2. Physical Exam of the Equine Neonate
History
• Mare current and past pregnancy complications
• Parturition - Duration - Complications
• Post foaling times for standing, nursing, etc.
• Medication or procedures performed post-birth
• Umbilical care
• Meconium passage
• Urination observed
• Environmental factors - Infectious disease present, previous farm
problems
Look at mare
current status and
past pregnancies
Need to know what happen in
stage all stages
4. Physical Exam of the Equine Neonate
Distance examination of neonate
• Mentation, degree of alertness and
maternal interaction
• Assess general conformation
-Watch movement and gait and look for evidence
of pain or lameness
• Respiratory rate and character
-Normal is 60-80 breaths/min if environmental
temperatures are moderate
** metabolic acidosis and response to pain causes
increased respiratory rate
Interaction with environment and
the mare
Look for angular deformities
Have a small abdominal
movement seen at the end of
respiration.
If there is exaggerated abdominal
movement, flaring of the nostrils
and exaggerated rib expansion
and grunting sound.
5. Physical Exam
of the Equine
Neonate
TPR
• Pulse/HR : 80-120 beats/min
• Temp. : 99-101.8°F (37.2-38.8°C)
-Environmental temperatures can alter the foal's
temperature
• Immediate post-birth rectal temperature can fall to
98.6°F
-Shivering in cold environments is normal for 3-4 hours to
generate heat
Go from the warm environment to a cold one
6. Physical Exam of the Equine Neonate
Cardiovascular
• Mucous membranes - Normally pink and moist
- Scleral injection seen with toxaemia or conjunctivitis
- Icterus, if severe suspect neonatal isoerythrolysis or liver problem
• CRT- 1-2 seconds
• Arterial pulse quality
- Normal is just detectable - Use fingertips, check facial, brachial and
great metatarsal
• Jugular pulses are abnormal
• Assess jugular distension, should fill up briskly if not hypovolemic
• Cardiac Auscultation - Murmurs
- Common to hear a holosytolic grade I-IV murmur on left side -
ductus arteriosus
• Distal extremities and ears should be warm with adequate
circulation
Color of the mucous membrane and the CRT is not a good
indicator of the degree of oxygenation in the foal. Use arterial
oxygenation.
Episcleral
haemorrphaging is
normal in first 3 days of
life due to pressure as it
passes through birth
canal
Or dehydration
One week foal
If greater than four could be VSD so a congenital
defect
7. Physical Exam of the Equine Neonate
Respiratory system
• Ausculted sounds are louder than in adult
- Increased rates may produce abnormally loud and harsh sounds
• Premature foals down lung can become quieter and congested just from
body position
• Changes in resp. rate over time may indicate increased compromise of
respiratory function as well as pain, environmental temp.
• Best pulmonary function test in veterinary medicine is an arterial blood gas
• O2 levels reflect respiratory component
• CO2 levels reflect ventilation component
**Coughing as a symptom is not a common component of severe pulmonary problems in
neonatal foals
8. Physical Exam of the Equine Neonate
Gastrointestinal System
• Examine oral cavity for bite, cleft palate, and pharyngeal paralysis
• Check medial canthus of eye and skin for meconium staining which
may indicate in utero stress
• Gut sounds - Normal to hear gurgling in four quadrants
• Observe any abdominal distension - Can be associated with:
• Gastric distension associated with over feeding in premature foals
• Uroperitoneum associated with ruptured bladder or urachus
• Fulminating peritonitis
• Check for passage of meconium (dark brown to black) and patency of
GI tract
• Atresia ani or coli in any breed
Overbite
Cleft
palate
More fluid sounds are heard
Rectal palpating
9. Physical Exam of the Equine Neonate
Umbilical Region
• Size, heat, tenderness, moisture, oedema
• Should learn normal appearance for age
• Patent urachus
• Moist hairs around navel or urine scald on
inside of legs
Eye
• Check for ulcers or uveitis
• PLR can be sluggish if foal is excited and has
sympathetic override
• Menace response is lacking in normal foals until
two weeks of age
• Entropion is common in sick and premature foals
Check for herniation, should know how it normally looks for a
foal
10. Physical Exam of the Equine Neonate
Musculoskeletal System
• Conformation
• Observe motion and gait
• Contracted tendons and weak flexor tendons often improve within a few
days
• Check joints and physis for heat, swelling or pain
• Fractured ribs at birth
• Passive range of motion is increased along with greater fetlock drop in
premature foals
11. Physical Exam of the Equine Neonate
Neurologic System
• General attitude and behaviour - Foals are normally "hyper", swift and
"jumpy"
• Stands within 2 hours
• Recognizes mother and mammary glands
• Usually easily aroused by individuals; however, can deeply sleep and require stimulation
to rise, especially after 2 weeks of age
• Cranial nerves
12. MEDICAL DISORDERS OF THE FIRST TWO
WEEKS OF LIFE
•Meconium Retention
•Neonatal Maladjustment Syndrome
•Ruptured Bladder & Uroperitoneum
•Neonatal Isoerythrolysis
•Diarrhoea
•Septicemia
•Umbilical Problems
•White Muscle Disease
•Septic Arthritis and Osteomyelitis
13. Meconium retention
Retained meconium or a meconium impaction is seen with unsuccessful attempts
to pass meconium within the first 12 to 36 hours of life
14. Meconium retention
Meconium-
Digested amniotic fluid, glandular
secretions, mucus, bile and epithelial
cells
Greenish black to dark brown, little
odor
Tarry consistency
Within 3 hours after birth
15. Meconium retention
Etiology
• High prevalence in males - narrowed pelvis
• Meconium is retained in the large colon (high retention) or
in the rectum - near the pelvic inlet (low retention)
Clinical Signs
• Develops 6-24 hrs following birth
• Restlessness, attempts to defecate, swishing or "flagging" of
the tail, tail elevation and straining
• Advanced signs are colic pain, lying down and getting up,
rolling, and lying dorsal recumbency
• May appear to be attempting to urinate frequently
If not passing urine but in the position may be meconium impact
in.
16. Meconium retention
Differential Diagnosis
• Colon torsion
• Intussusception
• Volvulus of the small intestine
• Enteritis
• Atresia coli
• Diaphragmatic hernias with bowel strangulation
• Ruptured bladder
• Cystitis
17. Meconium Retention
Diagnosis
• Based on clinical signs and by manual palpation of a firm mass(low
retention)
• Persistent signs of recurrent pain with lack of passage of the lighter
colour milk stool in a less than 36 hour foal are suggestive
• Abdominal radiography
• Abdominal ultrasound
18. Meconium Retention
Treatment
• Responds to 350 to 750mls of warm soapy water(Ivory liquid hand soap)
administered per rectum through a soft, flexible tube by gravity flow
• Forceps or firm metal instruments to grasp the meconium is not
recommended
Acetylcysteine - 30 F Foley catheter, 4-8oz infused slowly, retained for up to
45mins
Prevention
• Early post birth administration of a small enema such as Fleet® (C.B. Fleet)
• Allow early exercise
CAUTION
• Large volumes of any solution used as an enema can produce severe electrolyte
issues
• Fatal hyperphosphatemia has occurred in human infants with phosphate
retention enemas
Helps break up impacted meconium
Fill balloon and
Half or full bottle
Within first 24 hours
19. Neonatal Maladjustment
Syndrome
These foals appear healthy at birth, but shortly thereafter exhibit
neurological abnormalities. They are often, disoriented, unresponsive,
confused, and have trouble nursing
Gummy foal
syndrome
20. Neonatal Maladjustment Syndrome
Etiology
• Hypoxic encephalopathy suspected in 92% of cases
in earlier study
• Placental problems 55%, gestational problems 21%,
premature placental separation 34%, dystocia 30%
• Septicemia
• Earlier studies indicated up to 50% develop a
component of bacterial infection if no antibiotic
treatment
• Meningitis (rare cause)
• Congenital lesions - Hydrocephalus most common
21. Neonatal Maladjustment Syndrome
Etiology
• Reversion to foetal cortical status
Hypothesis - signals that "wake" the foal up from an in utero or "foetal
cortical state" have failed in some of these foals and neuropharmacological
modulation may provide some benefit
• CNS hemorrhage or oedema
• Metabolic insults - Hypoglycemia, electrolyte alterations, acidosis,
hypothermia
• Endotoxin
• In utero infection
22. Neonatal Maladjustment Syndrome
Clinical Signs
• May or may not be associated with an apparently normal birth
• Signs develop within 72 hours of birth
• Loss of awareness of environment
• Recumbency, Inability to stand
• Disorientation
• Struggling randomly
• Loss of affinity for mare and nursing, poor suck reflex
• Blindness, seizures, opisthotonus
• Airway origin bark ("Wanderbarker")
23. Neonatal Maladjustment Syndrome
Treatment
• Fluids: Don’t over-hydrate and contribute to CNS
oedema
• Antimicrobials: Open gut and high risk of infection
• Oxygen insufflation, respiratory stimulants if needed
• CNS treatment to stimulate "I have been born" signal
• Pergolide (0.5 mg-1.0 mg once daily orally for 48 hrs)
• Naloxone 5 mg IV once
• Apply "Madigan squeeze method“
https://www.youtube.com/watch?v=-oxGVrRzCYI
• Treat for cerebral oedema
• 10% DMSO solution intravenously
• Mannitol - 0.25 gm/kg IV q 6-8 hrs for 24 hr.
• Flunixin meglumine 0.5-1.0 mg/kg q 12 h for 24 hr
Especially within the first 24 hours as gut is still
open
24. Neonatal Maladjustment Syndrome
Treatment
• Nutrition: Tube feed with colostrum
and milk
• Drugs to control seizures – Valium
• Protected or padded environment and a
human holder
• A plasma transfusion may be needed if the foal
did not receive enough colostrum
25. Ruptured Bladder &
Uroperitoneum
Several causes of uroperitoneum in neonatal foals
Ruptured Bladder – most common
Urachal rents
Congenital or traumatic lesions of the ureter
26. Ruptured Bladder
Etiology
Higher incidence of bladder rupture in males than in females,
possibly because the narrower pelvis and the longer, narrower
urethra
Traumatic bladder rupture is thought to be caused by uterine
contractions
Most bladder tears are located on the dorsum of the bladder
Prematurity, neonatal encephalopathy, cystitis, ascending infection,
abdominal trauma may predispose the foal to bladder rupture
Lift foal at the forelimbs or stifle and not by abdomen
cause that can cause rupture.
27. Ruptured Bladder
Ruptured Bladder
History
• Clinical signs develop by less than 7 days of age, usually after Day 2
• Foal appears normal at birth
• In some hypoxic ischemic encephalopathy (HIE) - foals don’t perceive
bladder as full
28. Ruptured Bladder
Clinical Signs
• Depression, gradual anorexia
• ± Abdominal pain, usually mild
• Abdominal distension (uroperitoneum) - may feel percussion waves
across abdomen; rapid shallow breathing
• Dysuria and/or stranguria (dorsal-ventral flexion of the back and legs
extended caudally), decreased frequency and volume of urine
• Dribbling urine
• Some septicemic foals develop ruptured bladder associated with
cystitis
29. Ruptured Bladder
Diagnosis
• History and clinical signs
• Abdominal ultrasonography
• Free peritoneal fluid
• Abdominocentesis - large volume of fluid. May occasionally smell like
ammonia
• Compare serum creatinine vs. that in peritoneal fluid
• If abdominal fluid is urine, creatinine measured in peritoneal fluid should
be higher (1.75 - 2X) than that of serum
• BUN is not as reliable due to equilibration with plasma
• K+ in serum compared to peritoneal fluid is not reliable
• Foals may or may not be azotemic
30. Ruptured Bladder
Diagnosis
• Retrograde injection of new methylene-blue into
bladder and look for dye in peritoneal fluid via
paracentesis
• Contrast bladder radiography - use aqueous based
organic iodine solutions
• Blood gas and electrolyte imbalances
(hyponatremia, hypochloremia, hyperkalemia and
acidosis)
• These may be seen with conditions other than
ruptured bladder
• Electrolytes may be normal if foal has been on IV
fluids
31. Ruptured Bladder
Treatment - Medical
• Nonsurgical
• Small leaks have been managed with an indwelling urinary catheter
• Hyperkalemia can cause death; Do not administer K+ containing antibiotics or
I.V. fluids (use 0.9% saline)
• Surgical Considerations
Prognosis – Good, if no
other concurrent problems
Ruptures heal on their own
Large defects in the bladder. Have to ensure that
they are rehydrated and electrolytes replaced else
death
32. Uroperitoneum
Urachal Rent
History and clinical signs are similar to ruptured bladder
Concurrent infection of the urachus
• Associated with septicaemia, prematurity, or ICU foal
• urachal infection and cystitis
Peritoneal fluid
• Inflammatory cells and increased protein
• Creatinine - is 2X that of serum creatinine
Treatment - Surgical correction and aggressive antibiotic therapy and nursing
care; plasma transfusion, etc
**Ureter stenosis and ureter defect has been described as a cause of
uroperitoneum in a foal
33. Neonatal Isoerythrolysis
An immune-mediated haemolytic disorder of new-born foals due to absorption of
colostral immunoglobulins which contain antibodies against red cell antigens
inherited from the stallion
34. Neonatal Isoerythrolysis
Etiology
• Most commonly in multiparous Aa or Qa negative mares due to sensitization
to blood group factors during pregnancy or blood transfusion
• Other (Ua, Pa, Qc, Db)
****In horses there are 8 major blood groups: A, C, D, K, P, Q, U, and T
35. Neonatal Isoerythrolysis
Clinical signs
• Foal from high-risk mare - Foals are normal at birth and only develop
clinical signs after ingestion of colostrum
• Progressively developing anaemia, icterus or rarely haemoglobinuria
leading to depression, anorexia, collapse and death
36. Neonatal Isoerythrolysis
Diagnosis
• Progressive haemolytic anaemia
• Hyperbilirubinemia - Elevation of both direct and indirect bilirubin
• Blood typing (Serology Laboratory)
• Hypoglycaemia and acidosis may be present concurrently
• Coombs test
• Flow cytometry
• Serial tube agglutination test
37. Neonatal Isoerythrolysis
Treatment
Blood Transfusion
Minimize stress, and exercise- stall rest is imperative
• Provide monitoring and supportive care depending on degree of clinical
signs. N.I. foals need a warm, dry environment, adequate IV fluids,
correction of hypoglycemia, or acidosis and monitoring for concurrent
infection
• Sepsis due to partial failure of passive transfer of adequate antibodies,
due to compromised hepatobiliary function, or due to tissue hypoxia and
enhanced translocation. Administer antimicrobials to minimize the risk
38. Neonatal Isoerythrolysis
Management of the N.I. Mare
• Observe foaling and do not allow foal to nurse mare
• Milk mare by hand
• Provide alternative colostrum from colostrum bank tested negative
for alloantibodies
• Muzzle foal until colostrum milked from mare
• Check milk via colostrometer and it may be possible to return the foal
to the mare earlier
40. Diarrhoea
Foal Heat Diarrhoea
• Most frequently occurs at a time that would correspond with dam's
first postpartum oestrus; foal is 6-10 days old
• Foals BAR
• Duration is usually 2-5 days
• Usually, no therapy required other than perineum cleaning
Foal eating forage, mare farces or concentrates. Just a
change in gut flora
41. Diarrhoea
Nutritional
• Consumption of excessive amount of milk after a foal is separated
from its dam for a period of time, or in overfeeding ill or orphaned
foals
• Sudden changes in diet of the mare or foal
• Foreign material (sand, dirt)
• Examine feces for sand, digital exam of rectal mucosa for grit
• Carbohydrate intolerance
42. Diarrhoea
Parasites
Strongyloides westeri
• May cause diarrhoea in foals at 1-4 weeks of age
• Larvae in mare's milk beginning at 4 days postpartum and peak at 10-12 days
• Prepatent period in foal 6-14 days; - Use fresh faeces (faecal flotation)
Crytosporidium sp.
• Associated with diarrhoea in both immunocompetent and
immunosuppressed foals
• Incubation 9-28 days
• Oocysts found in feces by sugar float or direct FA test (FA is the best test)
• Found in 15-31% of normal foals beginning at 4 weeks
• Infected foals considered the source of infection for other foals
43. Diarrhoea
Bacteria and Viral
In a retrospective study at University of Florida, at least 1 infectious
agent was detected in 122/223 (55%) foals
Rotavirus (20%)
C. perfringens (18%)
Salmonella spp. (12%)
C. difficile (5%)
The survival rate was 87% (191/223)
44. Diarrhoea
• Rotavirus Affects foals 2 days to 4-5 months
- Younger foals more severely affected
- Outbreaks have been reported on farms
- Low mortality but high morbidity
- 1/3 of foals positive( asymptomatic)
- Fever, depression, watery diarrhoea and anorexia
The virus persists in the environment for up to 9months, Phenolic
disinfectants required (bleach not effective)
45. Diarrhoea
• Salmonella spp. Endotoxemia/diarrhoea
• Clostridium perfringens type C, - has been responsible for high
mortality in neonatal foals during the first 2 days of life
It may manifest as sudden death without diarrhoea
May affect >1 foal on a farm, causes illness in new-born foals within 72
hours of birth
• Clostridium difficile In foals < 3 days of age; two presentations:
• Fatal haemorrhagic necrotizing enterocolitis
• Severe watery diarrhoea
46. Diarrhoea
Clinical Signs:
These organisms have been isolated from the gut in large numbers
from foals
• Fever, Depressed mentation
• Profuse diarrhoea, shock and death
• However, peracute cases may manifest as sudden death without
diarrhoea
• Clostridium difficile Produces haemorrhagic necrotizing enteritis
characterized by colic, depression, shock and death in 12 hr - 4-day
old foals
47. Diarrhoea
Diagnosis
• Blood cultures if suspect septicaemia. Most bacteraemias are gram -ve and yield
more than one isolate
• CBC
• Leukopenia associated with (Salmonellosis, E. coli septicaemia, Clostridia sp.)
endotoxemia
• May be unremarkable in viral diarrhoeas
• Electrolytes
• Diarrhoea causes losses of sodium, bicarbonate, chloride, potassium and calcium
• BUN, creatinine, may be elevated due to hypovolaemia (pre-renal), nephritis
from infectious agents, or tubular damage from concurrent use of
aminoglycoside antibiotics
• IgG - Often is low (< 400 mg/dl)
• Acid/base status ??
Metabolic acidosis
48. Diarrhoea
Diagnosis
• Faecal culture (direct plating of faecal specimen in selective media)
• Submit 25-50 ml of liquid faeces
• Must evaluate within 24 hours - Keep refrigerated or freeze
• Virogen Rotatest – ELISA test for faeces – sensitive and specific
***E. coli is a frequent cause of septicaemia in which diarrhoea may be
a component; however, E. coli has not been frequently documented as
a primary cause of foal diarrhoea
49. Diarrhoea
Treatment
Parasites Strongyloides westeri. Benzimidazoles are effective against
adults in small intestine. Thiabendazole (44 mg/kg); Fenbendazole (10
mg/kg); oxibendazole (10 mg/kg)
Fluids: Electrolyte replacement and maintenance should be of utmost
concern. Fluids with NaCl, bicarbonate and K replacement can be
accomplished by PO or IV therapy
• Withhold milk from foal while administering oral fluids
Milk can make diarrhoea worse
50. Diarrhoea
Treatment
Plasma Transfusion - Indications
• Failure of passive transfer in presence of diarrhoea + septicaemia
• Protein loss through inflamed bowel wall may lead to hypoproteinaemia
Antimicrobial Therapy - Selection of appropriate antimicrobials should be
based on blood culture and sensitivity results
• Rotavirus infected foals will not need antimicrobials if CBC is normal
***Be aware of nephrotoxic potential of aminoglycosides due to
decreased renal perfusion in hypovolemic and dehydrated foals
51. Diarrhoea
Treatment
Internal Protectants:
Bismuth subsalicylate. It also acts to
neutralize bacterial toxins; 3-4
ounces/45 kg PO, every 6-8 hours
Kaolin and pectin; 3-4 ounces/45 kg
PO, every 24 hours
Activated charcoal: acts to neutralize
toxins, 0.5-1.0 oz (15-30 g)/45 kg,
every 12 hours
Di-tri-octahedral smectite
(Biosponge) can bind endotoxin and
has been shown to neutralize toxins
15-30 ml every 6 hours
52. Diarrhoea
Treatment
Mucilloid (Metamucil):via stomach tube beneficial in managing sand-
induced enteritis. 1-2 ounces
NSAID ***Caution must be exercised because of their potential
nephrotoxicity and role in gastroduodenal ulceration
• Minimum effective dosage should be used
• Flunixin meglumine appears to be safer than phenylbutazone
Total Parenteral Nutrition (TPN) should be considered
Prognosis: Good once organism is identified
Treatment is early
53. Septicaemia
Disease caused by the spread of bacteria and their toxins in the bloodstream, and
most common cause of death in foals admitted for intensive care
54. Septicemia
Etiology
• Causative agents - A gram-negative organisms - E. coli, Actinobacillus
spp, Klebsiella spp, Enterobacter spp, Pseudomonas spp were most
common
• Streptococcal - usually in conjunction with a gram-negative
• Onset within 3-4 days of age - Some infections develop in utero and will
be present at birth
Predisposing conditions
• Delayed access to colostrum
• Failure to ingest adequate quantity of colostrum
• Maternal risk factors
• Maladjustment syndrome(NMS)
Does not produce enough colostrum or poor auality
55. Septicemia
Clinical signs
• Often cannot differentiate from neonatal maladjustment syndrome
• Early signs may be depression, lethargy, decreased mammary sucking
and a behaviour change
• Fever (>102°F, 39°C) occurs in less than 50% of cases
• Hypothermia <100°F (37.8°C) not uncommon
Advanced
• Petechiation - Pinnae of ears, mucous membranes of oral cavity, vulva
• Anterior uveitis
• Diarrhoea
• Coma, convulsions
• Respiratory distress
• Dehydration
• Poor pulse quality
• Swollen joints
56. Septicemia
Diagnosis
• Clinical pathology of septic foals - Obtain Stat. <400 mg/dl serum IgG is
common; some are within the 400-800 mg IgG range
• Complete blood count - Always do a WBC differential count
• Neutropenia <4000/ul (Remember premature non-infected foals have
neutropenia)
• Neutrophilia >12,000/ul
• Toxic cells
• Fibrinogen >400 mg/dl
• Hypoglycemia -50% of cases have glucose <80 mg/dl (4.4 mmol/l)
• Arterial oxygen <70 mmHg in 40% of cases
• Acid-base status indicating a mild to severe acidosis is common
• Blood culture
-Take before antibiotics or at trough periods before next administration
-Negative in 50% of cases with septicemia
Failure of passive transfer or
partial ones
Left shift
57. • Localized or
generalized sepsis is
likely if score > 12
• The sepsis score
should be repeated
daily in the following
instance:
• The score is in the
questionable range on
day 1 (11-14)
Table . Modified Sepsis
Score
Findings
4 3 2 1 0
Placentitis, vulvar
discharge, high risk
foal
yes no
Premature
gestational
age(days)
<300 300-310 310-330 >330
Petechiation,
scleral injection
severe moderate mild none
Fever >102 <100
Hypotonia,
depression, coma,
seizures
marked mild normal
Uveitis, diarrhoea,
respiratory distress,
swollen joints,
wounds
yes no
Neutrophil
count(/ul)
<2000 2000-4000 4000-8000 normal
Toxic changes marked moderate mild none
Band Neutrophils
(/ul)
>200 50-200 >50 none
Fibrinogen
Blood
Glucose(mg/dl)
<50, >200 50-80 80-180
IgG(mg/dl) <200 200-400 400-800 >800
58. Septicemia
Treatment
Antimicrobial
• Based on a review of UCD equine neonatal septicemia isolates from field and in-
house cases, the probability for antimicrobial susceptibility:
100% Imipenem
90-99% Ciprofloxacin, Ceftazidime
80-89% Ceftriaxone, Amikacin, Netilmicin, Cefaperazone, Ceftizoxime
70-79% Aztreonam, Gentamicin
60-69% Ceftiofur, Chloramphenicol, Ticarcillin/Clavulanate,
Trimethoprim/sulfamethoxazole, Ipericillin, Azlocillin
50-59 Amoxicillin/clavulanate, Ampicillin/sublactam, Tetracycline, Cephalothin
40-49% Ticarcillin
20-39% Ampicillin, Penicillin G, Sulfamethazine
<20% Rifampin, Oxacillin, Erythromycin, Tylosin
• Plasma therapy to increase IgG
• Fluid therapy
• Correct any hypoglycemia
• Correct any acidosis and dehydration
• Shock and dehydration treatment
• Nutritional Support
• Prognosis is guarded with blood culture positive foals; mortality may be 50% even
with intensive care. When presented collapsed in semi coma prognosis very poor
Septicaemia is more likely a
gram negative so antibiotics are
more likely to work. Gentamicin
is what is commonly used as it is
available
60. Umbilical Problems
Umbilicus consists of 3 structures
Two arteries connect internal iliac arteries; these regress to
become the round ligaments of the bladder
One vein connecting the placenta to the liver and portal cava,
regresses to become the round ligament of the liver within the
falciform ligament
The urachus connects the fetal bladder to the allantoic cavity
61. Umbilical Problems
Septic Omphalophlebitis
• Foal may have a completely normal, dry appearing external navel and be
severely ill from an infected urachus, umbilical arteries or vein
• May extend to peritonitis, and produce a bacteraemia and subsequent
septic arthritis, also liver abscesses, pneumonia, or osteomyelitis
Diagnosis
• Ultrasound of umbilicus for abnormalities
• Leukogram may or may not be inflammatory
• In cases of septic arthritis examine umbilicus for evidence of infection
Treatment
• Traditionally surgical removal of the suspected infected tissue under GA
• Many cases are managed by medical means and long-term antibiotics
62. Umbilical Problems
Umbilical Hernias
• May occur during parturition
• Most umbilical hernias occur or are noticed weeks after foaling
• Decision on whether to repair depends on the size of the opening
• Repair is either with clamps or surgical reduction
• Strangulating hernias in neonates are presented as acute abdominal pain
cases
• Uncommon occurrence
• Umbilical area is swollen and hernia may be irreducible
• Enlarging umbilical mass due to evagination of urinary bladder can occur
63. Umbilical Problems
Umbilical Abscessation – Extra-abdominal
Clinical signs:
• Enlargement, which may be hot and painful, in a foal usually >1 week of age that
often is showing no signs of systemic infection
Diagnosis:
• History and clinical signs with or without ultrasound examination of area
• Differentiate from a hernia by palpation and needle aspiration
• Include a good physical exam and haematology to evaluate systemic
component
Treatment:
• Medical - Manage by hot packs, and drainage ± systemic antibiotics
• Surgical – Indicated no response to medical management or if foal begins to
show signs of septicaemia
65. White Muscle Disease
Epidemiology/Etiology
• Seen in Pacific Northwest and Eastern states in equine neonates
• May also be precipitated by birth asphyxia and oxidative stress
Two forms of NMD
• - Peracute or cardiac form
• - Subacute or skeletal form
66. White Muscle Disease
Clinical Signs
Peracute or cardiac form
• Animals found dead or exhibit cardiac failure, or cardiogenic shock
• Intercostal muscles and diaphragm may also be affected
Subacute or skeletal form
• Signs from birth to 11 months of age
• Weakness - Unable to rise without assistance, falls on attempting to
rise, often resembles colic
• Dysphagia - Seen as oral and nasal regurgitation of milk
• Stiff painful gait or neck
• Tense or painful muscles
• Elevated respiratory rate
• Dark urine
67. White Muscle Disease
Diagnosis
Clinical Pathology
-Elevated serum CK (subtypes for myocardium or skeletal muscle can be
differentiated)
-Elevated serum AST
-Elevated LDH
-Occult blood or myoglobin in urine
-Low serum glutathione peroxidase activity
• Submit whole blood in EDTA tube
• Normal level is 20-50 U/mg of hemoglobin/min
-Low blood selenium <0.07 ppm suggests deficiency
-Vitamin E level should be >1-2 ppm
-Hyperkalaemia and hyponatremia can be severe
68. White Muscle Disease
Treatment
• Vitamin E - Selenium injection - 1 ml E-Se/45 kg IM. It may need to be
repeated daily or q 2-6 weeks. Also use oral vitamin E 1000 unit/day
during acute phase
• Supplementation of pregnant mares at risk
• 1 mg/day Selenium to ration.
• 10 ml Vitamin E-Se® IM
• Metabolic support - I.V. fluids, correction of hyperkalaemia and
hyponatremia, diuresis for myoglobinuria, limit movement
To prevent further muscle damage
70. Septic Arthritis and Osteomyelitis
Common names: Joint-ill, navel ill, infectious arthritis, septic polyarthritis, septic
epiphysitis, and septic physitis
Most common in foals <30 days
Most commonly isolated organisms are gram-negative enteric organisms including E.
coli, Actinobacillus suis like spp., Klebsiella pneumoniae, and less commonly Salmonella
spp.
71. Septic Arthritis and Osteomyelitis
Sources of Infection
• Previous or concurrent bacteraemia ± failure of passive transfer
• Gastrointestinal tract
• Probably most common portal of entry
• May or may not be associated with obvious signs of diarrhoea or enteritis
• Umbilical infection
• Often exterior of navel appears normal, but can also be enlarged or swollen
• Infection may be associated with umbilical arteries, vein or urachus
• Concurrent pneumonia
• Concurrent pneumonia in approximately 35% cases
• Pneumonic lesion often focal
• Penetrating wounds - Rare in young foals (<60 day)
72. Septic Arthritis and Osteomyelitis
Clinical Signs
• Sudden onset of lameness with or without joint distension, pain and oedema
• Swollen joints with or without periarticular oedema
• Foals maybe BAR
• Onset of stiffness, with back or neck pain and a low-grade fever - consider
vertebral osteomyelitis
• Sudden onset of lameness with owner history of trauma to foal (mare
stepped on foal). In foal less than 45 days, any lameness should be proven
NOT to be related to an infectious etiology
• More than one joint may be involved in approximately 50% of cases
73. Septic Arthritis and Osteomyelitis
Diagnosis
• Based on history and clinical signs
• Fever, lameness (joint swelling in recumbent foal), inflammation,
hemogram, leukocytosis ± joint swelling and periarticular oedema
Ultrasound of joint
• Joint aspiration(arthrocentesis)
• Synovial fluid examination
• Culture synovial fluid
• Aseptic technique
• Aerobic and anaerobic cultures
• Attempt culture even if foal is receiving antimicrobials
Joint fluid is cloudy
or dark
74. Septic Arthritis and Osteomyelitis
• Culture of blood
• Culture any foal with systemic signs or those foals <14 days
• Greater probability of obtaining causative organism than joint culture - Do
both joint and blood culture
• Radiography
• May be normal on initial examination - Repeat in 5-7 days
• Examine metaphysis, physis or epiphysis for osteolysis, sclerosis, or reactive
cortical bone
• Soft tissue swelling
75. Septic Arthritis and Osteomyelitis
Treat early - within hours
• Systemic Antimicrobials - combine with intra-articular antimicrobial
therapy
• Gentamicin (25 mg) or amikacin (125 mg) into joint
• Use along with drainage, lavage and anti-inflammatory drugs
76. Septic Arthritis and Osteomyelitis
• Regional Limb Perfusion:
• High and persistent concentrations in joints (up to 100 x concentration after
IV administration)
• Drainage - Mechanical lavage and removal of debris. Removal of
degenerative neutrophils, fibrin, high WBC, proteolytic enzymes, will benefit
from aspiration and flush
• Flush
• Distension - irrigation with one puncture and 3-way stopcock and 2 syringes
with saline or preferably lactated Ringer’s. Use 500 ml to 1 liter total volume
• Through and through - two needles in joint and continuous lavage of 1-2
liters sterile fluid
• Arthroscopy - allows look at cartilage, removal of fibrin and synovectomy
(removal of bacteria sequestered in synovial membrane)
• Flushing generally repeated until WBC <30,000 cell/μl (clinical impression)
77. Septic Arthritis and Osteomyelitis
Prognosis
• Good with early treatment (1st day)
• Poor with a delay in treatment, use of procaine penicillin only and
radiographic evidence of bone involvement
