Principles of Neonate Care and Disorders of the Neonate Flashcards

1
Q

Let’s think about the differences between neonates and adults; how do neonates thermoregulate in comparison to adults?

A

· They have brown fat

· The neonate cannot regulate their own temperature

· Change in respiratory rate and increasing their metabolic rate

Thermoregulatory mechanisms are poorly developed so neonates tend to become hypothermic more quickly – also normal basal temperature is generally higher than that of adults.

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2
Q

Briefly describe how neonatal hepatic and renal function compares to adults?

A

Renal function in the preterm neonate is not only immature at birth but there is a significant delay in the renal function to achieve its full capacity. t is important for the clinician caring for neonates to be aware of the expected fluid shifts, electrolyte handling, and renal functional capacity as these “normal” changes will become quite relevant when medical or surgical pathology is present.

Renal System

ƒ Renal blood flow and glomerular filtration are low in the first 2 years of life due to high renal vascular resistance. Tubular function is immature until 8months, so infants are unable to excrete a large sodium load.

ƒ Dehydration is poorly tolerated. Premature infants have increased insensible losses as that have a large surface area large surface area relative to weight. There is a larger proportion of extra cellular fluid in children (40% body weight as compared to 20% in the adult).

Hepatic System

ƒ Liver function is initially immature with decreased function of hepatic enzymes. Barbiturates and opioids for example have a longer duration of action due to the slower metabolism.

Neonates have a higher volume of distribution (they are 75-80% water compared to 60% in adults) – this is combined with a not yet mature renal and hepatic function means that they are at a greater risk of developing hypovolaemia and hypoglycaemia (also they don’t have the same fat stores as adults do so they rely on glucose as the main source of energy).

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3
Q

What is in colostrum that makes it different from normal milk?

A

· Immunoglobulins - IgA, IgG, IgM

· Fats

· Sugars

Colostrum is rich in IgG, has some IgM and IgE and lymphocytes

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4
Q

When absorption does not occur, we speak of failure of passive transfer (FPT). List 5 risk factors which may lead to the development of FPT.

A

· Poor quality colostrum

· Disease to dam preventing standing

· Teats are too large

· Injury to the neonate preventing suckling

· Neonate fails to compete with siblings

· Poor quality colostrum

· Early lactation and colostral loss

· Primiparous animals

· Poor udder development

· Mastitis

· Lack of appropriate maternal antibodies

· Poor intake (quantity or time)

· Underlying neonatal disease

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5
Q

How can you differentiate FPT from other types of hypogammaglobulinemia (e.g. transient and congenital)?

A

Hypogammaglobulinemia – congenital types usually manifest once maternal (colostral) immunity has waned

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6
Q

How can you treat neonates with FPT

A

FPT can be addressed by administering IgG to the neonate, generally via a plasma transfusion (in foals particularly) though other colostrum supplements are available for oral administration (only in the first few hours of life while the neonate can still absorb the colostrum)

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7
Q

Why don’t we vaccinate neonates on their first day of life?

A

They still have maternal natural immunity at this point

The following picture shows the relationship between waning maternal immunity and timing for vaccination when the youngling is starting to develop a self-sufficient functioning immune system. Earlier vaccination would “use up” maternal IgG and potentially predispose to infections, later vaccination means exposing to the risk of infection as maternal immunity is waning. So getting the timing right is very important.

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8
Q

What are the range of parameters for foaling?

A
  • Foals are not miniature horses they have their own reference ranges of physical parameters
  • Horses have quick foaling as they are prey species
  • 1st stage= ideally less than 2-3 hours
  • 2nd stage= very quick exit of foal in 10-20mins when mare is extremly vulnerable
  • 3rd stage= delivery of placenta (always check it has been passed as retained placenta will make the mare very sick)
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9
Q

Discuss the approach to the normal and sick equine neonate?

A
  • Foal showing how intensive treatment can be.
  • Septic foal with SIRS, hypovolaemic and unconscious this is referral level not a day on competency.
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10
Q

What are the range of parameters for the newborn foal?

A
  • Should be sitting standing quickly
  • Should stand within an hour and suckling within 2 hours
  • After that should be able to move and follow mare around
  • Anything that deviates from normal is a sign of something that could degenerate very quickly. Be a hypercondriact parent with foals.
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11
Q

What is the normal foal TPR?

A

Foals tend to be tachycardia for first 24hrs

Temperature they are a bit warmer than adults

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12
Q

Describe day 1 foal exam?

A

–Examine the vulva, placenta and udder – when you get there following birth

–Examine placenta (make sure it has been passed completely, retained fetal membranes can lead to septic shock and death. Best case scenario of RFM just laminitis)

–Check foal can stand and suck – examine limbs for deformities

–Examine umbilicus – advise re dipping

•Chlorhexidine/ povidone iodine/ (blue spray)

–Examine general appearance of foal – does it look premature (premature foals have typical features: may not be ready to suckle, underdeveloped lungs causing resp difficulties, was it born prematurely due to in utero infection so born septic)

–Ask whether defecated/ urinated – depends when you get there. Check for meconium impactions. Check for ruptured bladder common in colts.

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13
Q

Continue your discussion of a foal exam day 1?

A

–CardioVascular exam

–Check for congenital defects

  • Parrot mouth (may prevent from nursing)
  • Cleft palate (may prevent from nursing)
  • Cardiac abnormalities
  • Hernias (usually umbilical)

–Ophthalmological examination (or day 2) When foals are born they have no menace response remember

–Administer tetanus anti-toxin (spend a lot of time on the ground so have a higher risk of getting tetanus)

–Enema?

–Antimicrobials?

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14
Q

Discuss insurance in the foal?

A
  • Most companies will not insure foals less than seven days of age and will not insure them above this if certain procedures have not been performed. CHECK THE REQUIREMENTS FOR SPECIFIC INSURANCE COMPANIES
  • This insurance is VERY expensive and is usually only taken out for very valuable foals – be that monetary or attachment
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15
Q

Summarise foaling?

A
  • Provide clean, dry, warm environment
  • Make sure they can drink/get their Colostrum (rich in antibodies and in the first 12-24hrs the foal’s gut is predisposed to absorb these and these will protect it for the next 6 months) and appropriate nutrition vital
  • Treat umbilicus appropriately as biggest route of infection in LA (large animals)
  • Assume sick neonates are septic until proven otherwise and treat promptly and aggressively
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16
Q

What are common conditions of the foal which can be treated in most common +/- ambulatory settings?

A
  • Meconium impactions
  • FPT (failure of passive transfer)
  • Flexural limb deformities

–Contracted (can try to splint)

–Lax tendons (will improve as foal runs around)

17
Q

What are common conditions which are best to refer?

A
  • Omphalitis/haernia
  • Diarrhoea
  • Bladder rupture
  • HIE
  • Colic
  • Pneumonia
  • Prematurity/dysmaturity
  • Sepsis
  • Congenital abnormalities
18
Q

What are the keys to success in treating foal conditions?

A
  • Early recognition of a problem
  • Rapid, aggressive treatment of problem otherwise will go down hill very quickly
  • Repeated major body system assessment and adaptation of therapy based upon clinical examination findings, urine output and USG, treatment of low MABP and high blood glucose
  • Know the limits of yourself and the practice

–Very time consuming and labour intensive

–If no over night care needs refering to place with 24hr care

–If in doubt refer and do the best for your client and the foal

19
Q

Discuss omphalitis and umbilical hernias?

A

More common in calves. Defect in closure of abdominal wall. Depending on size can heal as animal grows most of time needs treatment as is easier to fix when they are younger

20
Q

Discuss IV access?

A

•Foals

–Jugular vein (generally easiest spot)

–Clip and aseptic prep for catheters (they are relying only on maternal antibodies at this point so you need to be very aseptic)

–20G or 21G needle

•Calves/small ruminant

–Jugular vein

–20G needle

•Puppies/kittens

–Jugular vein

–22G in kitten, 21 or 22G in puppies

21
Q

What are good injection sites in neonates?

A
22
Q

What is the approach to the sick equine neonate?

A
  • Assume that a sick foal has SIRS due to bacteraemia/toxaemia until proven otherwise
  • Do NOT ignore mild clinical abnormalities
  • Time is of the essence

–Clients who want to treat foals that are sick will end up with smaller bills the sooner they are referred

–Warn clients with sick foals that wish no or minimal treatment of likely outcome

–Don’t half-heartedly treat foals in the field and convince yourself and the client that you are doing the best for the foal!!

23
Q

What are the clinical signs of sepsis?

A
24
Q

What is a premature foal?

A
  • <320d gestation
  • Low birth weight
  • Silky hair coat feel to it
  • Domed forehead not full developed
  • Floppy ears
  • Flexor laxity/hypotonia
  • Weak suck reflex/poor at feeding
  • Poor thermoregulation
  • Entropion (caused by hypovolamia hair then rubs on cornea)
  • Poor glucose regulation (not good at handling it may remain hypoglycaemic)
  • Immature renal function (creatinine will be high and stay high despite giving fluids)
  • Can take pictures of hocks, knees and carpi can see bones of carpus are not formed only cartilage there if fully formed should see some bones there
25
Q

What is a dysmature foal?

A

Similar to premature but born at term but suffered placental insufficiency

26
Q

What is post-mature?

A

Retained in Utero for too long tend to be bigger foals but a bit skinnier

27
Q

Discuss Hypoxic Ischemic Encephalopathy?

A

Aka Perinatal Asphyxia Syndrome (PAS)

Aka Dummy foal

Signs form birth to few hours later

Dystocia/premature placental separation, unrecognised in utero hypoxia

  • Neurological signs (unconsciousness, dull demeanour, inability to stand/suckle) Can see hold their tongue out walk around like a dummy
  • Respiratory compromise (lungs may not work properly)
  • Renal insufficiency (suffered hypoxic damage so may have renal failure at birth)
  • GI ileus (and have reflux)

Often result in FPT leading to sepsis

Often along with prematurity

28
Q

Discuss bladder rupture?

A

Classically 1-2 old colts as urethra is longer

Can be caused by trauma of falling over

Present with:

  • Neurological signs (weakness, not suckling)
  • Anuria/dribbling little urine
  • Straining to urinate
  • Abdominal distension
  • Tachycardia/tachipnoea

Do some blood work and electrolytes will confirm rupture bladder the below cocktail is indicative of this:

  • Hyperkaliemia
  • Hyponatraemia
  • Hypochloraemia
  • High creatinine
29
Q

Discuss Omphalitis?

A

Umbilical remnant contains:

1 vein, 2 arteries, 1 urachus

Reference ranges for size of it at different age

Often source of infection, often in association with FPT

If umbilicus looks too big for you refer

30
Q

Discuss respiratory distress in foals?

A

Foals are standing when in RD (foals tend to prefer to lie down when they can breathe properly a foal in resp distress will rarely sit down as it is harder to breath this way)

Give oxygen therapy ASAP

Identify and treat cause where possible

Hypoxaemia from other disease (HIE)

Pneumonia

  • Bacterial
  • Viral

Fractured ribs (during parturition)

•Pneumothorax

ARDS (acute respiratory distress syndrome)

•Can die very suddenly

31
Q

Discuss colic in the foal?

A

Rectal palpation not possible

Medical

  • Meconium impaction (can diagnose with finger)
  • Gastric ulceration
  • Necrotising enterocolitis

Surgical

  • Intussusceptions
  • Volvolus
  • Displacements
  • Diaphragmatic hernias
  • Obstructions
  • Etc
  • LI not as developed in foals the SI is as they are only drinking milk at this point so only require SI activity.

Congenital abnormalities

•E.g Atresia coli ani (intestine is a dead end)

32
Q

Discuss Diarrhoea in the foal?

A

Foal heat – 5-14 days (nothing to do with mare but can happen around the time the mare has the first heat after foaling) Generally is benign and goes away but can get worse so need to keep an eye.

Viral

  • Rotavirus – 5-35 days
  • Coronavirus – first few days of life
  • (Adenovirus, parvovirus)

Bacterial

  • C. perfringens, C. difficile
  • Salmonella spp
  • E. coli
  • Bacterioides, Aeromonas
  • Lawsonia intracellulare (6m.o.)

Parasitic

  • Strongyloides Westerii (transmammary!)
  • Strongylus vulgaris, Cyathostomes (>6m.o.)

Protozoal

33
Q

Describe the general approach to fluid therapy in the foal?

A
  • Initially (to a 50Kg foal) administer 1-2 litres of fluid (Hartmanns ideally) as a bolus depending on assessed fluid deficit
  • Repeat major body system assessment
  • REMEMBER THAT FOALS MAINTENANCE FLUID RATE IS TWICE THAT OF ADULTS – 5ML/KG/HR
  • Once parameters start to improve start plasma and further resuscitation fluids at approx twice maintenance
34
Q

Discuss the approach to the sick foal further?

A

Oxygen therapy via intra-nasal tube – well tolerated

If foal is down:

–On a mat

–Turn every few hours to prevent decubital ulcers and keep in sternal as improves oxygen uptake

–Near, but separated from mare – need person with foal at all times!! Mares presence perks the foal up a little bit.

–Urinary catheter – MEASURE USG regularly

Urine output means perfusion – should be 1-2ml/kg/hr

Normal urine of foals is -as they are on a liquid diet- HYPOSTHENURIC - <1.008!! If foal has renal disease then they probably will be isothenuric about 1.008 as they cannot concentrate/dilute urine

•Assess fluid therapy success as well as appearance of foal

35
Q

What is the care of the sick foal in the 1st 24 hours?

A

If down DO NOT ADMINISTER MILK ORALLY

–IF perfusion poor, will have ileus and the milk sits in gut and predisposes to necrotic enterocolitis=death

–IV glucose for max 24 hours or PPN for as long as required

–When foal better, can administer glutamine prior to gradually re-introducing milk (q 1hour)

NIBP (non-invasive blood pressure)

–Keep MABP >60mmHg

–Dobutamine and/or norepinephrine and/or vasopressin infusions

Blood gases – arterial – lateral metatarsal or brachial arteries (tell you about gas exchange)

Monitor and correct electrolytes and glucose

–K+ and Mg2+ low usually – change to maintenance fluids which are higher in these and lower in Na+ (e.g. Plasmalyte)

–Insulin to control high glucose – IM or infusion

36
Q

What needs to be considered at the end of the 24hr stage of sick foal treatment?

A

At this point need to decide if foal showing improvement

–If not, then consider euthanasia or discuss further financial commitment

–Usually £1000 for first 24 hours and total bill for septic/ dummy foal, depending how bad – in excess of £3000-5000. They are labour-intensive!!! May need 5-7 days of this type of care followed by 2-3 days of adaptation – help standing, re-introduction of milk and to mare!

37
Q

What further evaluation can be done for the sick foal?

A
  • Scan umbilicus (and abdomen if required)
  • Repeated examination of

–Joints

–Vein

•If in doubt, remove catheter and insert a new one

–Cephalic or saphenous veins NOT other jugular vein

–FPT means the catheter can be a strong site of infection