Conditions of the Foal Flashcards

1
Q

what are congenital abnormalities of the respiratory tract

A

Wry nose (see top photo)

Cleft palate - common so all foals should be checked at birth (palpate with a clean gloved finger)

  • May see milk from nose when nursing if present.

Choanal atresia (uncommon)

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2
Q

what are congenital cardiac abnormalities

A

Atrial Septal Defect (ASD)

Patent Ductus Arteriosus (PDA)

Ventricular Septal Defect (VSD)

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3
Q

what breeds are more prone to ventricular septal defects

A

very common in Welsh Section A ponies and linked to short ears

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4
Q

what are neurological congenital abnormalities

A

Cerebellar abiotrophy - occurs in Arabian and Eriskay foals - progressive neurological signs localized to cerebellum

Juvenile epilepsy - Arabian foals again… but it is self-limiting

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5
Q

what are congenital abnormalities of the GI tract

A

Atresia of colon, rectum, or anus

Congenital aganglionosis

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6
Q

what breed does congenital aganglionosis occur in

A

(overo lethal white foal syndrome) - occurs in American Paint horse with overo coat pattern

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7
Q

what are musculoskeletal congenital abnormalities

A

Flexural limb deformities

Angular limb deformities

May be severe and result in dystocia and require C section (the forelimbs of the foal in the photo were not able to be straightened any further)

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8
Q

what should be a routine assessment in the majority of sick foals

A

Umbilical ultrasonography

Is the basis for diagnosis of all umbilical conditions

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9
Q

what is a patent urachus

A

Urachal remnant remains open and urine drains out

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10
Q

when is a patent urachus commonly seen

A

Seen a few days after birth

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11
Q

what foals are at an increased risk of patent urachus

A

Foals with systemic illness, recumbent hospitalized ‘mat babies’ etc are at an increased risk of developing this

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12
Q

what can patent urachus result in

A

It can result in urine scalding of the skin on the ventral abdomen

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13
Q

how is patent urachus treated

A

Conservative management

  • Topical cleansing and monitoring for infection
  • Chemical cautery - silver nitrate, procaine penicillin

Surgical excision

  • Never needs to be addressed urgently, but this might be an option in some cases.
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14
Q

what is umbilical remnant infection

A

Foals with umbilical infections may be clinically normal, or show signs of systemic inflammation (or even sepsis)

The umbilicus may appear swollen, inflamed, hot, or have discharge

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15
Q

how does an umbilical remnant become infected

A

The infection may have occurred due to ascending infection (from the external environment) or be secondary to another site of infection (bacteraemia) (latter is more common than people think)

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16
Q

what are the areas that can be infected in the umbilical remnant

A

Urachitis

Omphaloarteritis

Omphalophlebitis

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17
Q

what are the treatment options for umbilical remnant infection

A

Any delay in treatment/resolution of infection increases the risk of infection spreading to joints and leading to septic arthritis (which is more difficult to treat)

Medical treatment:

  • This is usually the first line treatment plan
  • Broad- spectrum antimicrobials (until culture results obtained)
  • Prolonged treatment is required (several weeks)

Surgical treatment:

  • Excision of affected internal remnants
  • Exact surgery is planned based on US
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18
Q

what should you always check for in a colicky foal

A

Always check for the presence of an umbilical hernia in a colicky foal!

And at all newborn foal checks

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19
Q

how are hernias managed

A

Small hernias are not uncommon and may close without treatment

Larger hernias may be treated conservatively (belly band) or need surgery

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20
Q

when would bladder rupture occur and why

A

May occur in first few days of life, due to bladder wall failure occurring during parturition

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21
Q

where is the most common site for bladder wall rupture

A

dorsal wall

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22
Q

why is bladder rupture more common in colts

A

It is more common in colts compared to fillies (think about where pressure occurs around the abdomen during delivery relative to the position of the urethra in colts vs fillies)

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23
Q

what are the clinical signs of bladder rupture (uroperitoneum)

A

Straining to urinate (see photo, must distinguish this from straining to defecate)

Depression and weakness

Signs of hypovolemia

24
Q

what might be seen on clinical pathology with bladder rupture

A

Azotemia (increased creatinine - post renal)

Hyperkalemia (beware fatal bradycardia!)

Hyponatremia

Hypochloremia

Metabolic acidosis

25
Q

what should you beware with hyperkalemia in bladder wall rupture

A

fatal bradycardia

26
Q

what is seen on US with bladder wall rupture

A

Free abdominal fluid

Small bladder

Hole identified in bladder wall (usually dorsal bladder wall - see arrow)

27
Q

how is bladder wall rupture diagnosed using abdominocentesis

A

More risky to perform on foals cf adults - only do if essential for diagnosis or therapy

Creatinine in peritoneal fluid twice that of serum

May also be therapeutic - control hyperkalemia, reduce pressure on diaphragm, but FLUID THERAPY required to replace lost volume

28
Q

how is bladder rupture treated

A

These foals require EMERGENCY medical management:

Correct hypovolemia

Correct hyperkalemia

  • Add dextrose/glucose to fluids (will increase endogenous insulin)
  • Give insulin (will drive potassium into cells)

Place urinary catheter (will help drain abdomen)

Drain abdomen directly (only if essential)

Surgery will be required, but only once stable (there is no rush!)

29
Q

what is the prognosis of bladder wall rupture

A

Survival is good if diagnosed early

Delays in diagnosis or concurrent disease reduce prognosis.

Foals form abdominal adhesions following abdominal surgery (or even abdominocentesis!) very readily which can be a complication in these cases

30
Q

what is neonatal isoerythrolysis

A

Foals RBC destroyed by preformed maternal anti-red blood cell antibodies in colostrum

31
Q

what is the pathophysiology of neonatal isoerythrolysis

A

Mare exposed by placental pathology, during parturition or after blood transfusion

Foal must have consumed colostrum

Aa and Qa most commonly involved because there are more antigenic

Foal gets sires blood type

If mare during a previous pregnancy has formed antibodies to the foals blood type

These antibodies are in mare’s circulation and go into colostrum

When foal drinks colostrum these antibodies will go into the foal’s bloodstream and attack the RBCs

32
Q

what % does neonatal isoerythrolysis occur in

A

1-2%

33
Q

what are the clinical signs of neonatal isoerythrolysis and when do they occur

A

Normal at birth — develop signs 2-5d of age

Anemia and tissue hypoxia

Lethargy, weakness, tachypnea, tachycardia

Pale MM —> yellow icterus

Seizures (kernicterus)

Pigmenturia

34
Q

what is shown on clinical pathology in neonatal isoerythrolysis

A

Anemia:

  • Most 10-20% (normal 30-40%)
  • Decreased venous oxygen

Metabolic acidosis (lactic acidosis)

Hyperalbuminemia (indirect/unconjugated)

Thrombocytopenia?

Coombs test — (direct antiglobulin test)

35
Q

how is neonatal isoerythrolysis treated

A

Depends on severity of anemia and clinical signs

Moderately affected — supportive care, rest

Severely affected (PCV <12%) Restoration of oxygen carrying capacity Transfusion of RBC

Universal donor (Aa/Qa negative)

Mare washed RBC

  • To remove antibodies
  • Mare will be perfect donor, because there will be no more antibodies

Nasal oxygen?

  • Not significantly increase O2 carrying capacity
36
Q

how is neonatal isoerythrolysis prevented

A

At risk:

  • Aa/Qa negative mare

Mare with previous NI foal Muzzle foal at birth for first 24 hours

  • Means birth must be witnessed!
  • Provide donor colostrum or plasma
37
Q

what are causes of respiration disease in foals

A

Meconium aspiration

Milk aspiration

Rib fractures (leading to pneumothorax and/or hemothorax)

Bacterial pneumonia

Viral infections (EHV-1, EHV-4, EAdV, EAV)

Parasitic pneumonia

38
Q

how does meconium aspiration occur

A

All foals with meconium staining present at birth should be assumed to have meconium aspiration

When hypoxia occurs at the point of delivery this leads to foetal stress, which in turn leads to the unfortunate combination of meconium passage and gasping, and results in meconium aspiration

39
Q

how is meconium aspiration treated

A

Aspiration of nasal passages and pharynx on delivery (BEFORE the first breath is taken)

Oxygen supplementation

Anti-inflammatory therapy

Antimicrobials

40
Q

why might milk aspiration occur

A

Generalized weakness

Poor suckle reflex

Dysphagia (often prematurity or PAS)

Bottle feeding

Cleft palate (check all foals at birth, often see milk from nose but not always)

Vascular anomalies (rare)

Incorrect tube placement/feeding (be careful!)

41
Q

how is milk aspiration diagnosed

A

There are two aspects to diagnosis - confirming that milk aspiration is happening, and then diagnosis of the aspiration pneumonia

  • Auscultation of the trachea whilst nursing - you can hear the fluid running down the trachea/gurgling
  • Endoscopy of the pharynx/larynx - to assess for any abnormality in structure or function
  • Endoscopy of the trachea - to observe for milk in the trachea
  • Thoracic radiographs - alveolar pattern ventral lung (esp caudoventral)
42
Q

how is milk aspiration treated

A

Placement of an indwelling nasogastric tube will be required until the underlying disorder leading to aspiration is corrected. This may take many weeks in rare cases.

Antimicrobials will be require to treat secondary bacterial pneumonia.

Usual supportive care for pneumonia (oxygen, anti-inflammatories etc)

43
Q

what are the bacterial causes of pneumonia in foals and what is the lung pattern on radiographs

A

Hematogenous spread to lung secondary to bacteraemia

  • Diffuse radiographic pattern

Secondary to meconium or milk aspiration

  • Caudoventral radiographic pattern
44
Q

what bacteria cause pneumonia in the foal

A

The same ones which cause sepsis

E.coli, streptococci, Enterococcus, Actinobacillus, Enterobacter, staphylococci

45
Q

what types of bacteria cause pneumonia in older foals

A

Strep equi zooepidemicus

Rhodococcus equi

46
Q

besides lung abscesses where else do R. equi infect

A

Joints

Uveitis

Diarrhoea

Abdominal abscesses

47
Q

what are causes of colic in foals

A

Meconium impaction

Diarrhea

Dysmotility

Strangulating obstructions

Intussusceptions

Hernias

Ulcerations

Ovarian or testicular torsion

Ascarid impaction

Pyloric or duodenal strictures

Fecaliths

Etc

48
Q

what are causes of true neonate diarrhea

A

Necrotizing enterocolitis (NEC)

Asphyxia-associated enteric dysfunction

49
Q

what is foal heat diarrhea

A

Cause likely changes in fecal microbiota

Adding in hay and grain in their diet

50
Q

what age does foal heat diarrhea occur

A

5-15d of age

51
Q

how is foal heat diarrhea treated

A

mild, usually self limiting

52
Q

what age does rotavirus cause diarrhea

A

5-35d

53
Q

what are the signs of rotavirus diarrhea

A

Anorexia and depression

Acute, profuse watery diarrhea

54
Q

how is rotavirus diarrhea treated

A

Supportive care (IV fluids)

Lactase enzymes

Severe cases may need ‘enteral rest’

  • Off feed and providing parenteral nutrition
55
Q

what are causes of diarrhea

A

True neonates:

  • Necrotizing enterocolitis (NEC)
  • Asphyxia-associated enteric dysfunction

Foal heat diarrhea

Rotavirus

C. difficile and C. perfringens

R. equi

Strongyloides westeri

Older foals — proliferative enteropathy (Lawsonia)

56
Q

how is diarrhea treated

A

Maintain hydration

  • Fluid therapy

Check IgG

  • Provide plasma if low or low protein

Antimicrobials?

  • Different than adult horse
  • Can become bacteraemic and septic from diarrhea whereas adult horses do not

Symptomatic treatment

Transfaunation

Bio-sponge

Lactase supplementation

Nursing care — clean bum

  • Scalding

Enteral rest?

  • Referral for TPN
  • Not okay to just provide IV fluids need to actually provide IV nutrition
  • Hypoglycemia and high energy demands during this period