible and readily interpreted by the veterinary practitioner. These diagnostic methods should help in the early identification of renal disease in horses and therefore should allow veterinarians the option to treat renal disease before renal failure is advanced. In addition, practitioners may be able to offer more informed prognoses after a more complete evaluation of renal function.

Animals↗
PubMed1987

Equine herpes myeloencephalopathy.

The neurologic form of EHV-1 infection appears to be the result of central nervous system infarction caused by vasculitis, which is initiated in endothelial cells of small blood vessels. The etiologic agent is equine herpesvirus-1, subtype 1. There is some evidence to suggest that the neurologic form of the disease actually results from reactivation of a previous infection. Whether the vasculitis that causes the central nervous system injury is the direct result of the infection or an immune response to the infection has not been determined. The clinical signs are rapid in onset, nonprogressive, and many horses may improve. The diagnosis must often remain tentative, particularly in horses that recover, because there is no single reliable confirmatory test. The prognosis is generally good, although recovery may be slow and incomplete. Supportive therapy is essential, and administration of corticosteroids may be useful. There is no specific therapy for the virus or for the vasculitis. Currently no vaccine can be claimed to protect against the central nervous system form of the disease. Vaccination is recommended, however, to reduce the incidence of respiratory disease, abortion, and neonatal death on the farm. Repeated vaccination is necessary to maintain presumably protective antibody concentrations. Vaccination every 3 to 4 months may decrease the incidence of EHV-1 infection on the farm and therefore may indirectly prevent the occurrence of the neurologic form of the disease.

Animals↗
PubMed1986

Bilateral renal hypoplasia in four young horses.

Three horses less than or equal to 3 years old were evaluated because of stunted growth, weight loss, anorexia, depression, and lethargy of at least 1 month's duration. A neonatal foal was examined after its death. In each case, gross and microscopic renal lesions were compatible with bilateral renal hypoplasia (ie, cortical hypoplasia with severe medullary hypoplasia). In young horses with renal failure, bilateral renal hypoplasia should be considered in the differential diagnosis, and may represent a congenital lesion.

Animals↗
PubMed1986

24-hour renal clearance and excretion of endogenous substances in the mare.

Urine samples were obtained from 6 healthy mares. During a 2-day acclimation period, mares were kept in stalls, fed sweet feed and mixed grass hay, and allowed free access to water and trace mineral salt. The mares were crosstied in their stalls within reach of hay, salt, and water for 24 hours during which urine was obtained by constant flow via indwelling Foley catheters. Twenty-four-hour urine production was 7,649 to 11,904 ml/day (mean = 9,212 +/- 1,9285) or 14.7 to 25.1 mlĝ/day. (mean = 19.3 +/- 4.1). Urinary excretion and clearance of electrolytes and protein were determined from aliquots of well-mixed, pooled 24-hour urine samples. These values were sodium (Na) = 0 to 1.7 mEq/kg/day (mean = 0.4 +/- 0.7), chloride (Cl) = 2.0 to 4.2 mEq/kg/day (mean = 3.0 +/- 0.8), phosphorous (P) = 0.03 to 0.12 mg/kg/day (mean = 0.07 +/- 0.3), potassium (K) = 3.7 to 6.5 mEq/kg/day (mean = 5.3 +/- 1.4), and creatinine (Cr) = 32.1 to 53.9 mg/kg/day (mean = 40.3 +/- 8.5). Fractional excretions of electrolytes were Na = 0% to 0.46% (mean = 0.1 +/- 0.2), Cl = 0.48% to 1.64% (mean = 1.14 +/- 0.45), P = 0.04% to 0.16% (mean = 0.08 +/- 0.04), and K = 23.9% to 75.1% (mean = 51.7 +/- 17.3). Average clearances (ml/hr/kg) were Na = 0.12 +/- 0.19, K = 64.1 +/- 17.1, Cl = 1.21 +/- 0.33, and P = 0.09 +/- 0.51. Average endogenous Cr clearance (ml/min/kg) was 1.92 +/- 0.51.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Uroperitoneum in the foal.

The case records of 22 foals with uroperitoneum were reviewed. The most common cause was a defect in the urinary bladder. A sex predilection for males was apparent. Clinical signs were tachycardia, tachypnea, and abdominal distention. The history pertaining to micturition was variable. Hyponatremia, hypochloremia, and hyperkalemia were marked. A reliable means of diagnosis was considered to be the demonstration of a wide disparity in serum and peritoneal fluid creatinine values. Surgical repair was successful in 11 of 18 cases, although surgical and anesthetic complications were common. Some of the defects were believed to be congenital.

Animals↗
PubMed1982

Acquired inguinal hernia in the horse: a review of 27 cases.

Twenty-seven cases of acquired inguinal hernia in the horse were reviewed. The history, clinical signs, treatment, and complications were summarized. Mortality was 25.9%. Only 13 or the 27 cases were diagnosed prior to admission. With early diagnosis and treatment, mortality should approach zero. In 24 of these cases, the hernia was strangulated. In each case, the signs were colic, a firm slightly enlarged testicle in the scrotum, and small intestine displacement through the inguinal ring, as determined via rectal palpation. In was concluded that palpation of the scrotum and inguinal rings should be performed on every stallion with colic. The importance of early diagnosis in decreasing mortality was illustrated by the comparison of nonsurvivors to survivors.

Animals↗
PubMed1978

Effects of furosemide on plasma volume and extracellular fluid volume in horses.

The effects of IV administered furosemide upon plasma volume (PV) and extracellular fluid volume were determined in horses at rest and after exercise. Serum sodium, potassium, chloride, and osmolality determinations were made. Furosemide caused a significant (P less than 0.05) decrease in PV and serum potassium concentrations in resting horses only. Furosemide's effects upon PV and electrolytes were evident longer than its hemodynamic effects.

Animals↗
PubMed1978

Plasma volume and extracellular fluid volume in horses at rest and following exercise.

Plasma volume and extracellular fluid volume were determined in horses at rest and immediately after a standardized exercise test. Exercising during training demonstrated no detectable effect on plasma or extracellular fluid volume determinations when compared with resting values. An explanation of this finding and an argument for the proper analysis of plasma and extravascular fluid volumes are presented.

Animals↗
PubMed1977

Fibrous foreign body impaction colic in young horses.

OF 207 horses with colic seen over a 36-month period, 10 were determined to have impaction colic caused by ingestion of synthetic fencing material. In 6 cases, there was history of exposure to rubberized fencing products. All horses affected were less than or equal to 3 years of age, had signs of mild to moderate abdominal pain, and were unresponsive to usual symptomatic therapy. At surgery, each horse was found to have an impaction involving the distal right dorsal colon, transverse colon, or small colon, and in some cases, all 3 bowel segments. In 9 cases, the involved segment of bowel could not be brought out of the abdominal cavity, and in each of these cases, the foreign bodies were removed through one or more enterotomies. Five of the 10 horses survived.

Animals↗
PubMed1977

Plasma clearance of [51Cr] albumin into the intestinal tract of normal and chronically diarrheal horses.

Five clinically normal, mature horses and 11 with chronic diarrhea were given 51Cr-tagged Cohn fraction V equine albumin intravenously. All urine and feces were collected separately, and blood for plasma analysis was taken periodically for 5 to 8 days after injection of the isotope. Plasma clearance of albumin into the intestinal tract of normal horses was calculated as 0.67 +/- 0.23 (SD) ml/kg of body weight/day, with 1.33 +/- 0.69% of the 51Cr dose appearing in the feces in 5 days. Of the 11 diarrheal horses, 8 had a plasma clearance of 0.49 +/- 0.21 ml/kg/day with 1.12 +/- 0.68% of the dose of 51Cr in a 5-day fecal collection, suggesting that excessive losses of plasma protein into the bowel was not a component of their intestinal disease. The 3 other diarrheal horses had a marked protein-losing enteropathy; 1 of these horses had granulomatous enteritis due to Mycobacterium avium infection; another had severe intercellular edema of small and large intestinal mucosa, cause unknown; and intestinal biopsies were not obtained from the 3rd horse. The results suggest that: (1) as with other species that have been studied, daily loss of plasma protein into the bowel of horses is small; (2) most horses with chronic diarrhea do not have protein-losing enteropathy.

Albuminuria↗
PubMedDate not supplied

Selected aspects of the clinical pharmacology of visceral analgesics and gut motility modifying drugs in the horse.

Comparison of the visceral analgesic effects of xylazine, morphine, butorphanol, pentazocine, meperidine, dipyrone, and flunixin in a cecal distention model of colic pain indicated that xylazine produces the most relief from abdominal discomfort. Repeated administration of xylazine may reduce visceral pain so effectively that the seriousness of abdominal disease is obscured. Xylazine decreased propulsive motility in the jejunum and pelvic flexure of healthy ponies. Morphine and butorphanol also gave relief from visceral pain in the cecal distention model. Morphine may inhibit colonic, and butophanol jejunal, motility. Whether xylazine or opiate mediated decreases in gut motility cause clinically important slowing of ingesta transit is controversial and requires further investigation. The development of behavioral changes (i.e., apprehension and pawing) in horses given opiate therapy may limit the use of these drugs. Combinations of xylazine and morphine or butorphanol produce excellent, safe, visceral analgesia and sedation without untoward behavioral effects. Although flunixin fails to demonstrate good visceral analgesic effects in the cecal distention model, this drug produces analgesia in some cases of colic by blocking prostaglandin mediated induction of pain. Improvement of propulsive gut motility in patients with ileus may follow administration of neostigmine (which is particularly effective when the large bowel is hypomotile), naloxone (which experimentally stimulates propulsive colonic motility), and metoclopramide (which stimulates stomach and proximal small intestinal motility).

Analgesics↗
PubMedDate not supplied

Myeloid and megakaryocytic hypoplasia in related standardbreds.

Myeloid and megakaryocytic bone marrow hypoplasia in association with moderate to profound neutropenia was observed in 8 young Standardbred horses sired by the same stallion; 7 horses were intermittently thrombocytopenic. Evaluation of serial neutrophil counts in 2 horses suggested that a cyclic variation in neutrophil numbers was present, that lymphocyte numbers increased when neutrophil counts decreased, and that platelet counts decreased when neutrophil counts decreased. Preliminary bone marrow cultures indicated that myeloid progenitor cells were present and that these cells were able to respond to exogenous growth factors by differentiating. A bone marrow microenvironment or growth factor defect is suspected. Seven of 8 horses died or were euthanized. One horse with moderate neutropenia and a normal platelet count has been racing for 3 years. Necropsies in 4 horses did not reveal a cause for the myeloid hypoplasia. A familial basis for the disease is suspected.

Anemia, Aplastic↗
PubMedDate not supplied

Necrotizing enterocolitis in horses: a retrospective study.

The clinical and clinicopathologic characteristics of fatal necrotizing enterocolitis were examined in 16 horses (age 4 months to 12 years). At initial presentation, 8 of 16 horses were pyrexic (median temperature, 38.4 degrees C; range, 33.8 to 40.6 degrees C); all 16 were tachycardic (median heart rate, 93 bpm, range, 66 to 138 bpm); 13 of 16 were tachypneic (median heart rate, 36 bpm, range, 16 to 80 bpm), dehydrated, and had discolored mucous membranes. All horses that were pyrexic were also tachycardic and tachypneic. PCV was high (> 45%) in 14 horses. Six horses were leukopenic (< 5,000 cells/microL); 12 were neutropenic (< 2,300 cells/microL), and 14 had > 100 band neutrophils/microL. Twelve horses were acidemic (pH < 7.37; range, 6.88 to 7.33) and the venous bicarbonate concentration was low (< 23 mEq/L) in 14 horses. Median anion gap in 16 horses was 31.5 mEq/L (> 15 mEq/L in 15 horses). Eleven of 16 horses were hyponatremic (< 137 mEq/L), 1 horse was hypernatremic (> 143 mEq/L), 3 were hypokalemic (< 3.2 mEq/L), 6 were hyperkalemic (> 4.5 mEq/L), and 14 were hypochloremic (< 98 mEq/L). Serum creatinine concentrations were high (> 1.4 mg/dL) in 15 horses. Abdominal fluid was examined in 12 horses 4 had total protein concentrations > 2.5 g/dL and 6 had nucleated cell counts > 5,000/ microL and < 10,000/microL; none had > 10,000/microL. Eight of 12 samples revealed a nondegenerate neutrophilia (> 50%). Abdominal fluid collected from 4 horses immediately before death was normal in 2 horses and indicative of suppurative inflammation in 2. All 8 horses tested had low or nonexistent serum immunofluorescent antibody titers to Ehrlichia risticii. Four of 16 horses had Salmonella spp isolated from feces or tissues. All 16 horses either died (5 of 16; 31%) or were euthanized because of a grave prognosis. Median time to death was 45.5 hours (range, 7 to 113 hours) from the time of admission. Death was preceded by severe abdominal pain in 14 horses. Fatal necrotizing enterocolitis of horses is characterized by a brief course, profound dehydration, electrolyte derangements, acid-base abnormalities, and terminally, severe abdominal pain. Abdominal fluid analysis was frequently not indicative of the severity of disease.

Acid-Base Equilibrium↗
PubMedDate not supplied

Results of quantitative cultures of urine by free catch and catheterization from healthy adult horses.

Quantitative urine cultures were performed on 11 male and 11 female healthy adult horses. Urine was collected by free catch and catheterization using standard methods. Results showed that all samples collected by free catch contained less than 20,000 colony-forming units (CFU)/mL. All samples collected by catheterization contained 500 CFU/mL or less. A significant difference was found between collection methods (P < .005), with catheterization having less contamination. In samples collected by free catch, females had significantly greater contamination than did males (P < .03). Predominant bacterial species isolated included Streptococcus spp., Escherichia coli, Enterobacter sp., Bacillus sp., Staphylococcus spp., Diptheroids sp., Proteus spp., and Enterococcus sp. Many samples contained multiple bacterial species. Bacterial isolates were representative of the normal bacterial flora of the equine urogenital tract. This paper establishes reference values for quantitative urine culture results in healthy adult horses to aid in the diagnosis of urinary tract infections.

Animals↗
PubMedDate not supplied

Diagnostic validity of electroencephalography in equine intracranial disorders.

Electroencephalography (EEG) is a valuable diagnostic test to identify functional disturbances in brain activity. The purpose of this study was to assess the validity of EEG as a diagnostic indicator of intracranial diseases in horses. The validity of EEG was estimated by comparing clinical, clinicopathologic, and histopathologic findings to EEG findings in 20 horses examined for seizures. collapse, or abnormal behavior between 1984 and 1997. A bipolar left-to-right, back-to-front montage and a bipolar circular montage were recorded from sedated (4) and anesthetized (16) horses. Visual and semiquantitative masked analysis of EEG recording Ist was validated on 10 horses presented for problems other than intracranial diseases. EEG pattern was normal in 7 of the 20 clinically affected horses. Abnormal EEG patterns included high-voltage slow waves and discrete paroxysmal activity with or without generalized activity in 13 horses. Histopathologic diagnoses in 10 horses included meningoencephalitis, neuronal necrosis, congenital anomalies. cerebral edema. and abscess. All of these horses had abnormal EEG patterns (sensitivity, 100%) with a positive neuroanatomic correlation in 7 animals. Localization of histopathologic and EEG abnormalities did not correlate in 15% of the horses (3/20). The cause of neurologic signs could not be explained at postmortem examination in 10 animals and the EEG pattern was normal in 7 of these horses (specificity, 70%). In conclusion, equine EEG was a sensitive tool in the diagnosis of intracranial disorders.

Animals↗