Respiratory Distress

Respiratory distress is a clinical feature. The signs of labored or rapid breathing, flared nostrils and increased breathing efforts are not specific for a single cause. Remember that non pulmonary causes can be fever, neurological disease, pain, anxiety, excitement, severe anemia or drug induced hyperthermia.

I. Acute Respiratory Distress Syndrome (ARDS)

ARDS is a poorly understood condition with the common feature of impairment of the lung to adequately exchange gas at the alveolar level, which produces hypoxemia and carbon dioxide retention. Diffuse atelectasis and reduced lung compliance are features of the syndrome. Foals that experience asphyxia, deprivation of placental blood, or are premature or small for gestational age are at increased risk [1]. Surfactant deficiency has not been documented in term foals as a component of the syndrome.

II. Diagnosis

1. Clinical Findings

1. Flared nostrils and rapid breathing with chest wall collapsing inward during inspiration.
2. Poor entry of air into lungs on auscultation. Bronchovesicular sounds are diminished compared to the degree of effort, crackles may be audible.
3. Expiratory grunting and cyanosis may be present.

2. Blood gas abnormalities: PaO2 <50 mmHg and PaCO2 >60 mmHg without metabolic alkalosis [1]
3. Chest radiographs in foals with respiratory distress do not resemble the ground glass or reticulated pattern seen in human infants with ARDS. Air bronchogram indicating diffuse atelectasis can occasionally be seen but a generalized increase in interstitial density is the more common finding.
4. Ultrasonography reveals diffuse wide comet tails in most cases of ARDS (See Chapter 52).

III. Concurrent or Predisposing Factors

Occurs in three forms:

1. Any factor that leads to a decrease in efficiency of respiration or an increased demand can produce fatigue and progressive atelectasis [1].

1. Pneumonia; viral, bacterial.
2. Pneumocystis carinii [2]
3. Increased vascular permeability.
4. Pulmonary hypertension.
5. Fractured ribs.

2. Prematurity

1. Prematurity may lead to ARDS.
2. Whether or not ARDS develops in a premature foal, is not necessarily predictable based on gestational age alone.

1. Foals that are born at 300-320 day gestation or that have experienced in-utero stress (twins or other conditions) may have hastened pulmonary maturation and have mature lungs.

3. Amniotic fluid analysis for surfactant (Lecithin/sphingomyelin (L/S) ratio and phosphatidylglycerol (PG)) has not been able to predict lung maturity in foals [3].

1. Preliminary evidence does suggest L/S ratio of 2.2 and 2+ PG indicative of some degree of lung maturity in foals.

4. Corticosteroids to mare may hasten lung maturity.
5. Preventive measures are limited to avoiding elective early induction of labor. Avoid induction entirely unless absolutely essential.

3. Premature placental separation, dystocia or cesarean section, maternal medication, placentitis, in utero infection.
4. Sepsis or other conditions which cause a foal to be in prolonged recumbency can produce atelectasis.
5. Reversion to fetal circulation with high pulmonary arterial pressure and a shunting of blood through the ductus arteriosus away from the lung has been documented by the author by cardiac catheterization in a premature foal with ARDS and diagnosed via ultrasonography in a foal [4].
6. Meconium Aspiration - foals may have meconium staining on eyes, face and skin.

1. Occurs due to defecation associated with pre or intrapartum asphyxia.
2. Causes surfactant inactivation and inflammation.
3. Treatment is suctioning of airways, oxygen insufflation, mechanical ventilation, surfactant administration.

IV. Management - General Principles

The object is to support the respiratory system and entire patient while correcting undesirable conditions or allowing spontaneous resolution to occur. Sternal position to improve oxygenation efficiency is extremely important.

1. Airway Management

1. Coupage, airway suction as needed and early ambulation (Chapter 66).

2. Oxygen Therapy

1. Warm, humidified, O2 at sufficient rates to maintain PaO2 in lateral recumbency of 80-100 mmHg (Chapter 13).
2. Useful in foals with low O2 and normal or low PaCO2 (<60 mmHg).
3. Hypoventilation as evidenced by elevated PaCO2 may require ventilation therapy

3. Vascular Catheters

1. An indwelling arterial catheter for monitoring of blood gases is helpful.
2. Sites used have all been somewhat difficult to maintain but have included facial, brachial, femoral, and dorsal metatarsal artery.
3. Swan-Ganz thermodilution catheters to determine cardiac output, mixed venous blood gases, and pressures within pulmonary artery, atrium and right ventricle have been used by the author in management in conjunction with a cardiac output computer [5].

4. Acidosis

1. Metabolic acidosis with a base deficit of > 6 mEq/L requires evaluation of causes including shock, hypovolemia, hypoglycemia, hypothermia, infection, renal disease and sequelae of asphyxia.
2. If the arterial pH is less than 7.25 with a base deficiency of 6, correction is via volume expansion, glucose infusion if hypoglycemic, or plasma or whole blood. If refractory to volume expansion, use I.V. administration of diluted sodium bicarbonate if ventilation is adequate. Bicarbonate is converted to CO2 which must be capable of being eliminated by the lung.
3. Bicarbonate amounts are calculated by base deficit x body weight in kg x 0.4, due to the larger extracellular fluid of newborn foals.
4. Administer bicarbonate slowly – use an isotonic solution (See Fluid therapy, Chapter 22). Monitor arterial blood gas for evidence of CO2 increases.
5. A pure respiratory acidosis in the range of 7.2 - 7.3 may be tolerable. When the pH falls below 7.2 due to respiratory acidosis, assisted ventilation is indicated.

1. If assisted ventilation not possible, consider CRI of Doxapram.

5. Sudden Deterioration in Condition

1. Check mechanical portions of oxygen delivery system.

1. O2 amounts and pressure in tanks.
2. Obstruction of endotracheal tube by secretions.
3. Inadvertent positioning of the endotracheal tube into the esophagus or too far distal in an airway into a bronchus.

2. Check metabolic causes such as hypoglycemia and acidosis.

6. Respiratory Failure Management [1]

1. Reasons to intervene with pulmonary support techniques other than supplemental oxygen are inability to maintain a PaO2>52 mmHg in lateral recumbency and/or steadily rising PaCO2 above 60 mmHg (See Chapter 13).
2. See Section on nasotracheal intubation and positive pressure ventilation (Chapter 67).
3. Be prepared and make a commitment for the significant degree of effort to manage these patients.
4. Bronchopulmonary dysplasia has developed following treatment for ARDS in foals [6].

7. Differential Diagnosis - Transient Tachypnea Syndrome

1. Resembles respiratory distress
2. Has been seen in foals with significantly elevated respiratory rates of 60-120/min.
3. May have elevated body temperature but foals are alert, nurse, and not cyanotic or pale.
4. Differentiate by normal CBC, clinical chemistry, blood gases and acid base and chest x-ray.

1. Even though foals are hyperventilating, PaCO2 is normal which means foals are "panting".

5. Condition is self limited over 1-2 weeks. Clipping body hair in warm climates and keep in a neutral thermal environment. Avoiding higher environmental temperatures is helpful.
6. Cause is unknown but believed associated with immature or delayed development of central brain regulation of ventilation and thermoregulation.