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29 Cards in this Set
- Front
- Back
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What are the components of a foal wellness exam?
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vaccination hx of mare, problems w/ delivery, streaming milk, colostrum quality, gestation length, appearance of placenta, time to delivery, time to stand, time to nurse, attitude, behavior, complete PE, enema (owner usually gives: so foal passes meconium), umbilical care (1% Nolvasan)
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How is adequacy of passive transfer assessed?
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assess colostrum quality: appearance (should be thick, sticky), IgG content or SG (SG > 1.060 or IgG > 3000 mg/dl)
serum IgG at 12-18 hrs -radioimmunoassay: gold standard -stall side ELISA snap test: quick & generally reliable -glutaraldehyde coagulation: precipitation of Ig (cheap & fast) characterize passive transfer -IgG < 200 mg/dl: FAILURE OF PASSIVE TRANSFER (FPT) 200 mg/dl < IgG < 400 mg/dl: partial FPT -IgG > 400 mg/dl: adequate |
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What is the tx for failure of passive transfer?
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IgG supplementation: tx if FTP is partial or complete, esp. if risk factors for septicemia are present
if early: < 6 hrs. - colostrum by tube: equine is best, but can use bovine - if colostrum not available, commercial IgG supplement by tube if late: > 6 hrs. - give colostrum if foal has not suckled to provide local protective effects in gut & aid gut closure - plasma IV: 1-2 L - if plasma not available, commercial IgG supplement 12 hrs: usually too late to give anything orally recheck IgG to assess success of tx |
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What is the pathogenesis of neonatal septicemia?
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foal’s host defenses are overwhelmed
may occur in utero or after birth # & virulence of infecting organisms important bacteria gain access via GI tract, resp. tract, umbilicus, etc. Gram neg. enteric organisms most common: may be opportunistic (ex. E. coli) or pathogenic (ex. Salmonella sp.) |
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What are some risk factors for neonatal septicemia?
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- lack of good colostrum: FPT, poor local defenses, delayed gut closure
- illness: enteritis, pneumonia, etc. - sick mare - other complications: dystocia, hypoxia, placentitis, twins, prematurity, adverse environmental conditions, etc. |
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What are the clinical signs of neonatal septicemia?
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weakness, depression, stupor, coma, loss of suckle, hyperemic mm, dehydration, scleral injection, petechia, pyrexia or hypothermia
tachycardia, tachypnea, poor pulse quality, cool extremities |
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What are the common lab findings w/ neonatal septicemia?
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systemic inflammation: leucopenia, neutropenia w/ toxic change, bands, ↑ fibrinogen, thrombocytopenia
hypoglycemia, low IgG organ dysfunction: azotemia, ↑ LFT, ↑ bilirubin, high gap metabolic acidosis d/t poor tissue perfusion |
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How is neonatal septicemia diagnosed?
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sepsis score: predicts likelihood of sepsis (likelihood high if > 12)
blood culture: may not be very sensitive |
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What is the tx for neonatal septicemia?
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ABs: tx for 2 wks
- broad spectrum based on likely organisms prior to culture - drugs of choice: amikacin + penicillin - 2nd choice: ceftiofur or gentamicin + penicillin IgG - if early (< 6 hrs): colostrum or oral IgG supplement - if late: IV IgG supplement - plasma IV ALWAYS indicated regardless of time since birth fluids - isotonic crystalloids: rehydration, maintenance - colloids to support circulation - correct hypoglycemia & electrolyte/acid-base abnormalities nutrition - if not nursing, bottle feed only if strong enough to maintain sternal position; else, nasogastric tube - mares milk best, else goats milk or milk replacer - feed AT LEAST 15% of BW/day in milk, 20% if possible - total or partial parenteral nutrition if oral feeding not tolerated anti-inflammatories: NSAIDs (flunixin) O2 supplementation: based on arterial blood gas (nasal insufflation) other: pressors if needed (dobutamine or dopamine), +/- gastric ulcer prevention (ranitidine) |
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What is the pathogenesis of perinatal asphyxia syndrome (neonatal maladjustment)?
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often normal at birth & signs progressively appear over 12-72 hrs
cerebral hypoxia-peripartum asphyxia/hypoxia: placentitis, dystocia, prematurity/surfactant deficiency |
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What are the clinical signs of perinatal asphyxia syndrome?
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localize to forebrain: loss of suckle, wandering, blindness, vocalization, compulsive behavior, head pressing, circling, opisthotonus, seizures, depression/somnolence/coma
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How is perinatal asphyxia syndrome diagnosed?
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hx (foaling problems, gestation length, placental appearance)
PE CBC/Chem, arterial blood gas, blood culture, +/- CSF tap, +/- rads |
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What is the tx for perinatal asphyxia syndrome?
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cerebral edema
- mannitol IV: drug of choice - vitamin E PO: antioxidant - steroids: controversial - caffeine if hypoventilating - Mg sulfate infusions: standard of care; protect neurons from necrosis & death seizure control - diazepam IV for acute control - midazolam CRI: drug of choice - phenobarbital preventive ABs: high risk of septicemia |
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What is the pathogenesis of ruptured bladder?
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colts > fillies
etiology: birthing trauma?, infection?, other? uroperitoneum --> peritonitis, post-renal azotemia occ. hemoperitoneum or bacterial peritonitis |
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What are the clinical signs of a ruptured bladder?
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usually develop at 2-7 days of age
depression, stupor, coma, loss of suckle, stranguria or dysuria, colic, abdominal distension, encephalopathy: hyponatremia cerebral edema, bradycardia &/or arrhythmias: d/t progressive hyperkalemia (life threatening), high risk of septicemia: may see related signs |
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What are the lab findings assoc. w/ a ruptured bladder?
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hyponatremia, hyperkalemia (K > 6: ↑ mortality), hypochloridemia, hypocalcemia, metabolic acidosis, hypoosmolality, +/- azotemia, inflammatory leukogram
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How is a ruptured bladder diagnosed?
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measure peritoneal fluid &serum creatinine: diagnostic for uroperitoneum if Cr 1.5x higher in peritoneal fluid
abdominal U/S: can see peritoneal fluid |
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What is the tx for a ruptured bladder?
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medical
correct fluid & electrolyte imbalances - IV fluids: 0.9% saline (beware of acidosis) - +/- sodium bicarb to tx acidosis tx hyperkalemia - urinary catheter to keep bladder drained; may be sufficient to allow healing if only a small tear - drain uroperitoneum if possible (slowly) - consider peritoneal dialysis (abdominal lavage w/ warm saline) if K > 6 mEq/L glucose, insulin, bicarb: drive K into cells calcium: cardioprotectant broad spectrum ABs (ex. Cephalosporin): avoid potassium penicillin & aminoglycosides surgical - stabilize prior to sx: get K < 6, correct acidosis, drain abdomen - major complication: irreparable abdominal adhesions |
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What are some causes of enterocolitis (foal diarrhea)?
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nutritional: overfeeding (osmotic diarrhea), carbohydrate intolerance, esp. after enteritis (osmotic diarrhea), sand, change in diet
infectious: C. perfringens, Salmonellosis, C.difficile, Rotavirus, Coronavirus, Rhodococcus equi, Cryptosporidium, Lawsonia intracellularis, parasites, necrotizing enterocolitis |
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What are the clinical signs of foal diarrhea?
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diarrhea (+/- hemorrhagic), depression, stupor, coma, dehydration, signs of sepsis (fever, tachycardia or bradycardia, tachypnea, hyperemic mm, etc.), abdominal distension &/or colic (assoc. w/ ileus)
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How is enterocolitis diagnosed?
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blood culture if signs of sepsis: ALWAYS do if < 2 wks of age
Salmonella: fecal culture (3-5 serial samples) &/or PCR C. perfringens: fecal culture & toxin detection C. difficile: fecal cytotoxin A/B immunoassay rotavirus: fecal ELISA parasitism: fecal float |
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How is enterocolitis treated?
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fluid therapy
- isotonic crystalloid (plasmalyte R or LRS): resuscitation & rehydration - colloid if needed - maintenance: plasmalyte M ABs - broad spectrum if septicemia suspected - metronidazole (tx of choice) or penicillin IV d/t possibility of Clostridiosis - chloramphenicol for Salmonellosis mucosal protectants: bismuth subsalicylate (Pepto) gastric ulcer prevention: H2 blocker (ranitidine) or proton pump inhibitor (omeprazole) nutrition: +/- enteral or parenteral nutrition, probiotics? |
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What are prematurity & dysmatruity?
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prematurity: < 320 days gestational age
dysmaturity: > 320 days gestational age but physiologically premature (small); common in twins |
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What is the pathophysiology of prematurity/dysmaturity?
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- varying degrees of organ dysfunction
- immature immune system: prone to FPT - lungs: lack surfactant, alveolar collapse, ventilation/perfusion mismatch, pulmonary hypertension --> pulmonary failure (most common cause of death) - GI tract: ileus, susceptible to necrotizing enterocolitis, diarrhea - bones: incomplete ossification of cuboidal bones & sesamoids - CT: severe joint/tendon laxity - endocrine: hypoaldosteronism, hypothyroidism - blood-brain barrier: cerebral edema |
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What are the clinical signs of prematurity/dysmaturity?
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floppy ears, silky haircoat, thin skin, small size, domed forehead, joint laxity, incomplete ossification, resp. distress, tachycardia, ileus/diarrhea, forebrain signs, septicemia
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How is prematurity/dysmaturity diagnosed?
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gestational age, clinical signs
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What is the tx for prematurity/dysmaturity?
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- O2: insufflation or ventilation if hypoxia
- ABs: presume sepsis - plasma: presume FPT - parenteral nutrition - pressors - surfactant replacement? - physical therapy: must limit exercise to prevent crushing of cuboidal bones, but need some exercise & support of limbs (bandages, splints) - thyroid supplementation?: to speed ossification of bone |
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ddx for forebrain dz in neonates
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perinatal asphyxia syndrome, EHV-1 encephalitis, bacterial meningitis, hypoglycemia, trauma, endotoxemia/sepsis, electrolyte abnormalities (Na or Ca), acidosis, organ failure: hepatic encephalopathy, uremic encephalopathy, congenital anomaly
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ddx for ruptured bladder signs
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ruptured bladder, septicemia, SQ rupture of urachus: retrograde uroperitoneum, neurological dz, meconium retention & other colic, acute neonatal enterocolitis, hypoglycemia
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