Sepsis In Foals

Question 1

SIRS systemic inflammatory response syndrome refers to

Answer 1

A systemic response that results in 2 of the following: fever, tachcyardia, tachypnea or hyperventilation leukocytosis, luekopenia or relative increase in circulating neutrophils

Question 2

Sepsis definition

Answer 2

When SIRS occurs in response to a suspected or confirmed infectious process

Question 3

Infection with which class of bacterial organisms causes sepsis in neonatal foals?

Answer 3

Gram negative bacteria— release endotoxin

Question 4

Foal GI tract is an important portal of entry for pathogens via which route of absorption?f

Answer 4

Pinocytosis of macromolecules in the small intestine (little discrimination between maternal IGG and macromolecules)

Question 5

What is the predominant organism isolated from septic foals?

Answer 5

E coli

Question 6

Rare, but what is the most common systemic fungal infection in foals?

Answer 6

Candida albicans

Question 7

Common biochemical abnormalities in septic foals

Answer 7

Abnormal blood glucose
Azotemia/hyperbilirubinemia
Acidemia
Hyperlactatemia
Arterial hypoxemia & hypercapnia (can occur indepedent to resp dz)
INC triglyceride concentration
Inc albumin

Question 8

What is the gold standard for diagnosis of sepsis in a foal?

Answer 8

Blood culture

Question 9

Examples of medical treatment options for systemic candidiasis

Answer 9

Fluconazole
Itraconazole
Miconazole
Amphtoericin B

Question 10

Drugs that are antiendotoxic use to treat foals:

Answer 10

Flunixin meglumine
Polymyxin B
Pentoxifylline

Question 11

When to consider vasopressor therapy in hypovolemic/septic shock/hypotensive patients?

Answer 11

After appropriate fluid resuscitation should consider vasopressors & inotropes

Question 12

What is the incidence of pneumonia in septic foals?

Answer 12

28 to 50%

Question 13

What percentage of foals that have diarrhea the bacteremic?

Answer 13

About 50% of neonates

Question 14

How does uroperitoneum develop in foals?

Answer 14

Ischemia and Necrosis of bladder &/or urachus

Besides trauma

Question 15

CSF of a foal with meningitis

Answer 15

Pleocytosis (normally neutrophilic)

Question 16

Treatment of choice for meningitis in foals

Answer 16

3rd generation cephalosporin (ceotaxime)

Question 17

Major differentials for the neurologic neonate?

Answer 17

Meningitis
Neonatal encephalopathy (NE)

Question 18

What are some strategies to prevent sepsis in foals?

Answer 18

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

Question 19

Differentials for seizures in foals

Answer 19

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

Question 20

What is the basis of neonatal encephalopathy pathogenesis?

Answer 20

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

Question 21

After reversible hypoxic-ischemic brain injury, neuronal injury and or death occurs in what 2 phases:

Answer 21

1. Primary or acute phase of injury

2. Delayed phase of cell death

Question 22

Primary or acute phase of injury in the pathophysiology of neonatal encephalopathy involves:

Answer 22

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

Question 23

What is the role of microglia in the phase of primary energy failure of pathogenesis in neonatal encephalopathy?

Answer 23

Microglia migrate to the area of necrosis & release further inflammatory mediators that can damage the CNS

Question 24

Neonatal encephalopathy:

Delayed neuronal cell death or secondary energy failure occurs in what time period?

Answer 24

6 to 48 hours after initial hypoxic ischemic injury

Question 25

Neonatal encephalopathy: Delayed neuronal cell death/secondary energy failure is believed to be through/associated with what following mechanisms?

Answer 25

``` Excitotoxicity Accumulation of intracellular calcium & resultant activation of numerous enzymes & pathways Reperfusion injury (oxidative stress) Cytotoxic actions of activated microglia Inflammation Apoptosis ```

Question 26

Neonatal encephalopathy What is the pathway of glutamate in the healthy individual?

Answer 26

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

Question 27

Neonatal encephalopathy What impairs the glutamate transporters in astroglial cells in teh synpatic cleft?

Answer 27

Hypoxia or ischemia Decreased glucose delivery to teh brain —> RESULTS: increased glutamate concentrations & excessive calcium influx into neurons—> excitotoxicity—> cell apoptosis & necrosis

Question 28

Neonatal encephalopathy Why is the neonatal brain susceptible to oxidative injury?

Answer 28

High concentrations of unsaturated fatty acids High rate of oxygen consumption Low concentration of antioxidants

Question 29

Neonatal encephalopathy: Reactive oxygen spp (ROS) and reactive nitrogen spp (RNS) cause significant damage to what

Answer 29

``` Biological proteins (membrane protein degration) Lipids (lipid oxidation) Nucleic acids (DNA degeneration) ```

Question 30

Neonatal encephalopathy: What is a steroid that possibly contributes to neonatal encephalopathy in some foals?

Answer 30

Neurosteroids— ie plasma progestagens: progesterone, epitetestosterone, androstenedione

Question 31

What are recognized risk factors for the development Neonatal encephalopathy in foals?

Answer 31

``` 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

Question 32

Reported clinical signs in neonatal foals & percentages (from a retrospective study)

Answer 32

``` Abnormal udder seeking (59%) Abnormal suckle (55%) Inability to stand (42%) Abnormal GI motility (37%) Abnormal consciousness (34%) Seizure activity (22%) ```

Question 33

Neonatal encephalopathy in human infants diagnosis is supported by what modalities?

Answer 33

Neurologic exam MRI EEG Ultrasound

Question 34

Neonatal encephalopathy diagnosis in the foals is based on:

Answer 34

``` Clinical impression Historial information Neurologic examination Compatible clinical signs Exclusion of other disease processes ```

Question 35

What is an alternative therapy to doxapram to improve PaCO2 in foals with NE?

Answer 35

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

Question 36

Neonatal encephalopathy treatment: If hypoventilation and hypercapnia are observed what medication can be administered as a CRI as a respiratory stimulant?

Answer 36

Doxapram: at 0.02 to 0.05 mg/kg/hour

Question 37

For seizure control in foals, what medications can be used?

Answer 37

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

Question 38

What are possible side effects of phenobarbital?

Answer 38

Mild sedation Ataxia Hypothermia

Question 39

What medication can be administered if intractable cases of status epilepticus in foals?

Answer 39

Propofol CRI

Question 40

Proposed benefits of a hyperbaric chamber in NE foals?

Answer 40

Reduced apoptosis Promotion of neuronal stem cell prolifeartion Enhancement of oxygen radical scanvers Increased oxygen delivery to teh brain Increased activity of superoxide dismutase

Question 41

Medications used to combat edema and oxidative damage in foals with NE?

Answer 41

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

Question 42

What are the proposed benefits of magnesium sulfate in IV fluid therapy for NE foals?

Answer 42

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

Question 43

Reported survival rate in foals with NE (without complicating factors) is

Answer 43

70 to 80%

Question 44

Factors that decrease the prognosis for survival in foals with NE

Answer 44

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