Sepsis In Foals Flashcards
SIRS systemic inflammatory response syndrome refers to
A systemic response that results in 2 of the following: fever, tachcyardia, tachypnea or hyperventilation leukocytosis, luekopenia or relative increase in circulating neutrophils
Sepsis definition
When SIRS occurs in response to a suspected or confirmed infectious process
Infection with which class of bacterial organisms causes sepsis in neonatal foals?
Gram negative bacteria— release endotoxin
Foal GI tract is an important portal of entry for pathogens via which route of absorption?f
Pinocytosis of macromolecules in the small intestine (little discrimination between maternal IGG and macromolecules)
What is the predominant organism isolated from septic foals?
E coli
Rare, but what is the most common systemic fungal infection in foals?
Candida albicans
Common biochemical abnormalities in septic foals
Abnormal blood glucose Azotemia/hyperbilirubinemia Acidemia Hyperlactatemia Arterial hypoxemia & hypercapnia (can occur indepedent to resp dz) INC triglyceride concentration Inc albumin
What is the gold standard for diagnosis of sepsis in a foal?
Blood culture
Examples of medical treatment options for systemic candidiasis
Fluconazole
Itraconazole
Miconazole
Amphtoericin B
Drugs that are antiendotoxic use to treat foals:
Flunixin meglumine
Polymyxin B
Pentoxifylline
When to consider vasopressor therapy in hypovolemic/septic shock/hypotensive patients?
After appropriate fluid resuscitation should consider vasopressors & inotropes
What is the incidence of pneumonia in septic foals?
28 to 50%
What percentage of foals that have diarrhea the bacteremic?
About 50% of neonates
How does uroperitoneum develop in foals?
Ischemia and Necrosis of bladder &/or urachus
Besides trauma
CSF of a foal with meningitis
Pleocytosis (normally neutrophilic)
Treatment of choice for meningitis in foals
3rd generation cephalosporin (ceotaxime)
Major differentials for the neurologic neonate?
Meningitis Neonatal encephalopathy (NE)
What are some strategies to prevent sepsis in foals?
Maintain a clean environment
Reduce potential b act load introduced during udder seeking
Ensure GI intake of colostrum
Confirm adequate transfer of passive immunity
Ensure appropriate umbilical care
Monitor foals closely and tx suspect foals quickly
Differentials for seizures in foals
Neonatal encephalopathy Bacterial meningitis Viral encephalitis Benign juvenile epilsepsy Lavender foal syndrome Kernicterus Hepatic failure Congenital brain disease Hydrocephalus, hydranecephaly Head trauma Hypoglycemia Eectrolyte disorders (Hypocalciemia hyponatremia, hypernatremia) Tetanus Toxicities (ivermectin, moxidectin) Glycogen storage disease IV Hyperammonemia of Morgan foals
What is the basis of neonatal encephalopathy pathogenesis?
Reduction in cerebral blood flo w& oxygen to tissues during:
—Antepartum: maternal hypotension, severe hypoxia, infection, placental insufficiency
—Perpartum: cord occlusion, premature placental separation, dystocia
—Postnatal: neonatal shock, repsiraotry or cardiac arrest
After reversible hypoxic-ischemic brain injury, neuronal injury and or death occurs in what 2 phases:
- Primary or acute phase of injury
2. Delayed phase of cell death
Primary or acute phase of injury in the pathophysiology of neonatal encephalopathy involves:
Dec cerebral blood flow—> dec O2 & glucose delivery to the brain
—> switch to anaerobic respiration
—>Dec ATP & phosphocreatine & INC lactic acid production
—> DEC ATP results in inability to maintain Ca/Na/K regulation through the Na/K pump
—> cell swelling/edema & depolarization of neurons—> precipitates the release of neurotransmitter glutamate
What is the role of microglia in the phase of primary energy failure of pathogenesis in neonatal encephalopathy?
Microglia migrate to the area of necrosis & release further inflammatory mediators that can damage the CNS
Neonatal encephalopathy:
Delayed neuronal cell death or secondary energy failure occurs in what time period?
6 to 48 hours after initial hypoxic ischemic injury
Neonatal encephalopathy:
Delayed neuronal cell death/secondary energy failure is believed to be through/associated with what following mechanisms?
Excitotoxicity Accumulation of intracellular calcium & resultant activation of numerous enzymes & pathways Reperfusion injury (oxidative stress) Cytotoxic actions of activated microglia Inflammation Apoptosis
Neonatal encephalopathy
What is the pathway of glutamate in the healthy individual?
Glutamate released from presynpatic nerve terminals when signaled by neuronal depolarization
Rapidly removed from synpatic cleft by glutamate ransporters in astroglia & converted to glutamine
Transported back into nerve terminal for reuse
Neonatal encephalopathy
What impairs the glutamate transporters in astroglial cells in teh synpatic cleft?
Hypoxia or ischemia
Decreased glucose delivery to teh brain
—> RESULTS: increased glutamate concentrations & excessive calcium influx into neurons—> excitotoxicity—> cell apoptosis & necrosis
Neonatal encephalopathy
Why is the neonatal brain susceptible to oxidative injury?
High concentrations of unsaturated fatty acids
High rate of oxygen consumption
Low concentration of antioxidants
Neonatal encephalopathy:
Reactive oxygen spp (ROS) and reactive nitrogen spp (RNS) cause significant damage to what
Biological proteins (membrane protein degration) Lipids (lipid oxidation) Nucleic acids (DNA degeneration)
Neonatal encephalopathy:
What is a steroid that possibly contributes to neonatal encephalopathy in some foals?
Neurosteroids— ie plasma progestagens: progesterone, epitetestosterone, androstenedione
What are recognized risk factors for the development Neonatal encephalopathy in foals?
Dystocia Induced parturition Cesarean section Placentitis Premature placental separation Severe illness Post-term pregnancy (fescue toxicity) Maternal hypotension (endotoxemia, hemorrhage, anemia, severe respiratory disease)
Other possible risk factors: meconium aspiration, twin foals, fetal infection, congenital malformations, umbilical cord accidants
Reported clinical signs in neonatal foals & percentages (from a retrospective study)
Abnormal udder seeking (59%) Abnormal suckle (55%) Inability to stand (42%) Abnormal GI motility (37%) Abnormal consciousness (34%) Seizure activity (22%)
Neonatal encephalopathy in human infants diagnosis is supported by what modalities?
Neurologic exam
MRI
EEG
Ultrasound
Neonatal encephalopathy diagnosis in the foals is based on:
Clinical impression Historial information Neurologic examination Compatible clinical signs Exclusion of other disease processes
What is an alternative therapy to doxapram to improve PaCO2 in foals with NE?
Caffeine per os: loading dose of 7.5 to 12 mg/kg, followed by daily dose of 2.5 to 5 mg/kg if CRI is not feasible
Neonatal encephalopathy treatment:
If hypoventilation and hypercapnia are observed what medication can be administered as a CRI as a respiratory stimulant?
Doxapram: at 0.02 to 0.05 mg/kg/hour
For seizure control in foals, what medications can be used?
Diazepman: 0.1 to 0.2 mg/kg — given intermittently
Midazolam: 0.4 to 0.1 mg/kg IV or a CRI: 0.02 to 0.06 mg/kg/hour IV
Phenobarbital- for persistent seizure activity
—2 to 10 mg/kg IV over 15 minutes, then 5 mg/kg PO q12h
What are possible side effects of phenobarbital?
Mild sedation
Ataxia
Hypothermia
What medication can be administered if intractable cases of status epilepticus in foals?
Propofol CRI
Proposed benefits of a hyperbaric chamber in NE foals?
Reduced apoptosis
Promotion of neuronal stem cell prolifeartion
Enhancement of oxygen radical scanvers
Increased oxygen delivery to teh brain
Increased activity of superoxide dismutase
Medications used to combat edema and oxidative damage in foals with NE?
Mannitol: 0.5 to 2.0 g/kg as a 20% solution over 20 minutes IV q12-24 h
Furosemide: 1 mg/kg IV q12-24h
Dimethyl sulfoxide: 0.5 to 1 g/kg IV as a 10% solution over 30 minutes q12 to 24 hours
Thiamine: 5 to 10 mg/kg IV or sc q24h
Vitamin E: 20/kg IU/kg, sc or pO q24h
Vitamin C: 100 mg/kg/day IV
What are the proposed benefits of magnesium sulfate in IV fluid therapy for NE foals?
Prevents calcium entry into the cell by nonceompetitive voltage depedent inhibition of NMDA receptors
— blocks release of glutamate & antagonizes the influx of calcium
— protective against hypoxic-ischemic injury
Dose: 0.5 g/kg/h for first hour, then 0.025 g/kg/h IV as CRI
Reported survival rate in foals with NE (without complicating factors) is
70 to 80%
Factors that decrease the prognosis for survival in foals with NE
Demonstrate C/S at tiem of birth
Evidence of brainstem or spinal cord involvement
Have multiple organs affected by hypoxic-ischemic injury
Have complicating factors (ie sepsis)
Remain comatose or difficult to arouse
Show no improvement in neurologic function in first 5 days
Have severe recurrent seizures
