Diagnosing and treating respiratory emergencies (Proceedings)

The first and most important thing is to recognize the horse with a respiratory emergency.   They are often anxious, they may have noisy, rapid breathing, and an abnormal, elbows out stance may give us a clue that they find it painful to breath.  If you look at their mucus membranes, the color is often pale or bluish, and, altogether, we infer dyspnea.  I say that we infer this, because dyspnea means the sensation of having difficulty breathing. 

Three things cause respiratory distress: hypoxemia, hypercapnia and high work of breathing.  Hypoxemia is diagnosed by the presence of an SpO2 of less htan 90% or an ABG analysis that reveals a PaO2 of less than 60 mm Hg.  ABG analysis is essential for proper interpretation of cuases of hypoxemia, Pulse oximetry and capnography are also useful in diagnosis.  Hypoxemia with hypercapnia DEFINES hypoventilation as the underlying cause. 

Hypoxemia with normocapnia implies diffusion impairment, V/Q mismatch, or shunt as underlying causes.  Response to oxygen supplementation usually allows differentiation between VQ mismatch and shunting.  Typically, the patient with a VQ mismatch will demonstrate marked response (i.e.improved PaO2) with supplemental oxygen, whereas the patient with shunt only minimally shows improvement in PaO2, if at all.  By definition, refractory hypoxemia is seen with < 10 mmHg increase with at least 40% O2 administration. 

Hypoxemia is most important.  It takes quite a long time to die of the type of hypercapnia that comes with respiratory embarrassment or failure. 

High work of breathing is probably the biggest contributor to dyspnea.  High work of breathing may become unsustainable, in which case the animal will eventually die.  Obstructive lesions cause high work of breathing.  The animal will usually work to maintain normoxia and normocapnea for a limited amount of time before exhaustion and failure. 

With these thoughts in mind, the first goal in treating a respiratory emergency is to establish adequate oxygenation.  Establishment of normal blood CO2 is secondary only.  This is why in any code, the routine is to take care of Airway, Breathing, and then Circulation. 

Let's think about the tools that you have for a respiratory emergency in the field – they are usually history, physical examination, and auscultation.  Ancillary tools, that you may only have access to in a referral hospital, are an O2 sat monitor, ABGs, capnograph, radiographs, ultrasound, and lung function testing. 

Physical examination, history, and auscultation often take place more or less simultaneously.  You must quickly decide if the site is extra-thoracic or intrathoracic.  Typical signs of extra-thoracic disease are: stridor, stertor, facial swelling and edema, pharyngeal swelling, and nasal discharge or deformity.  Upper airway obstructions often require an emergency tracheostomy BEFORE definitive diagnosis.  In order to make this determination, you should auscult from the nose to the chest. 

Inspiratory stridor is usually loudest at the site of the obstruction.  Facial swelling and edema can be due to anaphylaxis, EVA, purpura hemorrhagica, trauma, or snake bite.  Pharyngeal swelling can be from strangles, clostridial infections, or guttural pouch tympany.  Facial and nasal deformities are often slowly progressing, and can be due to sinusitis, granuloma, ethmoid hematoma, neoplasia, maxillary cysts, fungal granuloma, and head trauma. These animals often have malodorous breath.

What are the signs that we associate with intrathoracic disorders?  They include expiratory or mixed inspiratory and expiratory distress, absence of lung sounds, and adventitious lung sounds.  Intrathoracic obstructive disorders usually cause high airway resistance (think RAO or heaves).  Intrathoracic restrictive disorders usually cause low compliance (think of pneumonia, pulmonary fibrosis, pleuritis). What do you see on physical examination? Expiratory respiratory embarrassment usually reflects high airway resistance due to airway obstruction. 

Often, and exaggerated inspiratory effort will also be present.  Absence of lung sounds usually is seen with restrictive diseases with inadequate expansion of lung fields.  Penumothorax is associated with dullness especially in the dorsal lung fields, whereas pleural effusion is usually associate with dullness in the ventral lung fields.  Cardiac sounds will often be louder, and you may be able to percuss a fluid line.  Ultrasound is very helpful. 

How to approach the airways:

Clear the airways if possible.  It is not easy in horses, because their mouths do not open very much! Think about how much easier it is to intubate a dog than most of our long-nosed large animal species.  After clearing anything possible, the choices will then be to intubate or perform a tracheostomy.  Once you're familiar with the technique, tracheotomy is often the quickest.  It is best to do a tracheotomy before it is a true emergency.  This is usually preceded by striderous, stertorous, or labored breathing referable to the upper airway.  To perform a tracheotomy, you should use sedation unless the horse has actually collapsed. 

Scrub and clip your site in the cranial 2/3rds of the neck unless it is truly emergent – in that case, just cut.  The trachea is cleanly palpable in this area where the sternothyrohyoid muscle is thing.  Infiltrate with carbocaine if there is time.  Make a long incision – at least 10 cm – otherwise you'll be working in a hole.  Try to keep the head straight.  Have a clear view of the trachea – use fingers or scissors to quickly bluntly dissect , and then make a stab incision into the trachea.  Cut the annular ligament no more than halfway.  Insert the tracheostomy tube, and ideally, don't leave it in longer then 48 hours.  

Nasotracheal intubation is quite easy in a sedated horse, but can be very difficult in a frantic horse.  Try to do it, therefore, before it has become a matter of life or death.  If you have the equipment, it is a good idea to oxygenate with a mask for 5 minutes beforehand.  Sedate!! It makes everything easier.  It is best to have 14,16, 18, and 20 mm nasotracheal tubes.  After sedating the horse, lubricate the ventral meatus of the nostril and the nasotracheal tube. 

Insert as for an NG tube.  Feel for a swallow.  Then, extend the head as straight as possible.  Rotate the tube slightly while inserting into the trachea.  To check, you can feel for  ‘two tubes'.  You can also feel air flowing, but this can be deceiving – it may be gas from the stomach.  The best test is to use the capnograph.  Orotracheal intubation is best if the horse is already down.  You must use a mouth speculum – you can use a roll of half-used duct tape in an emergency, or a pre-made spec made of PVC piping. 

You may need to do pleurocentesis if the horse has a pneumothorax or pleuropneumonia.  Remember that the horse's mediastinum is fenestrated, so there is the chance of inducing a penumothorax if the horse hasn't already got one.  First, as for the tracheostomy, sedate.  It is easiest to locate your site with ultrasound.  Then, scrub and clip, and do a block, as pleurocentesis is painful.  Once you insert the chest tube, you must place either a Heimlich valve or you can make a valve using half of a condom.  If a horse presents with pneumothorax, first, place a bandage over the point of entry wound to prevent further ingress of air, then do a DORSAL pleurocentesis and aspirate the air. 

Horses may acquire pulmonary edema secondary to upper airway obstruction, from electrocution, or from ARDS.  The most important thing is to remove the inciting cause, whether this be sepsis or electrocution.  Furosemide remains the mainstay of treatment (1.0 mg/kg IV), however, it is important to remember that this will be much less effective in the face of leaky capillaries, e.g. ARDS. 

How to administer emergency oxygen:

The first question is, how much oxygen does the horse need? Well, to start with, minute ventilation is RV X RR.  In the normal horse, where TV = 8, and RR = 12, this is close to 100 liters per minute.  Horses in respiratory distress may need 250 lpm or more.  The best that we can achieve with an E tank and nasal canulae is ~ 10 – 20 lpm.  Here is where a tracheostomy may help – even without upper airway obstruction, the nose and neck of a horse represent an astounding amount of dead space and increased work of breathing.  Bypassing this may decrease your need for oxygen. 

That said, and E tank has enough psi to inflate the lungs (2200 psi) – so be careful, as you can rupture the lung.  A demand valve is a good thing – it can deliver a flow rate of ~ 200 lpm.  If you're in a real jam, you can intubate with an NG tube, attach the tube to the regulator, and turn the regulator on and off to ventilate.  BUT, and this is an important but, an E tank only contains 660 liters of oxygen – so use it sparingly, and carry extras.  If your demand valve is set at 200 lpm, you only have 3 minutes or so to work with. 

Emergency treatment of bronchospasm:

Luckily, even horses in a heaves crisis rarely die, unlike human asthmatics.  That said, the horse with bronchospasm has very high work of breathing, and will become exhausted.  You can treat with inhaled beta-two agonists, such as albuterol, or with parasympatholytic inhaled drugs, such as Atravent.  Atropine is a very effective drug at 0.01 mg/kg IV, however, you risk inducing ileus and tachycardia.  Clenbuterol, an oral B2-sympathomimetic, is NOT a rescue drug, as it is too slow.  Dexamethasone likewise is not a rescue drug, but is very useful in decreasing inflammation. 

Horses in anaphylactic shock need epinephrine.  It is the most important rescue drug in this situation.  Corticosteroids may not influence the course of the disease, and are of much lower priority. You can give 1 ml/100 lbs of body weight of the 1:1000.  It is rapidly metabolized (< 10 minutes) and there is a dose-related response for alpha, B1, and B2 receptors.  Of course, you must also consider the airway and oxygen. 

In summary, hypoxemia kills much, much faster than hypercapnia.  Establish an airway and deliver oxygen.  You don't need to know an exact diagnosis at first.  Alleviate the hypoxemia, THEN diagnose.