Vet Clin Equine 19 (2003) 19–33
Lower respiratory problems of the neonate
Pamela A. Wilkins, DVM, MS, PhD
University of Pennsylvania, New Bolton Center, 382 West Street Road,
Kennett Square, PA 19348, USA
The transition to extrauterine life
Early recognition of abnormalities in the respiratory tract is of utmost
importance for the successful management of critically ill foals. To recognize
abnormal, the normal must be known. Immediately after birth, foals
undergo several important physiologic and behavioral changes. Chief
among these changes is the adaptation of the cardiovascular and respiratory
systems to extrauterine life. The normal transition of the respiratory tract
involves opening closed alveoli and absorption of fluid from the airway,
accomplished by a combination of breathing efforts, expiration against
a closed glottis (‘‘grunting’’), and a change in sodium flux across the
respiratory membrane from net secretion to net absorption [1–5]. The
transition from fetal to neonatal circulatory patterns requires resolution of
the pulmonary hypertension present in the fetus, normally shunting blood
flow through the lower resistance ductus arteriosus in the fetal state, so as to
direct cardiac output to the pulmonary vasculature for participation in gas
exchange. This change is achieved by the opening of alveoli, decreasing
airway resistance, and providing radial support for pulmonary vessels,
functional closure of the ductus arteriosus, and increased oxygen tension in
the lung, which reverses pulmonary vasoconstriction mediated by hypoxia
[6,7]. Pulmonary tree vasodilators (prostacyclin and nitric oxide [NO]) and
vasoconstrictors (endothelin-1 [ET-1] and leukotrienes) play apparently
well-coordinated but as yet not fully elucidated roles. In the normal newborn, this change is smooth and rapid. These critical events are undermined
by factors like inadequate lung development, surfactant deficiency (primary
or secondary), viral or bacterial infection, placental abnormalities, in utero
hypoxia, and meconium aspiration.
Spontaneous breathing should begin in the neonate within 1 minute of
birth; many foals attempt to breathe as their thorax clears the pelvic canal
E-mail address: [email protected]
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doi:10.1016/S0749-0739(02)00064-0
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P.A. Wilkins / Vet Clin Equine 19 (2003) 19–33
[8,9]. During the first hour of life, the respiratory rate of a healthy foal can
be as high as 80 breaths per minute but should decrease to 30 to 40 breaths
per minute within a few hours. Similarly, the heart rate of a healthy
newborn foal should have a regular rhythm and be at least 60 beats
per minute at the first minute [8,9]. A continuous murmur can usually be
ausculted over the left side of the heart, although its loudness may vary with
position. This murmur is thought to be associated with some shunting
through the ductus arteriosus. Variable systolic murmurs thought to be flow
murmurs may be ausculted during the first week of life [10]. Murmurs that
persist beyond the first week of life in an otherwise healthy foal should
be more thoroughly investigated, as should any murmur associated with
persistent hypoxia. Auscultation of the thorax shortly after birth should
reveal a cacophony of sounds as airways are opened and fluid is cleared.
End-expiratory crackles are consistently heard in the dependent lung during
and after lateral recumbency. It is not unusual for a normal newborn foal to
appear slightly cyanotic during this initial adaptation period, but this should
resolve within minutes of birth. The equine fetus, like all fetuses, exists in
a moderately hypoxic environment, but the equine fetus has a greater PO2,
around 50 mm Hg [11]. Because the fetus is well adapted to low oxygen
tensions, cyanosis is rarely present in newborn foals once adaption occurs,
even those with low oxygen tensions. Although in many species, the fetal
blood oxygen affinity is greater than that of the maternal blood, in the
equine fetus, the oxygen affinity of its hemoglobin is only approximately
2 mm Hg greater than that of the maternal blood because of decreased levels
of 2,3 diphosphoglycerate (DPG) compared with other species [12]. The
result is enhanced oxygen unloading in the equine fetus compared with other
fetuses. DPG concentration increases after birth in the foal and reaches
mature levels by 3 to 5 days of age. The presence of significant cyanosis
that persists should prompt the clinician to evaluate the foal for cardiac anomalies resulting in significant right-to-left shunting or separated
circulations, such as transposition of the great vessels.
The chest wall of the foal is compliant, facilitating passage through the
pelvic canal during parturition. This compliance requires that the foal
actively participate in both inspiration and expiration, with several potential
consequences. First, restriction of the thorax or the abdomen can result in
impaired ventilation. This can easily occur when restraining a foal and may
result in spuriously abnormal arterial blood gas values. Second, foals with
primary pulmonary parenchymal disease resulting in poorly compliant lungs
develop paradoxic chest wall motion, with the thorax moving inward during inspiration [13–16]. The work of breathing can be greatly increased,
resulting in respiratory failure because of respiratory muscle fatigue. A foal
in which a previously abnormal respiratory rate and pattern seem to improve suddenly may in fact be in greater respiratory difficulty because of
fatigue. A reduction in respiratory rate or an abnormal breathing pattern
can be observed in premature/dysmature foals or foals subjected to
P.A. Wilkins / Vet Clin Equine 19 (2003) 19–33
21
peripartum hypoxia/asphyxia. Foals attempting to maintain an adequate
lung volume expire against a partially closed glottis, called the ‘‘Valsalva
maneuver,’’ producing an audible ‘‘grunt.’’
Hypoxemia in the neonate
Arterial blood gas determinations are the most sensitive indicator of
respiratory function readily available to the clinician. The most easily accessed arteries for sampling are the metatarsal arteries and the brachial/
decubital arteries. Portable arterial/venous blood gas analyzers are now
making arterial blood gas analysis more practical for use in the field, and the
technique is no longer reserved for large institutions or referral practices. It
is veritably impossible to manage an equine neonate with severe respiratory
disease without knowledge of arterial blood gas parameters. Pulse oximetry
is being more commonly employed in some institutions and referral centers,
but these monitors only measure oxygen saturation of hemoglobin. Desaturation can occur rapidly in critically ill neonates. The utility of these
monitors in the foal, although holding promise, has yet to be clearly
demonstrated, particularly in cases with poor peripheral perfusion [17]. The
most common abnormalities recognized with arterial blood gas analysis are
hypoxemia with normo- or hypocapnia and hypoxemia with hypercapnia.
There are five primary means by which hypoxemia develops in any animal
with a heart and lungs. For our purposes, hypoxemia is defined as decreased
PaO2, and hypoxia is defined as decreased oxygen concentration at the level
of the tissue, with or without hypoxemia. Hypoxia results from hypoxemia,
decreased perfusion of the tissue bed in question, or decreased oxygencarrying capacity of the blood as a result of anemia or hemoglobin alteration.
Hypoxemia develops from (1) a low concentration of oxygen in the
inspired air (FIO2), such as that seen at high altitude or in an error in mixing
ventilator gas; (2) hypoventilation; (3) ventilation/perfusion mismatch;
(4) diffusion limitation; or (5) intrapulmonary or intracardiac right-to-left
shunting of blood. Hypoxemia is not an uncommon finding in neonates,
particularly those with respiratory disease, but it must be evaluated in terms
of the current age of the foal, difficulty in getting the sample, and the foal’s
position [18–22]. Normal arterial blood gas parameters for varying times
postpartum for foals in lateral recumbency are presented in Table 1. The
normal foal has a small shunt fraction (10%) that persists for the first few
days of life and contributes slightly to a blunted response to breathing 100%
oxygen when compared with the adult. If the lung is significantly involved in
the underlying pathologic changes, such as with severe pneumonia, acute
lung injury (ALI), or acute respiratory distress syndrome (ARDS), increased
PaCO2 may be present, representing respiratory failure [23].
Hypoxemia is usually treated with intranasal humidified oxygen insufflation at a rate of 4 to 10 L/min. Hypercapnia is not a simple matter to
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P.A. Wilkins / Vet Clin Equine 19 (2003) 19–33
Table 1
Normal arterial blood gas values for foals
Postnatal age
pH
2 minutes
15 minutes
30 minutes
60 minutes
2 hours
4 hours
12 hours
24 hours
48 hours
4 days
7.31
7.32
7.35
7.36
7.36
7.35
7.36
7.39
7.37
7.40
PaCO2 (mm Hg)
0.02
0.03
0.01
0.01
0.01
0.02
0.02
0.01
0.01
0.01
54.1
50.4
51.5
47.3
47.7
45.0
44.3
45.5
46.1
45.8
2.0
2.7
1.5
2.2
1.7
1.9
1.2
1.5
1.1
1.1
PaO2 (mm Hg)
56.4
57.5
57.0
60.9
66.5
75.7
73.5
67.6
74.9
81.2
2.3
3.6
1.8
2.7
2.3
4.9
3.0
4.4
3.3
3.1
Reported values are assumed not to be temperature corrected. All foals were term and
sampled in lateral recumbency. Values are mean SEM.
Data from Stewart JH, Rose RJ, Barko AM. Respiratory studies in foals from birth to seven
days old. Equine Vet J 1984;16:323.
treat. Most foals presented in acute respiratory distress are in the acute
stages of respiratory failure, but chronic adaptation begins to occur within
6 to 12 hours and is maximal in 3 to 5 days. An increase in bicarbonate should
be noted, particularly if the acidosis is primarily respiratory in origin. The
administration of intravenous sodium bicarbonate to correct acidosis is to
be undertaken with caution in these cases, because carbon dioxide retention
may only be increased. Also, 1 mEq of sodium is administered with each
milliequivalent of bicarbonate; hypernatremia has been seen in foals treated
exuberantly with sodium bicarbonate. Foals with hypercapnia of several
days’ duration may also develop a blunted respiratory drive to increased
carbon dioxide. In these cases, oxygen administration, although essential
to treat hypoxemia, may further depress ventilation and further decrease
pH. This is caused by a loss of hypoxic drive secondary to oxygen therapy.
These foals should be considered candidates for mechanical ventilation if
the PaCO2 is above 70 mm Hg or is contributing to the poor condition of the
foal, such as causing significant pH changes. If hypercapnia is a result of
central depression of ventilation, which is frequently seen in foals with
perinatal asphyxial syndrome or neonatal encephalopathy, caffeine can be
administered (10-mg/kg loading dose, then 2.5 mg/kg as needed) per rectum
or orally in foals with normal gastrointestinal function. Continuous rate
infusions of doxapram hydrochloride (Dopram) (400-mg total dose at
0.05 mg/kg/min) is used by some clinicians in these cases. If these therapies
fail, mechanical ventilation should be considered. Mechanical ventilation of
foals with central respiratory depression is quite rewarding and may only be
necessary for a few hours to days. The reader should be aware that foals
with primary metabolic alkalosis have compensatory respiratory acidosis.
Treatment of hypercapnia is not necessary in these cases because it is in
P.A. Wilkins / Vet Clin Equine 19 (2003) 19–33
23
response to the metabolic condition. These foals do not respond to
caffeine, and they should not be mechanically ventilated if this is the only
disorder present.
Persistent pulmonary hypertension of the newborn
Persistent pulmonary hypertension (PPH) is also known as reversion to
fetal circulation or persistent fetal circulation, and its genesis lies in the
failure of the fetus to successfully make the respiratory and cardiac transition to extrauterine life or reversion of the newborn to fetal circulatory
patterns in response to hypoxia and/or acidosis. Differentiating this problem
from other causes of hypoxemia in the newborn, such as sepsis or bacterial
or viral pneumonia, or from congenital cardiac malformation requires some
investigation, and multiple serial arterial blood gas analysis is necessary to
confirm suspicion of this problem. The condition should be suspected in any
neonate with hypercapnic hypoxemia that persists and worsens; these foals
are in hypoxemic respiratory failure. The fetal circulatory pattern with
pulmonary hypertension and right-to-left shunting of blood through the
patent foramen ovale and ductus arteriosus is maintained in these cases.
Pulmonary vascular resistance falls at delivery to approximately 10% of
fetal values, whereas pulmonary blood flow increases accordingly [24]. Early
in the postnatal period, these two changes balance each other out and mean
pulmonary and systolic pressure remains increased for several hours. The
direct effects of lung expansion and increasing alveolar oxygen tension
probably provide the initial stimulus for pulmonary arteriolar dilation. This
is partly caused by direct physical effects, but vasoactive substances are
released in response to physical forces associated with ventilation, for
example, prostacyclin [24]. Other vasoactive mediators thought to play a
role in regulating pulmonary arteriolar tone include NO, prostaglandins D2 and E2, bradykinin, histamine, ET-1, angiotensin II, and atrial
natriuretic peptide (ANP). The increase in alveolar and arterial oxygen
tensions at birth is required for completion of resolution of pulmonary
hypertension. It is thought that much of this is mediated by NO, with
evidence for this being the parallel increase during gestation of the pulmonary vasodilation response to hyperoxia and the increase in NO synthesis
[25]. Inhibition of NO synthesis does not eliminate the initial decrease in
pulmonary artery resistance occurring as a result of opening of the airways,
however [26].
It is when these mechanisms fail that PPH is recognized. Right-to-left
shunting within the lungs and through patent fetal conduits occurs. This can
be secondary to many factors, including asphyxia and meconium aspiration,
but in many cases, the precipitating trigger is unknown. Inappropriately
decreased levels of vasodilators (NO) and inappropriately increased levels of
vasoconstrictors (ET-1) are being currently examined as potential mechanisms. Chronic in utero hypoxia and/or acidosis may result in hypertrophy
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P.A. Wilkins / Vet Clin Equine 19 (2003) 19–33
of the pulmonary arteriolar smooth muscle [27]. In these cases, reversal of
PPH can be extremely difficult and is not achieved rapidly.
Treatment of PPH is two-pronged: abolishment of hypoxia and
correction of the acidosis, because both abnormalities only bolster the fetal
circulatory pattern. Initial therapy is provision of intranasal oxygen (INO2) at
a rate of 8 to 10 L/min. Some foals respond to this therapy and establish
neonatal circulatory patterns within a few hours. Failure to improve or
worsening of hypoxemic respiratory failure after provision of INO2 should
prompt intubation and mechanical ventilation with 100% oxygen. This
serves two purposes, one diagnostic and one therapeutic. Ventilation with
100% oxygen may resolve PPH; if intrapulmonary shunt and altered ventilation/perfusion relations are causing the hypoxic respiratory failure,
PaO2 should exceed 100 mm Hg under these conditions. Failure to improve
PaO2 suggests PPH or large right-to-left extrapulmonary shunt as a result of
congenital cardiac anomaly. The vasodilators prostacyclin and tolazoline
(an a-blocking vasodilator) cause pulmonary vasodilation in human infants
with PPH, but the effects on oxygenation are variable, and the side effects
(tachycardia and severe systemic hypotension) are unacceptable [28].
Recognition of NO as a potent dilator of pulmonary vessels has led to a
significant step forward in the treatment of these patients, because inhaled
NO dilates vessels in ventilated portions of the lung while having minimal
effects on the systemic circulation [29]. Based on evidence presently available, it seems reasonable to use inhaled NO at an initial concentration of
approximately 20 ppm in the ventilatory gas for term and near-term foals
with hypoxic respiratory failure and PPH that fails to respond to mechanical
ventilation using 100% oxygen alone [29,30]. We have used this approach in
our clinic, administering a range of 5 to 40 ppm NO, with success.
Meconium aspiration syndrome
Meconium aspiration is thought to occur secondary to acute pre- or
intrapartum asphyxiation associated with severe fetal distress, subsequent
passage of meconium by the fetus, and aspiration of meconium during fetal
gasping efforts. Neonates with meconium aspiration syndrome (MAS) have
marked surfactant dysfunction. Airways and alveoli of affected neonates
contain meconium, inflammatory cells, inflammatory mediators, edema
fluid, protein, and other debris. MAS can present clinically with different
degrees of severity, ranging from a mild form of respiratory compromise to
severe forms that may result in perinatal death despite respiratory management, up to and including mechanical ventilation and extracorporeal
membrane oxygenation (ECMO). Advances in our knowledge concerning
MAS have revealed that many cases of severe MAS in human beings may
not be causally related to the aspiration of meconium but are caused by
other pathologic processes occurring in utero, primarily chronic asphyxia
P.A. Wilkins / Vet Clin Equine 19 (2003) 19–33
25
and infection [31]. Current treatments being investigated in the management
of human infants with MAS include surfactant administration, surfactant
administration combined with partial liquid ventilation, and surfactant
lavage [32,33].
Bacterial pneumonia
In the neonate, bacterial pneumonia is usually secondary to sepsis or
aspiration during sucking. Foals with sepsis can also develop ALI or ARDS
as part of the systemic response to sepsis, and this is frequently a contributor
to the demise of foals in septic shock (Fig. 1). Diagnosis of bacterial
pneumonia is supported by transtracheal aspirate culture and cytology, but
blood culture can aid in early identification of the causative organism and
allow for early institution of directed antimicrobial therapy. Radiography and thoracic ultrasonography are useful additional diagnostic aids.
Auscultation and percussion of the thorax should be performed, and any
noted abnormalities should be addressed; however, thoracic auscultation
can be surprisingly unremarkable in some foals with significant pulmonary
disease. The isolated organisms from this type of bacterial pneumonia of the
neonate reflect those commonly isolated in sepsis in newborns, including Escherichia coli, Klebsiella spp, and Actinobacillus equuli [34,35]. Initial
antimicrobial treatment should be a broad-spectrum bactericidal combination, such as penicillin and amikacin. Antimicrobial therapy can then be
altered based on culture and sensitivity patterns of the isolated pathogens
(Table 2) [35]. Serial white blood cell counts, differentials, and determinations of plasma fibrinogen concentration are useful for monitoring
Fig. 1. Thoracic radiograph of neonatal foal with aspiration pneumonia. Note alveolar pattern
overlying and obscuring the caudal cardiac silhouette.
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P.A. Wilkins / Vet Clin Equine 19 (2003) 19–33
Table 2
Antimicrobial drug doses
Drug
Dose
Route
Frequency
Amikacin sulfate
Ampicillin trihydrate
Sodium ampicillin
Amoxicillin trihydrate
Cefotaxime
Cefuroxime (Ceftin)
Cephalexin
Ceftiofur (Naxcel)
Enrofloxacin
Erythromycin stearate
Erythromycin lactobionate
Gentamicin sulfate
Imipenem
Metronidazole
25–30 mg/kg
20 mg/kg
50–100 mg/kg
20–30 mg/kg
50–100 mg/kg
30 mg/kg/d
10 mg/kg
2–10 mg/kg
2.5–10 mg/kg
20–30 mg/kg
5 mg/kg
6.6–8.8 mg/kg
10–20 mg/kg
15 mg/kg
25 mg/kg
20,000–50,000 U/kg
IV
PO
IV
PO
IV
PO
PO
IV
IV, PO
PO
IV
IV
IV
PO, PR
IV
SID
TID
QID
TID
QID
BID–TID
QID
BID–QID
SID
TID–QID
Q 4–6 hours
SID
QID
QID
BID
QID
5 mg/kg
50–100 mg/kg
50–100 mg/kg
30 mg/kg
8 mg/kg loading, 4 mg/kg
PO
IV
IV
PO
PO
BID
QID
QID
BID
BID
Potassium penicillin
Sodium penicillin
Rifampin
Ticarcillin
Ticarcillin þ clavulanic acid (Timentin)
Trimethoprim potentiated sulfa
Fluconazole
Abbreviations: BID, two times daily; IV, intravenous; PO, per os; PR, per rectum; Q, every;
QID, four times daily; SID, once daily; TID, three times daily.
Data from Palmer JE. Neonatal drug doses. 2000.
response to therapy. The distribution of bacterial pneumonia secondary to
sepsis tends to be generalized throughout the lung.
A second frequent cause of bacterial pneumonia in the neonate is
aspiration caused by poor suck reflex or dysphagia associated with perinatal
asphyxial syndrome (PAS), sepsis, or weakness (Fig. 2). Multiple organisms
may be isolated from transtracheal aspirates with this form of pneumonia.
The distribution tends to be cranioventral. Care must be taken to ensure that
aspiration is not iatrogenic in foals being bottle-fed. Foals being bottle-fed
should be positioned in sternal recumbency or standing. Additionally, foals
with nasoesophageal tubes in place for feeding should be kept in sternal
recumbency or standing for 5 minutes after standing to prevent passive
esophageal regurgitation after changes in positioning of the head and neck.
Some foals with neonatal encephalopathy and poor suck reflexes do not
protect their airway well and aspirate their own saliva even when not allowed to suck from their dam or a bottle. Auscultation over the trachea
while the foal is sucking helps to identify occult aspiration in sucking foals.
Occult aspiration pneumonia should be suspected in any critically ill neonate
that is being bottle-fed or is sucking on its own and has unexplained fever,
fails to gain weight, or has a persistently increased fibrinogen concentration.
P.A. Wilkins / Vet Clin Equine 19 (2003) 19–33
27
Fig. 2. Thoracic radiograph of neonatal foal with viral pneumonia. Note alveolar pattern
distributed throughout entire lung field with prominent air bronchograms. This pattern can also
be seen with acute respiratory distress syndrome after overwhelming sepsis and in the surfactant
deficiency seen in extremely premature foals, usually those less than 280 days’ gestation.
Older foals develop bacterial pneumonia, frequently secondary to an
earlier viral infection [36]. Bacterial pneumonia of weanlings and older foals
is discussed in depth in other articles, but a few comments specific to the
neonate are presented here. Auscultation and percussion of the thorax
should be performed, but the results may not closely correlate with the severity of the disease. The most commonly isolated bacterial organism in
this primary foal pneumonia is Streptococcus zooepidemicus, and it may be
isolated alone or as a component of a mixed infection [34,36,37]. A transtracheal aspirate for culture and cytology is recommended, because mixed
gram-positive and gram-negative infections are common and antimicrobial
susceptibility patterns can be unpredictable. The obtained aspirate should
be split and submitted for bacterial culture, virus isolation, and cytology.
Additional diagnostics include radiography, ultrasonography, and serial
determination of white blood cell counts (with differential) and blood
fibrinogen concentrations. Treatment is by administration of appropriate
antimicrobial therapy. Some foals may benefit from nebulization with saline
or other local products. Ascarid larval migration through the lung can
mimic bacterial pneumonia [38]. In these cases, the foal may not respond to
antimicrobial therapy and should be dewormed with ivermectin. Deworming of the mare within 1 month of parturition and frequent deworming of
the foal prevent ascarid migration pneumonia in most cases.
Viral pneumonia
The most commonly identified causes of viral pneumonia in foals are
equine herpesvirus (EHV) 1 and 4, equine influenza, and equine arteritis
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P.A. Wilkins / Vet Clin Equine 19 (2003) 19–33
virus (EVA). EHV-1 is probably the most clinically important, but outbreaks of EVA in neonates have occurred and are devastating [39–45].
Adenovirus is reported sporadically and as a problem in Arabian foals with
severe combined immunodeficiency disease (SCID) [46–48].
In the neonate, infection with EHV-1 or EVA is almost uniformly fatal,
and antemortem diagnosis is difficult, even once an outbreak on a particular
farm is identified. Several factors seem to be common to foals with EHV-1,
including icterus, leukopenia, neutropenia, and petechial hemorrhage, but
these problems are also identified in foals with severe sepsis [45,49,50]. The
antiviral drug acyclovir (10–16 mg/kg administered orally or per rectum four
to five times per day) has been used in cases of EHV-1 in neonates, with
some evidence of efficacy in mildly affected foals or foals affected after birth
[49]. If viral pneumonia is a possibility, blood and tracheal aspirates should
be collected at presentation for bacterial and virus isolation. The lungs of
foals with EHV-1 or EVA are noncompliant, and pulmonary edema may be
present. Mechanical ventilation of these cases may prolong life, but death
is generally inevitable because of the magnitude of damage to the lungs.
Foals that are suspected of having either EHV-1 or EVA should be isolated
because they are generally shedding large quantities of virus and pose
a threat to other neonates and any pregnant mares. Foals with EVA are
generally born to seronegative mares, and treatment with intravenous
plasma with a high titer against EVA may prove beneficial, because passive
immunity seems to have a large role in protection against this disease in
neonates [40,51].
Older foals and weanlings may be affected by EHV. The disease is usually
mild, although a fatal pulmonary vasculotropic form of the disease has been
recently described in young horses [52,53]. Clinical signs of disease are
indistinguishable from influenza and include a dry cough, fever, and serous
to mucopurulent nasal discharge, particularly if secondary bacterial infection occurs. Rhinitis, pharyngitis, and tracheitis are all potentially present, and the disease is not limited to the upper respiratory tract. Treatment
of these foals is primarily supportive. Foals may also become infected with
EHV-2. The predominant clinical signs are fever and lymphoid hyperplasia
with pharyngitis [54,55]. Diagnosis is by virus isolation.
Other causes of respiratory signs in foals
Rib fractures have been recognized in 3% to 5% of all neonatal foals and
can be associated with respiratory distress [56]. Potential complications of
rib fractures include fatal myocardial puncture, hemothorax, and pneumothorax. Rib fractures are frequently found during physical examination by
palpation of the ribs or by auscultation over the fracture sites. Diagnosis can
be confirmed by radiographic and ultrasonographic evaluation. Usually,
multiple ribs are affected on one side of the chest. Specific treatment is
generally unnecessary, but direct pressure on the thorax should be avoided
P.A. Wilkins / Vet Clin Equine 19 (2003) 19–33
29
in all cases. Some specific patients may benefit from surgical stabilization of
some fractures, particularly those fractures overlying the heart.
Pneumothorax can occur spontaneously or secondary to excessive
positive-pressure ventilation [57]. It can also occur secondary to tracheostomy surgery or trauma. Any foal being mechanically ventilated that suddenly presents with respiratory distress and hypoxemia should be evaluated
for pneumothorax. Diagnosis is by auscultation and percussion of the
thorax but can be confirmed with radiographic and ultrasonographic evaluation of the thorax. Needle aspiration of air from the pleural space also
confirms the diagnosis. Treatment is required in cases where clinical signs
are moderate to severe and/or progressive and involves closed suction of the
pleural space. Subcutaneous emphysema can complicate treatment of this
problem.
Idiopathic or transient tachypnea has been observed in Clydesdale,
Thoroughbred, and Arabian foals primarily. In human infants, transient
tachypnea can be related to delayed absorption of fluid from the lung,
perhaps caused by immature sodium channels [58]. In foals, it is generally
seen when environmental conditions are warm and humid and is thought
to result from immature or dysfunctional thermoregulatory mechanisms.
Clinical signs are primarily an increased respiratory rate and rectal temperature. Signs develop within a few days of birth and may persist for
several weeks. Treatment involves moving the foal to a cooler environment,
body clipping, and provision of cool water or alcohol baths. These foals are
frequently treated with broad-spectrum antimicrobial drugs until infectious
pneumonia can be ruled out.
Bronchointerstitial pneumonia and acute respiratory distress have been
described in older foals and seem to be distinct entities from the ARDS seen
in neonatal foals in association with sepsis (Fig. 4) [59]. The underlying
etiology has not been identified, but the genesis is probably multifactorial,
with several potential pathogens having roles. Affected foals present with
acute respiratory distress with marked tachypnea, dyspnea, nostril flare, and
increased inspiratory and expiratory effort. Auscultation reveals a cacophony of abnormal sounds, including crackles and polyphonic wheezes in
all lung fields. Loud bronchial sounds are heard over central airways, and
bronchovesicular sounds are lost peripherally. Affected foals are cyanotic,
febrile, and unwilling to move or eat. Foals may be found acutely dead.
Laboratory abnormalities include leukocytosis, hyperfibrinogenemia, and
hypoxemia with hypercapnic acidosis. Foals can be severely dehydrated and
have coagulation changes consistent with disseminated intravascular coagulation. Hypoxic injury to other organs, primarily the kidneys and liver,
can be recognized. Chest radiographs reveal a prominent interstitial pattern
overlying a bronchoalveolar pattern that is diffusely distributed throughout
the lung (Fig. 3). This syndrome is a respiratory emergency. Treatment is
broad based and includes administration of oxygen, nonsteroidal antiinflammatory agents, broad-spectrum antimicrobial therapy, nebulization,
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P.A. Wilkins / Vet Clin Equine 19 (2003) 19–33
Fig. 3. Thoracic radiograph of neonatal foal with pneumothorax secondary to multiple rib
fractures and lung laceration. Note pleural line in caudal dorsal lung field.
judicious intravenous fluid therapy, nutritional support, and corticosteroid
therapy. Hyperthermia needs to be managed. Corticosteroid therapy seems
to have been life-saving in most of the reported surviving foals. Because
this syndrome is associated with high environmental temperatures in some
areas, prevention involves control of ambient temperatures, not transporting foals during hot weather, and keeping foals out direct sun on hot days,
particularly foals being treated with erythromycin for suspected or confirmed Rhodococcus equi infection [60].
Fig. 4. Thoracic radiograph of neonatal foal with acute respiratory distress syndrome. Note
diffusely distributed patchy interstitial pattern and enlarged pulmonary artery suggestive of
pulmonary hypertension.
P.A. Wilkins / Vet Clin Equine 19 (2003) 19–33
31
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