Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Boards_2024 > Neonatology > Flashcards

Neonatology Flashcards

1
Q

What is the normal foetal heart rate at various stages in gestation?

A

Early rates can be as high as 135 +/-6

By 120 days this should decrease to ~90bpm

By 330 days this should decrease to 60-80

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What treatments may be useful for increasing foetal oxygen delivery in-utero?

A
  • Intra-nasal O2 insufflation to the mare at 10-15L/min will increase the partial pressure of O2 and O2 saturation in the arterial blood so may improve O2 deliver to the foetus.
  • Pentoxyfylline - has anti-inflammatory effects as well as rheologic effects that may enhance O2 delivery by improving microcirculation.
  • Vitamin E has been used in management of high-risk pregnancies as an antioxidant.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the first step in activation HPA axis in the foetus for neonatal life?

A

Foetal cortisol begins to rise approximately 5 days before birth and prepares the foal for extra-uterine life/processes including respiration, renal Na conservation and glucose metabolism. Cortisol continues to rise in the first few hours after birth before decreasing to normal values by 1 day of age in healthy foals.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What role do neurosteroids play in the peripartum period?

A

High circulating concentrations of neurosteroids, in particular, allopregnanolone and pregnenolone play a role in maintaining the foal in a sleepy state in utero (along with other factors). These inhibitory neurosteroids are synthesised from progesterone primarily within the placenta during late gestation and act on the cerebrum.

Following delivery, their concentrations in normal neonates decline rapidly, usually over the first 48 hours of life and it is this loss of cerebral inhibition, in combination with the stimulation associated with transiting the birth canal, the onset of breathing and onset of multiple external stimuli that leads to the rapid increase in activity and awareness in the neonate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What heart rate and respiratory rates do you expect in the neonate and how do these change over the first days of life?

A

Respiratory rate:

  • 50-75 rpm for first 20-30 min,
  • decreasing to 30-40 rpm for the first 2 days, then
  • decreasing to ~20 rpm by 2-3 days of age.

Heart rate:

  • 60-80 bpm for the first 40-60 min,
  • increasing to 120-150 bpm by 1-2 hours and
  • stabilising at 100-120 bpm by 3 hours after birth.
  • This usually decreases to 80-100 bpm by 1 day of age.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Within what time frame should a “normal” foal nurse?

A

Within 3 hours.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What mechanisms are involved in intestinal absorption of macromolecules in colostrum?

A

Pinocytosis, lymphatic transport and exocytosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What variables affect the duration of gestation in mares?

A
  • Breed (light breeds typically shorter than heavy breeds)
  • Foetal gender
  • Foetal weight
  • Maternal age/parity
  • Placental functionality (eg mares with lots of cysts have a smaller placental area for transfer of nutrients so may have an increased gestation length)
  • Environmental factors (month of conception, maternal nutrition, climate)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are common findings (physiologic rather than appearance) in dysmature foals?

A
  • Impaired thermoregulation
  • Abnormal glucose metabolism/regulation (endocrine dysfunction, possibly due to impaired insulin production or peripheral insulin insensitivity)
  • Impaired cardiovascular function (most commonly persistent hypotension poorly responsive to pressor therapy. Increased vascular permeability may also be present).
  • Impaired pulmonary function (can be surfactant dysfunction, most commonly is associated with decreased respiratory drive, weak muscles of respiration, a highly compliant chest wall and poorly compliant lungs).
  • Impaired gastrointestinal function.
  • Impaired renal function (may manifest primarily as decreased urine output rather than azotaemia - fluid overload is a risk).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the goals or targets of treating hypotension in foals?

A

you should target maintenance of perfusion rather than a specific blood pressure range due to the risk of fluid overload.

you can use IVFT, inotropes and pressor support.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the normal neutrophil:lymphocyte ratio and what do aberrations in this ratio suggest?

A

Normal N:L ratio is >2.0. Reversal of this ratio (such as ratio of <1.0 suggests prematurity and is directly due to impaired adrenocortical function.

Maturation of the HPA axis normally occurs in the last few days of gestation and continues in the first weeks and even months after birth; hence premature foals exhibit low cortisol concentrations at birth, in combination with elevated ACTH. Some normal foals have ration <2.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are typical features of post-mature foals?

A
  • Normal-high birth weight
  • Large frame size but poor body condition
  • Long silky haircoat
  • Fully erupted incisors
  • May have flexor contracture.
  • May share functional characteristics with premature foals such as impaired thermoregulation, abnormal glucose metabolism, impaired GIT and renal function etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the most common conditions that are associated with a need to resuscitate?

A

Post-partum (absence of breathing, irregular gasps, RR <10rpm); primary lung disease, septic shock, hypovolaemia, metabolic acidosis, hyperkalaemia, hypoglycaemia, vasovagal reflex and hypothermia.

Cardiac causes include secondary myocardial damage from hypoxia or stress, myocarditis, congenital cardiac defects, endocarditis with coronary artery embolism and cardiac tamponade.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What rate and volume of ventilation should be provided during the resuscitation of foals?

A

Tidal volume of 10mL/kg
Rate of 10 breaths per minute.
Excessive ventilation will limit cardiac return and coronary perfusion and is associated with worse outcomes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What would be a benefit of ventilating a foal with 100% O2 briefly immediately after delivery?

A

May assist with reversal of foetal circulation. Prolonged use is contraindicated unless underlying respiratory dysfunction is noted.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe the process of cardiopulmonary resuscitation including frequency of checks and cut-offs for intervention.

A
  • Start with pulmonary support as pulmonary arrest followed by cardiac arrest is a more common scenario.
  • Following 30 seconds of ventilation stop and observe for spontaneous breathing while assessing cardiovascular function. If HR >50bpm but respiration is not, resume ventilation but stop every 2 min to check for spontaneous efforts.
  • If heat beat is absent or rate is too low then immediately initiate thoracic compressions (check for rib fractures first!). Cardiac compressions are applied at 100bpm, stopping every 2-3 min to check for a heartbeat, but resume within 10 seconds if not detected.
  • First-line medication is adrenaline either IV at 0.01mg/kg every 3-5 min or intratracheally at 0.1mg/kg diluted in 3-5mL sterile water. Vasopressin can be used adjunctively at a single dose of 0.6U/kg IV following the first dose of adrenaline.
  • Doxapram is contraindicated as it doesn’t reverse secondary apnoea and decreases cerebral blood flow while increasing cerebral oxygen consumption
  • Atropine and glycopyrrolate are not indicated as high vagal tone is not the cause of bradycardia although a single dose of atropine is unlikely to be harmful.
  • Corticosteroids, Ca gluconate, lignocaine, MgSO4 and NaHCO3 are not indicated unless it is primary cardiac arrest due to cardiac disease.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What charge should be applied with defibrillation and in what specific cases?

A

Cases of ventricular fibrillation and pulseless ventricular tachycardia.
Initially 2J/kg then increasing to 4J/kg for subsequent attempts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What monitoring techniques are useful in resuscitation?

A

ECG can be misleading as electrical activity doesn’t necessarily represent contractility.

EtCO2 is useful if capnography is available - a normal resting EtCO2 in a healthy patient is 35-45mmHg. During resuscitation a reasonable target is 10mmHg.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Define SIRS and its consequences

A

SIRS is a common terminal phase of the inflammatory response, characterised by malignant global activation of multiple proinflammatory pathways. SIRS can lead to shock which is characterised by severe hypotension (not responsive to IVFT) which can then result in hypoperfusion and organ dysfunction such that homeostasis cannot be maintained without intervention - this process is termed multiple organ dysfunction (MODS).

Typically the first system affected is the cardiovascular system followed by involvement of respiratory, hepatic, GIT, renal, cardiac and neurologic systems, most likely due to tissue hypoperfusion and changes in cellular metabolism secondary to hypoxia. The result is refractory hypotension, lactic acidosis, oliguria and potentially progression to death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

List mediators and describe their involvement in the progression of SIRS

A

The inciting cause of SIRS may be associated with trauma or microbial invasion that release damage-associated molecular patterns (DAMPS) or pathogen-associated molecular patterns (PAMPS) respectively (eg endotoxin, exotoxin, LPS etc); however, the development of an inflammatory response is dependent on the production (primarily by the activated mononuclear phagocyte) of numerous inflammatory mediators (incl. TNFα, IL1, IL6, inducible NOS, phospholipase A2, COX2, and adhesion molecules). Transcription of many of these mediators is dependent on nuclear factor Kß which might be a target for intervention of SIRS.

In addition to phagocytosis of foreign material, macrophages at the site of injury release proinflammatory cytokines (IL1, TNFα, IL6, IL12, IL18 which increase production of secondary inflammatory mediators including prostaglandins, thromboxane A2, leukotrienes and ROS. IL6, IL1 and TNFα initiate the acute phase response. Part of this is a counter-regulatory anti-inflammatory component that regulates inflammation and resolved the inflammatory response, including inhibiting macrophage activation, antagonises the receptors of the proinflammatory mediators and maintains a balance between pro and anti-inflammatory. In SIRS this balance is not maintained.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What causes endothelial activation during SIRS and what is the effect of this?

A

Inflammatory cytokines cause endothelial activation early in the process of SIRS. Activated endothelial cells produce NO, prostaglandins and endothelin 1. Activated endothelial cells retract from one another increasing the size of the intercellular pores, exposition of extracellular matrix and allowing for increased vascular permeability, and also increase their production of tissue factor and von Willebrand factor, resulting in localised thrombosis and platelet adherence.

An early systemic effect is pulmonary vasoconstriction leading to pulmonary hypertension followed by systemic hypotension due to decreased arterial tone and decreased left ventricular afterload combined with venous vasodilation in capacitance vessels, reducing venous return to the right heart. This can lead to hyperdynamic shock with tachycardia and increased cardiac output as a compensatory mechanism to maintain tissue perfusion.

Arteriolar vasoconstriction develops and in addition, you get adherence of neutrophils to the endothelium, endothelial cell swelling and accumulation of fibrin and aggregates of platelets and RBCs that occlude the vasculature and exacerbate tissue hypoperfusion. A-V shunting occurs in some tissues, and increased vascular permeability leads to oedema. These all culminate in the end result leading to MODS.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What factors lead to activation of coagulation and development of DIC?

A

Primarily via the extrinsic pathway.

Normally accumulation of fibrin (secondary to neutrophil degranulation and associated platelet adhesion) would be prevented by the fibrinolytic system (specifically plasmin). However, in the presence of SIRS, the fibrinolytic system is inhibited by plasminogen-activator inhibitory type 1.

The combination of impaired fibrinolysis and depression of the inhibitors of coagulation can result in a consumptive coagulopathy potentially leading to DIC.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Is Gram + or Gram - more common as an isolate from blood culture in septic neonates?

A

Gram - is more common, even if in the past decade there has been an increased incidence of Gram+ findings, although these are often present in mixed infections.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

In addition to sepsis, what are the differentials that should be considered for a sick neonate without localising signs?

A
  • NNE
  • EHV-1
  • EVA
  • C. psittaci (usually signs of respiratory dysfunction but not always initially)
  • NIE
  • Aspiration pneumonia? (usually signs localised to the respiratory tract)
  • Colitis (usually signs of colic or diarrhoea)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

List common bacterial isolates from foals with sepsis.

A

Gram -:

  • E. coli,
  • Klebsiella pneumoniae,
  • Actinobacillus, Enterobacter,
  • Pseudomonas aeruginosa,
  • Citrobacter,
  • Pasteurella,
  • Salmonella,
  • Serratia,
  • Acinetobacter.

Gram +:

  • B-haemolytic strep,
  • other strep,
  • Staphylococcus,
  • Clostridia,
  • Enterococcus.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Describe fluid resuscitative techniques for foals.

A

Initial resuscitation: 20mL/kg boluses given over 10-30min with assessment of volume status between boluses, up to a maximum of 3 boluses (60mL/kg total).

If hypotension is fluid refractory, should use of inotropes or vasopressors may be indicated. Fluid for resuscitation should be isotonic balanced replacement solutions such as Hartmann’s.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the advantages and disadvantages of placing an indwelling urinary catheter in a recumbent sick foal?

A

Pro’s: greatly helps nursing care/hygiene, reduces the risk of decubital ulcers, enables monitoring/quantification of urinary output.

Con’s: Increased risk of urinary tract infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What neurologic signs/reflexes are present or absent in neonates?

A
  • Menace: develops by 1-2 weeks of life
  • Dazzle: present from birth
  • PLR (direct & consensual): present from birth but may be slow
  • Globe position: may be slightly ventromedial but resolves by 1 month
  • Cutaneous reflexes: present from birth
  • Limb reflexes: present from birth
  • Crossed extensor reflex: present from birth but absent after the first 3 weeks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Describe the pathophysiology of organ dysfunction with hypoxic injury/HIE.

A
  • GIT and renal are typically most susceptible
  • Shift towards anaerobic metabolism leads to depletion of ATP, accumulation of lactate and failure of cellular homeostasis.
  • Decreased activity of transcellular pumps that rely on ATP leads to intracellular accumulation of Na, Ca and H2O.
  • Membrane depolarization leads to release of glutamate, accumulating in extracellular spaces. This acts on NMDA receptors, opening NMDA channels and potentiating Ca influx into the neurons, contributing to neuronal injury.
  • Hypoxia (and subsequent reperfusion) increases production of ROS and NO causing reperfusion injury/tissue damage and cell death and activation of apoptotic cascades.
  • The stimulated inflammatory response exacerbates vascular permeability, oedema formation and tissue injury.
  • The role of neurosteroids is poorly understood - they may be both protective and damaging.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

List differentials for NNE.

A
  • HIE
  • SAE
  • Elevated neurosteroid concentrations?
  • NIE - Kernicterus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What factors make neonates more susceptible to seizures?

A
  • Relative excitability of the developing brain.
  • High risk of brain injury in the neonatal period (hypo or hyperglycaemia, electrolyte derangements, hypoxia etc).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

List the signs of seizure in neonates.

A

Subtle signs: abnormal eye movements, tremors, excessive stretching, excessive extensor tone, hyperaesthesia, apneustic breathing.

Overt signs: rapid nystagmus, paddling, hyperextension, excessive mouth movements.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

List clinical signs of bacterial meningitis.

A

Lethargy, weakness, recumbency, decreased suckle reflex, abnormal PLR, hyperaesthesia, cervical pain, fever, blindness, seizure and coma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are the common bacterial isolates in meningitis and what would be suitable antibiotic choices?

A

*Typically similar bacteria to those associated with neonatal sepsis (E. coli, Actinobacillus, Klebsiella, Streptococcus, Salmonella).

Drugs that penetrate the BBB: ceftriaxone, cefotaxime, imipenem, chloramphenicol, rifampicin with TMPS.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What type of botulism is most common in foals?

A

Toxicoinfectious (spores from the environment are ingested and germinate in the GIT and spread toxin).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How does botulism affect the nervous system?

A

Toxin acts presynaptically at the neuromuscular junction by inhibiting release of acetycholine, resulting in weakness, trembling, dysphagia and sometimes acute death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the common toxin types in botulism and their associated prognosis?

A

Type B and C are most commonly associated with equine cases.
Toxin A has been associated with more severe clinical signs and higher fatality rate than type B and C.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the signalment characteristics of foals with tetanus and what are the common clinical signs?

A

Typically over 7 days age; history of anaerobic infection, often of the umbilical remnants.

Tetanospasmin inhibits release GABA by spinal interneurons leading to disinhibition of spinal motor neurons hence excessive motor activity and spastic paralysis.

Clinical Signs: rigidity, excessive autonomic activity, episodic muscle spasms leading to trismus, facial spasm, third eyelid prolapse and dysphagia. Recumbency may occur and death is due to respiratory muscle paralysis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

List the common metabolic encephalopathies and their cause.

A
  • Hypoglycaemia: associated with central and peripheral neuronal degeneration - unless insulin therapy is being used this typically results in only transient injury and dysfunction.
  • Hypo or hypernatraemia: only if severe, or with acute changes in serum Na concentration that cause dramatic fluid shifts in tissues of the CNS - hyponatraemia is associated with development of cerebral oedema; hypernatraemia may be associated with an osmotic demyelination syndrome. Correction of Na derangements should be done slowly (should not exceed 0.5 mmol/L/h).
  • Hypocalcaemia: often asymptomatic but may be associated with tetany and seizures.
  • Hyperbilirubinaemia: bilirubin is neurotoxic and can cause neurologic dysfunction and irreversible brain damage (NIE-kernicterus)
  • Hyperammonaemima: can be secondary to hepatic insufficiency, portosystemic shunts or increased gastrointestinal production. Hyperornithinemia-hyperammonemia-homocitrullinuria (HHH) syndrome is a genetic defect in the urea cycle resulting in persistent hyperammonemia in Morgan foals.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

List typical findings in foals with occipito-atlanto-axial malformation.

A
  • Paresis and ataxia of all 4 limbs or may be born dead or comatose.
  • May have a head tilt, abnormal head carriage or clicking sound with head movement.
  • Neurological deficits range from inapparent to quadriplegia.
  • Familial in Arabians. Can occur in other breeds.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the mode of inheritance for cerebellar abiotrophy and time frame presentation?

A

Autosomal recessive trait, whit clinical signs detectable at 1-6 months.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What specific lineage of Arabians does juvenile idiopathic epilepsy occur in?

A

Egyptian

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the mainstay of treatment of NNE?

A

Stabilise the patient to enable restoration and maintenance of CNS perfusion with O2 and glucose.

  • IVFT +/- glucose supplementation +/- vasopressors and inotropes
  • Maintain euvolemia (overhydration can be equally detrimental to CNS perfusion)
  • Intranasal O2 insufflation to support O2 delivery (transfusion)
  • Control seizures (if present) with benzodiazepines (boluses or CRIs) or phenobarbital; other medications may also be useful.
  • Minimal evidence to support DMSO as an anti-inflammatory but it may be useful.
  • Mannitol may be useful for reducing cerebral oedema. Hypertonic has more beneficial effects but its use in foals is often contraindicated due to such high Na concentrations.
  • MgSO4 is an NMDA receptor antagonist and may stabilise cell membranes, inhibit free radical production and reduce secondary CNS inflammation and associated injury.
  • Pentoxyfylline has anti-inflammatory and immune-modulating effects and may improve local tissue perfusion.
  • Head hypothermia (33-35°C)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

List differentials for acute respiratory distress immediately postpartum (new-born)

A

Causes of URT obstruction:

  • Bilateral choanal atresia
  • Stenotic nares
  • Laryngeal oedema or collapse
  • Dorsal displacement of the soft palate
  • Subepiglottic cysts
  • Severe congenital pulmonary abnormalities

Congenital cardiac anomalies: malpositioning of the great vessels causing severe right-to-left shunts may be involved.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Define acute lung injury (ALI/EqALI) and acute respiratory distress syndrome (ARDS/EqARDS)

A

Syndromes of respiratory failure associated with non-cardiogenic pulmonary oedema, decreased pulmonary compliance and ventilation-perfusion mismatching associated with exaggerated and self-perpetuating inflammatory response which results in severe tissue damage within the lung.

Protein-rich oedema fluid accumulates within the alveoli and interstitium resulting in impairment of gas exchange causing hypoxaemia. These are not primary diseases, merely secondary effects of another primary disease.

EqARDS: PaO2/FiO2 ratio of <200mmHg

EqALI: PaO2/FiO2 ratio of <300mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is the expected influence of lateral recumbency on arterial blood oxygenation?

A

Reduction by 10-14mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

List the mechanisms that can cause hypoxaemia in foals?

A
  • Hypoventilation
  • V/Q mismatch
  • Impaired diffusion
  • Intrapulmonary or extrapulmonary shunts
  • Decreased concentration of O2 in inspired air
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the complications of mechanical ventilation in cases of ARDs/ALI?

A
  • Trauma to the URT from intubation
  • Increased risk of LRT infection
  • Pulmonary barotrauma and volutrauma
  • Air leak syndromes (pneumothorax)
  • Haemodynamic complications including impaired venous return
  • Bronchopulmonary dysplasia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Which radiographic pattern is expected in cases of ARDS/ALI?

A

Ranges from diffuse interstitial pattern to a focal or diffuse coalescing alveolar pattern with multiple bronchograms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

List common differentials for ARDS/ALI in foals?

A
  • Bacterial pneumonia
  • Fungal pneumonia
  • Viral pneumonia
  • Smoke inhalation
  • Repeated transfusion of blood products
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is a key consideration in the treatment of ARDS/ALI in older foals?

A

Ensuring that R. equi is covered in the spectrum of activity of selected antimicrobial. Particularly if the tracheal wash showed evidence of Gram+ coccobacilli within pulmonary macrophages.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

List treatments for foals with ALI/ARDS

A

General supportive care including nursing, IVFT, electrolyte derangement correction etc.

  • Antimicrobials
  • Intranasal oxygen insufflation
  • Corticosteroids
  • Bronchodilators are often contraindicated as bronchoconstriction is not a feature and bronchodilation may worsen V/Q mismatch resulting in death; if used, it must be after administration of O2.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is persistent pulmonary hypertension?

A

Also known as persistent foetal circulation or reversion to foetal circulation; it is a syndrome characterised by sustained increases in pulmonary vascular resistance, possibly combined with decreased right ventricular function hence you get right to left shunting through the ductus arteriosus and/or foramen ovale. While it can be idiopathic, it may develop secondary to systemic sepsis, hypoxaemia or acidosis.

It should be suspected in any foal exhibiting progressive or refractory hypercapnic hypoxaemia, particularly if intranasal O2 supplementation does not result in significant increase in PaO2. Must rule out primary congenital cardiac anomalies.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are the treatment options for persistent pulmonary hypertension?

A

If response to intranasal O2 insufflation is insufficient, mechanical ventilation with 100% O2 may be indicated both to address hypoxia and also to stimulate pulmonary vascular relaxation. Following a brief period of hyperoxia, it is recommended to taper the O2 concentration to target PaO2 of 60-100mmHg.

  • Inhaled nitric oxide is the only approved pulmonary vasodilator in humans and its use is reported in foals but it’s impractical in most settings.
  • Sildenafil (phosphodiesterase type 5 inhibitor) may be effective at doses of 0.5-0.25mg/kg PO up to every 4 hours.
  • Pentoxyfylline (non-selective phosphodiesterase inhibitor) may also be useful.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

List congenital URT disorders and their treatment.

A

Wry nose: surgical repair is salvage only; prognosis for athletic function is poor.

Choanal atresia: surgical repair is salvage only; chronic airway narrowing likely prevents athletic function.

Subepiglottic cyst: results in persistent palatal displacement. Surgery may be curative. Concern for aspiration pneumonia as a sequelae.

Cleft palate: surgical correction of smaller defects may be possible; likewise conservative management of small defects may be possible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

List the pathophysiologic mechanisms leading to pulmonary dysfunction in meconium aspiration.

A
  • Mechanical airway obstruction
  • Regional air trapping
  • Surfactant inactivation
  • Surfactant displacement
  • Chemical pneumonitis and alveolitis
  • Persistent pulmonary hypertension.
57
Q

List the treatments for meconium aspiration.

A

O2 insufflation or mechanical ventilation (latter is challenging due to degree of pulmonary inflammation and airway compromise and severity of V/Q mismatch), may CPAP or SIMV.

Anti-inflammatories including corticosteroids are useful.

Pentoxyfylline has been useful in some animal models.

Lung lavage and/or surfactant replacement theraphy.

Broad-spectrum antimicrobials to reduce the risk of secondary bacterial pneumonia.

58
Q

What is the expected radiographic pattern for aspiration pneumonia?

A

Alveolar pattern with or without air bronchograms in the caudoventral lung, possibly localised to the perihilar region.

59
Q

In which breeds has idiopathic/transient tachypnoea been described in and what are the goals of treatment?

A

Clydesdale, TB and Arabian foals.
Treatment is aimed at controlling hyperthermia (clipping, alcohol baths, housing in a cool/shaded area). Generally resolves in a few days-weeks.

60
Q

What are potential sequelae of rib fractures?

A

Pulmonary contusion, lung lacerations, laceration to major arteries - heart or diaphragm; pneumothorax, haemothorax and diaphragmatic herniation.

61
Q

What diagnostic imaging modality is best for diagnosis of rib fractures in foals?

A

Ultrasound.

62
Q

List common viral infections of neonatal foals.

A
  • EHV-1
  • EHV-4
  • EI
  • EAV
  • Equine adenovirus
63
Q

What are the common clinical and clinicopathologic findings with EHV-1 in neonates?

A

Cardiovascular and respiratory insufficiency, congested and icteric mucous membranes. May see dilation of retinal vasculature with reddish discolouration of the optic disc.

Clinicopathologic abnormalities include leucopenia, neutropenia, toxic neutrophils, lymphopenia. Bone marrow examination shows depletion of myeloid cell lines.

64
Q

What are the common signs of equine influenza in neonates?

A

Severe broncho-interstitial pneumonia leads to respiratory distress.

65
Q

What is the prognosis for neonatal Equine Arteritis Virus?

A

Associated with severe interstitial pneumonia which has been uniformly fatal. Other presentations are still primarily respiratory and include initially oedema, weakness and depression, ultimately progressing to terminal respiratory distress although acute death has also been reported. GIT involvement is reported in some cases but not consistently.

66
Q

Which fungal agent has been associated with placentitis, abortion and birth of infected foals with multisystemic disease including granulomatous pneumonia?

A

Histoplasma capsulatum.

67
Q

What are the common isolates of bacterial pneumonia in neonates?

A

Typically the same as those involved in neonatal sepsis as its often haematogenous spread.

  • E. coli (most common)
  • Klebsiella
  • Actinobacillus
  • Pasteurella
  • Salmonella
  • Streptococcus
  • Staphylococcus
  • Enterococcus.
68
Q

What are the risk factors for pneumonia in older foals and what is the link between viral and bacterial pneumonia in older foals?

A

Risk factors include stresses of weaning, sales preparation, transport, confinement in crowded and dusty environments that enhance exposure to respiratory pathogens.

The above risk factors also facilitate spread of viruses such as EHV-1, EHV-4 and EHV-2 which can cause pulmonary inflammation and injury, and in the case of EHV-2, directly impairs pulmonary immune responses, facilitating development of secondary bacterial pneumonia. EIA may also lead to pulmonary inflammation and injury.

69
Q

What are the genetic predispositions to R. equi infection that have been identified?

A

Polymorphisms in the transferrin and SLC11A1 genes have been associated with infection in TB and Arabian Foals respectively.

TRPM2 gene on Chromosome 26 associated with neutrophil function was found to be positively associated with R. equi pneumonia - foals with single nucleotide polymorphisms in this region were 3-4 x more likely to be clinically affected.

70
Q

What are the common extra-pulmonary disorders associated with R. equi?

A
  • Diarrhoea
  • Ulcerative enterotyphlocolitis
  • Presumed IMM-synovitis
  • Intra-abdominal lymphadenitis or abscessation
  • Uveitis
71
Q

What are the common radiographic findings in foals with R. equi pneumonia?

A
  • Diffuse interstitial or alveolar pattern
  • Tracheobronchial lymphadenopathy
  • Intrapulmonary abscess
  • Pleural effusion
72
Q

What cumulative abscess score cut off is used for treatment of R. equi pneumonia?

A

Typically foals with a total abscess score of less than 8-10 don’t require treatment.

73
Q

What are the indications for mechanical ventilation?

A
  • Hypercapnoea (PaCO2 >60mmHg) that is inadequately responsive to respiratory stimulants, or more severe hypercapnoea (PaCO2 >70mmHg), such as in patients with severe respiratory disease resulting in respiratory failure eg ARDS, Sepsis, aspiration of meconium/milk, severe pneumonia.
  • Failure of respiratory muscles as with toxins such as botulism and tetanus.
  • Neurologic dysfunction with suppressed respiratory drive (obtunded or comatose foals)
74
Q

Why is provision of O2 insufflation inadequate in correcting hypoxaemia with concurrent hypercapnia?

A

O2 insufflation will increase the FiO2 but if there is V/Q mismatch this may not equate to increases in PaO2.

Increasing the FiO2 may help to increase the PaO2 (if there is no/minimal V/Q mismatch) however the presence of hypercapnia suggests hypoventilation which is not addressed by O2 supplementation. Hence mechanical ventilation or stimulation of increased respiratory rate/depth is necessary.

75
Q

Describe the process of mechanical ventilation in a foal.

A

Positive pressure ventilation is most commonly used and involves generating positive pressure which overcomes the resistance within the patients airways, the lungs and the thoracic wall.

In awake patients naso-tracheal intubation is best (ensure the tube is within the cervical trachea) - caution with cuff pressure - excessive pressure can cause pressure necrosis

Change endotracheal tubes every 12-24hr

Need to have a humidifier (active humidifier or passive humidifier (HME) but the latter should only be used for short periods due to clogging with airway discharge.

FiO2 should be set to the minimum level required to maintain adequate PaO2 but not below atmospheric (21%) - FiO2 >50% are associated with oxygen toxicity to respiratory mucosa.

Set tidal volume so that peak inspiratory pressure does not exceed 25-35mmH20 to avoid trauma.

Avoid excessive peak flow rates as these will result in overly rapid lung inflation.

Initial starting points could be FiO2 of 50%, tidal volume of 5mL/kg, peak flow of 70L/min and breath rate of 20-30rpm.

76
Q

List the common ventilator techniques.

A
  • Synchronised intermittent-mandatory ventilation (SIMV)
  • Pressure support ventilation (PSV)
  • Continuous positive airway pressure (CPAP)
77
Q

What are the three types of ventilator-induced lung injury (VILI)?

A
  • Barotrauma (damage caused by change in air pressure).
  • Volutrauma (exceeding the normal physiologic functional residual capacity of the ventilated regions of lung, resulting in development of pulmonary oedema and initiation/amplification of the local inflammatory response).
  • Atelectotrauma (repeated opening and closing of lung units during tidal ventilation causes a syndrome of low-volume injury resulting in the initiation of an inflammatory response.
78
Q

What is the preferred way to discontinue mechanical ventilation?

A: turn off the ventilator but maintain an intubated airway? or

B: Turn the ventilator off and immediately extubate the patient?

A

B because maintenance of an endotracheal tube increases the resistance to airflow and increases the patients work of breathing so extubation is preferred.

Maintenance of intranasal O2 insufflation should be provided.

79
Q

What are the common sites for meconium impaction?

A

Small colon or pelvic inlet

80
Q

List the different enemas for meconium impaction and their appropriate use.

A
  • Sodium phosphate enema: once daily to avoid hyperphosphataemia
  • Soapy water enema: not more than once daily due to irritation
  • Acetylcysteine retention enema: repeat up to 3 times at 12-24 hours intervals
81
Q

What is the common presentation of colic associated with ascarid burden?

A

Signs of small intestinal obstruction (often associated with recent anthelmintic treatment or a stressor such as transportation of weaning)
Secondary sequelae to luminal obstruction such as volvulus or intussusception commonly occur, necessitating surgical intervention.

82
Q

What are the diagnostic techniques for identification of atresia of various parts of the intestinal tract and the treatment options for each?

A
  • Atresia ani: visual and or digital rectal palpation; surgical correction is often straightforward and typically successful albeit anal sphincter function may be abnormal. it is commonly accompanied by penile malformations (hypospadias) that will also require surgical correction.
  • Atresia of the rectum: progressive colic and distention, absence of faecal material or meconium staining of enema fluids; retrograde contrast radiography or colonoscopy may be diagnostic. Surgical correction is dependent on accessibility.
  • Atresia coli may require surgical exploration for diagnosis. Surgical resection and anastomosis may be successful but generally the outcome is poor due to additional underlying neurologic and motility disorders, so it is typically fatal.
83
Q

What is the mutation and gene involved in overo lethal white syndrome, what is the disease, and what is the inheritance pattern?

A

Gene: endothelin receptor B gene
Inheritance: autosomal recessive
Disease: aganglionosis of the distal small intestine and large intestine resulting in lack of intestinal motility and hence colic.

84
Q

What is necrotising enterocolitis in foals and how is it diagnosed?

A

It is likely multifactorial pathophysiology that involves intestinal immaturity, haemodynamic instability, inflammation, genetic factors, formula feeding and dysbiosis.

Clinical findings are similar to asphyxia-associated disorders and include ileus, gastroduodenal reflux, intolerance of enteral feeding, abdominal distention, colic and diarrhoea. Diagnosis is via radiographic and ultrasonographic evidence of intramural gas in the intestinal wall or surgical/PME evidence of GIT necrosis. Has been associated with clostridia.

85
Q

List common infectious causes of diarrhoea.

A
  • Rotavirus is detected in up to 77% of foal diarrhoea cases. Age range is 5-35 days.
  • Equine coronavirus and adenovirus have been identified in faeces of diarrhoeic foals but pathogenicity has not been confirmed.
  • Clostridium perfringens (typically type A and C, with C often more severe; it is the ß toxin that is primarily responsible for intestinal injury)
  • Clostridium difficile (requires toxin A and/or B)
  • Cryptosporidium although its role as a primary pathogen is debated.
  • Lawsonia intracellularis
  • R. equi diarrhoea in older foals
  • Strongyloides westeri
86
Q

What is the pathogenesis of rotavirus in foals?

A

Infects the epithelial tips of the villi in the duodenum, jejunum and ileum but does not affect the crypt epithelium. Replication occurs within the villous epithelium and is release with cell lysis, resulting in desquamation of villous tips and reduction of absorptive capacity and reduction in production of lactase. Viral enterotoxins inhibit sodium-glucose cotransport, dysregulate Ca homeostasis and activate the enteric nervous system.

Often occurs in large comingled groups. Foals typically exhibit anorexia, depression, profuse water diarrhoea. Highly contagious, high morbidity, but low mortality. Dx is via ELISA, PCR. It persists in the environment and is resistant to disinfectant

87
Q

What is the risk of using proton pump inhibitors as a preventative for EGUS in foals?

A

Associated with an increased risk of undifferentiated diarrhoea, hence should only be used if there is documented evidence of EGUS with clinical signs.

88
Q

What are the common findings associated with gastroduodenal ulcer syndrome (GDUS) in foals?

A

Unthriftiness, pot-bellied appearance, small for age, signs of gastric outflow obstruction such as ptyalism and bruxism;
Gastroscopic examination shows oesophagitis, squamous and glandular lesions, pyloric ulceration and pyloric stricture. Examination of the duodenum may not be possible due to pyloric stricture.

89
Q

What is the treatment of gastroduodenal ulcer syndrome?

A
  • Supportive care including IVFT, parenteral nutrition.
  • Frequent gastric decompression
  • Acid suppression (primarily proton pump inhibitors such as omeprazole; or H2 receptor antagonists eg ranitidine or cimetidine) and gastro-protectants (eg sucralfate, misoprostol [enhanced epithelial repair via closure of tight junctions following re-epithelialisation] oral antacids such as aluminium hydroxide and Mg)
  • Prokinetics such as bethanechol
  • Surgical correction/bypass of pyloric strictures may be necessary
  • Antimicrobials
  • Anti-inflammatories/analgesics
90
Q

Foals born to mares treated for EPM during pregnancy have been associated with what congenital malformation of the urogenital tract?

A

Renal dysplasia

91
Q

What is the most common site of bladder rupture in neonates and which gender is more commonly afflicted?

A

Dorsal bladder wall; colts.

92
Q

What are the common clinicopathological derangements in foals with uroperitoneum?

A

Azotaemia (creatinine more consistently than urea), hyponatraemia, hypochloraemia and hyperkalaemia with metabolic acidosis. K absorbs across the peritoneal lining easily, as does the water content of the urine within the peritoneal cavity, hence you get dilution of the intravascular Na and Cl with sequestration of these electrolytes in the peritoneal cavity.

93
Q

What is the main potential complication of hyperkalaemia and how may it be detected, and what are other less common complications?

A

Fatal bradyarrhythmias. Identified on ECG by:

  1. initially peaked T waves and
  2. shortened Q-T interval with progression to
  3. lengthening of the PR interval and
  4. loss of P waves followed by
  5. widening of the QRS complex - cardiac arrest can ensue.

Less common complications include 3rd degree AV block, VPCs and VF.

94
Q

What therapy needs to accompany peritoneal drainage?

A

IVFT (start before peritoneal drainage, but ensure you have a urinary catheter in place first).

IVFT reduces the risk of reflex hypovolaemia and hypotension from 3rd space fluid loss.

95
Q

What components of IVFT are important in cases of uroperitoneum?

A

IVFT with low K fluids such as hartmann’s solution (has some K but the negative of this is outweighed by the buffering effect of the lactate; it’s less acidifying than NaCl) or 0.9-0.45% NaCl. Additionally:

  • Glucose in a separate CRI helps to drive K intracellularly
  • Ca gluconate helps to stabilise cells in the face of hyperkalaemia
  • Insulin CRI may be required in addition to glucose in refractory cases, to drive K intracellularly.
  • NaHCO3 may aid in lowering K and help address concurrent hyponatremic metabolic acidosis, as long as the respiratory function is adequate and pressure on the diaphragm from peritoneal effusion has been adequate relieved
96
Q

What are the normal findings of ultrasound examination of the umbilical remnants?

A
  • Arteries should be non-pulsatile by 24 hours of age although the lumen may be filled with clotted blood
  • Urachus should be collapsed down and the lumen should be difficult to appreciate <13mm
  • Transverse view of the urachus and umbilical arteries taken at the apex of the bladder should be <25mm in total diameter
  • The vein should measure <5-10mm
97
Q

What are the most common toxic causes of renal injury in foals?

A
  • Aminoglycoside antimicrobials
  • Oxytetracycline (particularly for tendon contracture)
  • Haemoglobin secondary to NIE
  • Myoglobin secondary to myopathies
98
Q

What are the limitations of identifying renal disease in foals?

A
  • BUN is very insensitive for AKI in foals
  • Serum creatinine is insensitive although remains the best biomarker for renal function in foals
  • Due to the large renal reserve, it is likely that substantial renal injury has occurred by the time there are abnormalities in BUN or Cr identified.
  • Urine output!
99
Q

How can you differentiate elevations in creatinine associated with renal disease and hypercreatinaemia associated with placental insufficiency or neonatal hypoxia?

A

If associated with neonatal hypoxia or placental insufficiency it typically reduces by 50% within 24 hours and returns to normal by 72 hours.

100
Q

How can you measure endogenous creatinine clearance?

A

Obtain baseline serum sample and empty the bladder, perform a timed urine collection over several hours or ideally 24 hours, collect a second serum sample at the end of the collection and do the following calculation:
Endogenous creatinine clearance (mL/min/kg)
= urine [creatinine] x urine output [mL] / body weight [kg]
plasma[creatinine] time [mins]
Reported values for ClCr in normal foals are 1.78-2.17mL/min/kg.

101
Q

Aside from azotaemia what are other indicators of renal dysfunction?

A
  • Persistent isosthenuria despite changing hydration status
  • Proteinuria (normally present up to 24 hours of age but then abnormal, although mild spurious increase associated with alkaline urine can be detected on dipstick)
  • Enzymuria, as detected by elevation in the urine GGT : creatinine ratio above 25 (urine GGT/urine creatinine x 100) which suggest proximal tubular injury (expected in foals receiving aminoglycosides)
102
Q

What is the expected urinary output in a neonatal foal?

A

At 4 days old foals should produce approximately 6mL/kg/hr; aim for at least 2/3 of fluid provision.

103
Q

Describe the normal process of activation of the HPA axis in a foal and the effects of cortisol on the body.

A

Activation of the HPA axis leads to secretion of CRH and AVP; CRH stimulates secretion of ACTH which acts on the zona fasciculata cells of the adrenal glands to produce cortisol.

Cortisol is released into the systemic circulation where some of it is free (a larger proportion in foals cf adults) and some is bound to cortisol binding globulin or albumin. The amount of free cortisol increases with inflammation, stimulated by neutrophil elastase or 11ß hydroxysteroid dehydrogenase (two types, type 1 generates active cortisol from cortisone; type 2 generates cortisone into cortisol).

Free cortisol enters the cell where it acts in critical illness to support cardiovascular function, regulate immune response and increase the availability of glucose as an energy source.

104
Q

How can you assess the function of the HPA axis?

A
  • Determination of neutrophil:lymphocyte ratio (<1.0 suggests impaired HPA axis function)
  • Basal serum cortisol concentration
  • Basal serum ACTH concentration
  • ACTH:Cortisol ratios
  • ACTH stimulation test to measure ability to produce cortisol
105
Q

What are the limitations of assessing the HPA axis?

A
  • Activation and response of the HPA axis is highly dynamic with rapid changes in a short period of time and substantial variation even on an hour to hour basis
  • Measurement of total cortisol doesn’t reflect free cortisol
  • Serum cortisol doesn’t give information about cortisol levels at the tissue or intracellular level
  • ACTH stimulation testing may not accurately reflect HPA axis function in critical illness.
  • Variation among assays makes it difficult to compare results.
106
Q

What recommendations (based on human medicine) are made for treatment of foals with suspected critical illness related cortisol insufficiency (CIRCI) and what is the clinical indication that this condition is present?

A

Clinical indication: IVFT refractory, vasopressor-resistant hypotension.

Tx: Physiologic doses of hydrocortisone via a 3-5 day tapering course of 1-3mg/kg/day divided into q4h IV injections in foals 2-6 days old. Longer courses (7-10 days) with subsequent tapering may be suitable.

107
Q

Are thyroid hormone concentrations higher or lower in foals compared with adults?

A

Higher in foals despite normal TSH levels, suggesting a difference in the HPT axis in foals.

108
Q

What are the findings in the syndrome of congenital hypothyroidism and dysmaturity?

A

Thyroid hyperplasia (goiter), increased gestational length, dysmaturity, flexural limb deformities, rupture of the common digital extensor tendon, incomplete ossification of cuboidal bones, mandibular prognathism, incomplete closure of the abdominal wall. Thyroid hormones may be low or normal but response to TSH is consistently decreased.

109
Q

What is the gold standard assay for measurement of IgG?

And what is the limitation of this test?

A

Single radial immunodiffusion assay.

Limitation is the long incubation period and hence delay in obtaining results making it clinically less useful.

Electrophoresis is proposed as a faster test and good Sp&Se.

110
Q

What increase in IgG can be expected from administration of 1L of commercial plasma?

A

200mg/dl or 2g/L.

111
Q

Which blood factors are considered the most antigenic or most often associated with NIE in foals?

A

Aa in the A system and Qa in the Q system.

112
Q

What are differentials for haemolytic anaemia in a foal and how might you confirm NIE?

A
  • NIE
  • DIC secondary to sepsis
  • Bacteria-induced haemolysis
  • Incompatible blood or plasma transfusions

Confirmation of NIE: Haemolytic crossmatch of mare serum with foal red blood cells using exogenous rabbit complement. The jaundiced foal agglutination test is performed using red blood cells from the foal with colostrum from the mare with agglutination as the end point. This test lacks sensitivity and specificity but is fast and easy to perform.

113
Q

What are the treatment options for hyperbilirubinaemia and hepatic failure secondary to NIE?

A
  • Plasma exchange
  • Deferoxamine mesylate (20mg/kg SC) to increase urinary excretion and reduce hepatic accumulation of iron.
114
Q

What are the conditions neonatal alloimmune thrombocytopaenia and neonatal alloimmune neutropenia, what are the clinical findings and how are they diagnosed?

A

These conditions are similar to NIE in which foals ingest maternal antibodies via the colostrum that are directed against their own platelets or neutrophils, resulting in destruction/removal from circulation.

Clinical findings include ulcerative dermatitis, thrombocytopenia and neutropenia, as well as increased susceptibility to secondary infections.

Diagnosis is based on confirmation of thrombocytopaenia/neutropenia in the absence of other diseases that might cause this (eg sepsis) and the presence of antibodies bound to the patients platelets or neutrophils. Direct fluorescent antibody tests, ELISA, immunoradiometric tests and flow cytometry may confirm this.

Tx is supportive although whole blood or platelet-rich plasma transfusions can be given if there is clinical bleeding diathesis.

115
Q

What clinical and clinicopathologic changes might be expected in cases of hepatic disease in foals?

A
  • Anorexia, depression, fever, weight loss and abdominal pain +/- CNS dysfunction
  • Bleeding disorders, oedema, ascites, diarrhoea or dermatitis
  • Elevations in conjugated and unconjugated bilirubin, liver enzyme activities, serum bile acids, serum ammonia and prothrombin time.
  • Hypoglycaemia, metabolic acidosis, low BUN, polycythaemia (these changes are not liver-specific but may be supportive if seen).
116
Q

What is the causative agent of Tyzzer’s disease and typical age at presentation?

A

Clostridium pilliform.
7-42 days age.

117
Q

List differentials for hepatitis in foals

A

Often secondary to systemic sepsis.
Bacterial:

  • C. pilliform (Tyzzers)
  • Actinobacillus spp
  • Strep equi subsp zooepidemicus
  • Bartonella henselae
  • Leptospirosis (pomona)
    • C. psittaci (in conjunction with pneumonia/ARDS)

Viral: EHV-1 (marked icterus but otherwise signs of hepatic disease are often mild but on PME there is marked hepatic necrosis)

Other:

  • Hepatic lipidosis secondary to hyperlipaemia (most common in mini’s) - insulin therapy is often critical in facilitating resolution
  • NIE (hepatocellular injury from excessive bilirubin accumulation, anaemic hypoxia and iron toxicosis. Tx with deferoxamine mesylate
  • Iron toxicity often iatrogenic due to administration of iron fumarate, particularly before the first suckle as protective factors in colostrum may reduce hepatotoxicity of iron.

Inherited or Congenital:

  • Glycogen storage disease Type IV (glycogen branching enzyme 1 in QH).
  • Persistent hyperammonaemia in Morgan foals thought to be associated with an inherited disorder of hepatic ammonia metabolism and possibly other amino acids.
  • Congenital hepatic fibrosis in Swiss Franches-Montagnes and Swiss Frieberger
  • Portosystemic shunts
118
Q

What are the clinical signs and progression of foals affected by glycogen branching enzyme 1 deficiency (GBE1)?

A
  • Seen in QH and paints
  • Severe impairment of glucose homeostasis
  • Foals may be born alive but weak and hypothermic
  • Intermittent hypoglycemic seizures may develop
  • Signs of fever, tachypnoea, tachycardia leading to respiratory failure and sudden death with even mild exercise.
  • Persistent elevations in CK, AST, and GGT may be seen.
  • Foals don’t survive beyond 18 weeks, most die by 6-8wk
119
Q

What is nutritional myodegeneration, what are the clinical signs, diagnostic tests and how is it treated?

A
  • Non-inflammatory degenerative disease of foals less than 30 days associated with low serum Se and Vit E concentrations
  • Affects skeletal muscle and cardiac muscle
  • Deficiency is in the mare associated with deficient soils and feeds
  • Subacute form involves muscular weakness, dysphagia due to weakness of muscles of mastication and swallowing and often leads to FPTI and aspiration pneumonia.
  • Acute form is associated with rapidly progressive weakness leading to recumbency and death within a few days. May have involvement of the myocardium and respiratory musculature.
  • Diagnosis: clinical signs and serum Vit E, glutathione peroxidase and Se levels.
  • Tx: injectable Se and Vitamin E
  • Prognosis is guarded but improved in foals that regain ability to stand.
120
Q

Why should isotonic replacement fluid solutions not be administered for maintenance in foals?

A

Na and Cl concentrations are too high - they would result in hypernatraemia and hyperchloraemia in addition the K concentration is too low so hypokalaemia may occur.

121
Q

What rate of Na and K supplementation should be provided per day in foals?

A

Na: <3mEq/kg/day

K: 1-3mEq/kg/day (can equate to addition of 20-40mEq/L to a hypotonic maintenance solution. However, ensure it is not administered at a high rate (not more than 0.5mEq/kg/hr)

122
Q

Why is PCV a less reliable marker of fluid balance in foals?

A

PCV will be increased in hypovolaemia but not necessarily in dehydration, so measurement of lactate and USG, as well as clinical examination, are important for establishing fluid/hydration status. If possible, measurement of CVP (through an over the wire catheter is often possible) is useful - maintain between 3-8cmH2O

123
Q

What is the lowest minimum MAP in foals before intervention is necessary?

A

60mmHg

124
Q

In addition to MAP, what other parameters are critical to monitoring tissue perfusion?

A

Heart rate, mentation, central venous oxygen tension, urine output, A/B status and trends in lactate concentration.

125
Q

What is the typical first-line choice of inotrope and/or vasopressor in foals?

A
  • **Dobutamine (positive inotrope) with primarily ß1 and slightly less ß2 effects with minimal α1. ß1 agonist effects increased cardiac output through increased myocardial contractility. Hence use of a vasopressor concurrently is used in humans.
  • *Dopamine but shown to be less effective inotrope than dobutamine and less effective and consistent vasopressor than noradrenaline.
  • Noradrenaline is a primary α adrenergic agonist but also has limited ß1 and ß2 effects. It induces arterial and venous vasoconstriction, increasing MAP, effective circulating volume, venous return and pre-load with minimal increase in heart rate or stroke volume. It is reported to be effective in increasing MAP and urine output in hypotensive foals that were nonresponsive to both fluid administration and dobutamine therapy. The combination is commonly used.
  • Vasopressin is a popular choice in humans however there is conflicting evidence in foals due to concerns regarding splanchnic hypoperfusion.
126
Q

What are the main potential negative effects of dobutamine?

A
  • Splanchnic vasodilation (ß2) can decrease systemic vascular resistance and MAP if not used in conjunction with a vasopressor
  • Increased myocardial contractility also increased myocardial oxygen requirements which can be detrimental in cases of impaired oxygen delivery
  • Stimulation of ß1 receptors causes tachycardia and arrhythmias at higher doses.
127
Q

Compare common vasopressors including positive and negative effects.

A
  • Noradrenaline is a primary α adrenergic agonist but also has limited ß1 and ß2 effects. It induces arterial and venous vasoconstriction, increasing MAP, effective circulating volume, venous return and pre-load with minimal increase in heart rate or stroke volume. It is reported to be effective in increasing MAP and urine output in hypotensive foals that were nonresponsive to both fluid administration and dobutamine therapy. The combination is commonly used.
  • Vasopressin is a popular choice in humans however there is conflicting evidence in foals due to concerns regarding splanchnic hypoperfusion. It has stronger vasoconstrictive effects on large arterioles than noradrenaline. In vasodilatory shock, decreases HR improves haemodynamics and reduces inotrope requirement. May be useful in catecholamine refractory hypotension.
  • Adrenaline is an α and ß adrenergic receptor agonist with negative effects on splanchnic and renal perfusion. It increases MAP by increasing cardiac output and vascular tone but has been associated with hyperglycaemia, hypokalaemia, lipolysis, tachycardia, decreased splanchnic perfusion increased lactate and increased platelet aggregation.
  • Phenylephrine has α1 activity but no cardiac effects, it works via constriction of the peripheral vasculature and is primarily used for arrhythmias resulting from dobutamine and or noradrenaline Tx. Not suitable for neonatal critical care.
128
Q

What are the nutritional requirements of a neonate and how does this change over the first few weeks-months of age or with disease in the neonatal period?

A
  • Neonate: 150kcal/kg/day. If sick, decreases to 45-50kcal/kg/day
  • 3 weeks: 120kcal/kg/day
  • 1-2mo: 80-100kcal/kg/day
129
Q

What is the approximate percentage of sugar, protein and fat in mares milk?

A

Sugar: 64%
Protein: 22%
Fat: 13%

130
Q

What are the long term implications of nutrient provision in utero for foals?

A

A restricted uterine environment can lead to lifelong impairment of growth and development.

An enhanced uterine environment can lead to enhanced growth rates out to 3 years of age.

131
Q

What is the potential impact of high carbohydrate feeding to mares in late gestation?

A

Decreased insulin sensitivity in the foal at 160 days age. There is speculation that this may pre-programme affected foals for metabolic disease later in life.

132
Q

What are the potential consequences of overfeeding carbohydrates, protein and fat in sick neonates?

A

Overfeeding carbohydrates: increased generation of CO2 which may be detrimental if compromised respiratory function; and hyperglycaemia which is a proinflammatory stimulus.

Overfeeding protein: increased protein catabolism and can potentiate or cause azotaemia.

Overfeeding fat: may result in hypertriglyceridaemia.

133
Q

What is the ideal milk replacer if commercial products are unavailable?

A

Semi-skimmed (2% fat) cows milk with 20g/L dextrose added.

134
Q

What is the recommended introduction rate for enteral feeding and how should this be increased with time?

A

Start: 2-3mL/kg/hr as bolus feeds
Increase to: 4-5mL/kg/hr on the second day
Increase to: 6-8mL/kg/hr on the third day (now at 10-15% of bodyweight)
Final volume/normal foal: 20-22% body weight/day.

135
Q

At what rate should parenteral nutrition be provided and how should this be increased with time or discontinued?

A

An initial caloric goal would be 40-60kcal/kg/day, and the starting rate would be administered at 25% of this.

Increase the rate gradually every 1-3 hours with monitoring of blood glucose concentration hourly.

If the patient tolerates parenteral nutrition well, consider increasing the caloric goal to 50-60kcal/kg/day

When discontinuing, decrease it by 25% increments every 4-6hours while gradually introducing enteral feeding and monitoring blood glucose.

136
Q

What monitoring is important in patients on parenteral nutrition and at what frequency?

A

Blood glucose, initially every 3-6 hours then decreasing to every 12 hours if stable over the first 36 hours.

CBC & serum biochem daily in critical cases or q72h in more stable patients

Serum electrolytes twice daily or more, in particular K (and P if patient was inappetent for a while, less relevant to foals) due to risk of hypokalaemia, particularly with concurrent insulin therapy.

137
Q

What are the recommendations for insulin dosing for SC boluses and for CRI?

A

SC boluses: 0.1-0.5IU every 12 hours. Risk of hypo or hyperglycaemia is high.

CRI: 0.07iu/kg/hr of regular insulin. Note, it takes 90 minutes after starting the infusion for maximum results to be seen or for adjustments in rate to be effected so don’t adjust the rate too quickly. A safer, more conservative rate would be 0.01IU/kg/hr. Monitor blood glucose closely (at least hourly initially) but avoid adjusting insulin and glucose infusions simultaneously as this results in a see-saw effect. If hyperglycaemia persists beyond 2-3hrs of initiating Tx, then increase the insulin; if hypoglycaemia develops give a bolus of 0.25-0.5mL/kg 50% dextrose over 3-5min and re-assess blood glucose in 30 and 90 min; if hypoglycaemia persists, a second glucose bolus should be given and insulin rate decreased by 50%.

138
Q

Over what time frame should insulin be discontinued?

A

Wean off in parallel with the discontinuing of parenteral nutrition (ideally over 24-36hrs) and importantly provide enteral nutrition during this time period.

139
Q

What are the structural changes in MRI that might be evident with equine neonatal encephalopathy?

A

Notable findings on MRI included hyperintensity of :

  • the basal nuclei
  • superficial layers of the ventral cerebral hemispheres
  • ventral thalamic nuclei
  • rostral aspect of the ventral midbrain.

Boards_2024 (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions