Initial Triage and Resuscitation of Small Animal Emergency Patients

ByAndrew Linklater, DVM, DACVECC, BluePearl Specialty + Emergency Pet Hospital;Annie Chih, DVM, DACVECC, Animal Medical Center of Seattle
Reviewed/Revised Nov 2020

Triage is the art of assigning priority to emergency patients and their problems based on rapid assessment of historical and physical parameters ( see Table: Parameters to Evaluate During Triage). Several historical or observed problems warrant transfer of the animal to the treatment area regardless of physical findings, and they are listed below; all members of the veterinary medical staff should be able to recognize these common presenting complaints so that rapid (STAT) evaluation by a veterinarian can occur; these conditions may either require rapid intervention or can potentially lead to rapid decompensation:

  • allergic reaction

  • bleeding

  • cardiopulmonary arrest

  • collapse, not moving, unable to walk, loss of consciousness or severe alteration in mental state

  • difficulty urinating or inability to urinate in male cats

  • dystocia

  • heat stroke

  • hypothermia

  • pale, weak (anemia)

  • profuse vomiting and/or diarrhea

  • prolapsed or eviscerated organs

  • respiratory difficulty

  • seizures

  • significant pain

  • snake bite

  • swollen abdomen or nonproductive retching (gastric dilatation and volvulus)

  • toxin ingestion

  • trauma or open wounds

Table

Airway, breathing, and circulation are evaluated sequentially, followed by examination for sources of hemorrhage, and determination of the level of consciousness and level of pain.

The most common reasons for an animal in catastrophic distress include:

Airway—airway obstruction or disruption

Breathing—cyanosis from tension pneumothorax, alveolar flooding (edema, blood, or inflammatory fluid), severe bronchoconstriction with air trapping or brain-stem pathology affecting ventilation

Circulation— shock (decreased perfusion), cardiopulmonary arrest, extreme bradyarrhythmias or tachyarrhythmias, cardiac tamponade, and acute intravascular volume loss usually due to internal or external hemorrhage.

Airway

Life-threatening airway pathology (catastrophic or severe) includes complete large airway obstruction and partial obstruction of the large and small airways.

Diagnosis of Airway Disorders in Animal Emergency Patients

  • Rapid assessment to establish the cause of an airway disorder and begin treatment is essential

Clinical evaluation and intervention for a patient with airway disease must occur rapidly. Animals with complete large airway obstruction are unconscious and apneic. Partial large airway obstruction causes noisy breathing (stridor or stertor), heard without the aid of a stethoscope. Cyanosis and anxiety are often present with loud referred airway sounds heard throughout the thorax on auscultation. Compromise of the extrathoracic airway (nasal passages, pharynx, larynx, or cervical trachea) causes inspiratory stridor; compromise of the intrathoracic trachea or bronchi causes expiratory stridor. Stertor is most common with pharyngeal disease.

Possible causes of large airway pathology include:

  • foreign body

  • edema or hemorrhage

  • laryngeal paralysis/paresis

  • tracheal collapse or obstruction, including trauma

  • brachycephalic airway syndrome (elongated soft palate, stenotic nares, hypoplastic trachea, and everted laryngeal saccules)

  • aspiration of saliva or stomach contents

  • neoplasia

  • pharyngeal neoplasia

Animals with severe small airway obstruction have labored breathing with an expiratory push of the diaphragm, cyanosis, and anxiety. Auscultation reveals high-pitched wheezes throughout the lung field. In severe life-threatening situations, the animal is cyanotic, open-mouth breathing, collapsed, and asphyxiating. Common causes include anaphylactic reactions; asthma (cats); and bronchial obstruction from edema, mucus, exudates, or foreign material.

Treatment for Airway Disorders in Animal Emergency Patients

  • Complete airway obstruction requires immediate treatment to re-establish air flow and deliver oxygen.

  • Oxygen should also be provided for animals with partial airway obstruction or small airway obstructive disease.

Breathing

Diagnosis of Breathing Disorders in Emergency Treatment of Animals

  • Changes in respiratory rate, posture, and obviously labored breathing are followed by changes in mucous membrane color.

Treatment of Breathing Disorders in Animal Emergency Patients

Circulation

Diagnosis of Circulatory Disorders in Animal Emergency Patients

Animals with circulatory compromise can have alterations in the following physical perfusion parameters:( see Table: Parameters to Evaluate During Triage

  • heart rate

  • mucous membrane color

  • capillary refill time

  • rectal temperature

  • pulse quality

  • level of consciousness

Careful auscultation of the heart for a murmur, gallop, arrhythmia, or muffled heart sounds and of the lungs for evidence of fluid is important to help identify heart failure as a cause of poor perfusion. Measurement of arterial blood pressure, central venous pressure, central venous PaO2, and serum lactate provide objective data for reaching resuscitation endpoints and monitoring trends of change after resuscitation. A complete history and physical examination will help identify the reason for shock.

In the early compensatory stages of hypovolemic shock in dogs, there is tachycardia, pink to red mucous membranes, rapid CRT, and bounding pulses; the animal is most often alert and responsive. Animals with a significant amount of pain or anxiety may appear to be in compensatory shock, so administration of appropriate analgesics is warranted along with time for the animal to acclimate to the environment. Tachycardia is often the first and only sign, so persistent tachycardia must be considered a sign of altered perfusion. This stage is rarely identified in cats.

As the pathology progresses, dogs begin to have pale mucous membranes, prolonged CRT, weak pulses, tachycardia, and a decreased level of responsiveness—the classic signs of the middle or early decompensatory stage of shock. Cats have gray mucous membranes, slow CRT, weak or absent pulses, hypothermia, and a normal or low heart rate. As shock approaches the terminal stages, the heart rate slows in both dogs and cats, and animals begin to lose consciousness. Clinical signs in this terminal stage include heart failure, pulmonary edema, severe hypotension, oliguria, and abnormal respiratory patterns. Cardiopulmonary arrest is a common sequela.

Treatment of Circulatory Disorders in Animal Emergency Patients

The therapeutic goal with shock is to deliver oxygen and substrate to the tissues. This requires a heart that effectively pumps blood and adequate hemoglobin, intravascular volume, vascular tone and patency, as well as sufficient oxygen and substrate for cellular metabolism. General guidelines for treatment of hypovolemic and distributive shock are described below, but modifications may be needed for specific animals or disease processes. ( See also Fluid Therapy in Animals.)

Oxygen Supplementation

Oxygen (at least 40%–60% inspired concentration) should be administered by flow-by technique, mask, hood, nasal cannula, endotracheal tube, or transtracheal catheter.

Hemostasis

Control of ongoing hemorrhage is essential for stabilization and often required before restoration of circulation. The animal must be carefully and thoroughly examined for any evidence of external hemorrhage. Direct pressure should be immediately placed over the bleeding skin site, and bleeding arteries clamped. When blood slowly oozes from a skin wound, a compression bandage should be placed. If more aggressive hemostasis is required, a blood pressure (pneumatic) cuff or tourniquet can be temporarily placed until coagulation occurs or surgical intervention is used to stop the bleeding. Tourniquets should not remain in place for >10 minutes because they compromise normal blood flow required for healing.

Intrathoracic or abdominal hemorrhage may be difficult to detect and may be exacerbated when blood pressure and circulation are restored. The focused abdominal and thoracic sonography for trauma (AFAST, TFAST) technique may be used to rapidly identify free abdominal or thoracic fluid. In the abdomen, the probe is focused on the ventral midline caudal to the xiphoid, over the urinary bladder, and on the right and left dependent flank regions; for the thorax, the probe is used to examine a minimum of 4 points of each hemithorax. A four-quadrant abdominocentesis can be performed if ultrasound is not immediately available. The TFAST may be used to identify pleural fluid as well.

Coagulopathy should be ruled out or treated before invasive procedures. PCV of thoracic or abdominal fluid the same or higher than that of peripheral blood confirms hemorrhage. Significant volumes of cavitary hemorrhage may be collected in sterile, empty IV bags or blood transfusion bags for autologous blood transfusion, if necessary.

Ongoing abdominal hemorrhage is initially managed with damage control techniques to avoid a lethal triad of acidosis, hypothermia, and hypocoagulation. Damage control resuscitation includes small volume fluid resuscitation to low-normal endpoints (see below) and early use of blood products during resuscitation. Damage control surgery is a limited abdominal procedure to arrest hemorrhage, including the use of intra-abdominal packing and minimizing further contamination without definitive surgical exploration to minimize anesthesia time. Definitive care is delayed until the patient is stable. For patients with hemorrhage due to ruptured neoplasia, organ or mass removal is often necessary. Abdominal and hindlimb counterpressure may be used in patients when surgical exploration is delayed or is not possible.

Ongoing intrathoracic hemorrhage should be managed with thoracocentesis or a thoracostomy tube to evacuate the blood and to allow measurement of the volume lost. Exploration of the thorax may be required for definitive hemostasis.

Intravascular Volume Replacement

Intravenous or intraosseous catheters are used, with multiple catheters placed for rapid, large-volume infusion in larger patients. Isotonic crystalloids can be administered by low-volume (10–15 mL/kg) or high-volume (20–30 mL/kg) boluses, each delivered over 10–15 minutes until desired endpoints of resuscitation are reached (see below). The concurrent use of colloids (blood products or hydroxyethyl starch, 2–10 mL/kg bolus) can reduce the amount of crystalloid required, rapidly expand the intravascular space with a smaller volume of fluid infused, and reduce the amount of fluid extravasating into the interstitial spaces of vital organs (eg, lung, brain). Hypertonic saline (7%) may be used in patients that are not dehydrated nor at risk for hypernatremia at a dosage of 4 mL/kg.

Small volume resuscitation is used with low-normal endpoints (normal perfusion parameters with a mean arterial pressure of 60–80 mmHg) is used to avoid volume overload or hypertension and is ideal for animals with head injury, pulmonary edema or contusions, abdominal or intrathoracic hemorrhage, heart disease, and all cats in hypovolemic shock. Large volume resuscitation with high-normal endpoints (normal perfusion parameters with a mean arterial pressure of 80–100 mmHg) is used in patients with GI disease, sepsis, or systemic vasodilation. The least amount of crystalloids and colloids possible are used to obtain and maintain a systolic blood pressure of 90 mmHg, restore a normal heart rate, and improve CRT and pulses. For an in-depth explanation, see Fluid Therapy.

Pain Control

Analgesia is provided as indicated during initial fluid resuscitation for optimal cardiovascular response and relief of anxiety. Ideally, pure mu opioids should be used because they have the benefit of being reversible. Opioids are administered systemically, and local anesthetics can be infiltrated into the affected area along with other medications such as ketamine, lidocaine, anti-inflammatory medications, and others, depending on the underlying disease. Many patients may require multimodal analgesia using a combination of medications, routes, and methods of administration. (Also see Pain Assessment and Management.)

Warming

Animals in shock should be slowly warmed during fluid resuscitation until rectal temperatures are >98°F (36.5°C). This is best accomplished by increasing the environmental temperature using warm air blowers, warm water blankets, and IV fluid warmers. Hot water bottles and hot rice bags should be avoided due to potential burn risk. Gastric, peritoneal, or urinary lavage may be needed for severe hypothermia. Surface warming is instituted only after initial volume resuscitation has provided enough intravascular volume to offset the peripheral vasodilation. Care must be taken in animals with cardiogenic shock or pericardial disease to avoid excessive peripheral vasodilation, because this may exacerbate a relative hypovolemia (due to decreased cardiac output).

Corticosteroids

Corticosteroids are administered when a deficiency is suspected (ie, hypoadrenocorticism, critical illness–related corticosteroid insufficiency). High-dose steroid administration has not been proved to reduce mortality in hypovolemic, septic, or cardiogenic shock and has been associated with increased morbidity, so it is not recommended.

Cardiovascular Support

Pharmacologic agents (positive inotropes, systemic vasopressors) can be used when fluid infusion has adequately replaced intravascular volume but fails to restore blood pressure and perfusion, or when poor cardiac contractility is thought to contribute to hypotension.

A positive inotropic agent can be administered to increase cardiac contractility in diseases such as sepsis and dilated cardiomyopathy (eg, dobutamine at 2–20 mg/kg/minute, initial dose 2–5 mcg/kg/minute, and the dosage titrated for optimal cardiac output). Stroma-free hemoglobin (dogs 5 mL/kg; cats 1–3 mL per cat, slowly) can be administered, and repeated as indicated, for its colloid effect as well as its mild vasopressor effect; it is particularly useful in animals with concurrent anemia, but it is not currently available in the USA. Pressor agents delivered as an IV constant-rate infusion such as dopamine (5–20 mcg/kg/minute), norepinephrine (0.05–2 mcg/kg/minute), epinephrine, phenylephrine, or vasopressin (extralabel, 1–4 mU/kg/minute) are other options to support blood pressure; they should be delivered in the smallest dosage needed to maintain arterial systolic pressure >90 mmHg.

The blood flow to the kidneys and GI tract, as well as other organs, may have been significantly impaired during shock. Urine output, heart rate, blood pressure, ECG, pulse intensity, and mucous membrane color should be closely monitored, because further vasoconstriction can worsen organ blood flow and function. If organ function declines or if arrhythmias become a problem, the vasopressor should be stopped.

Hindlimb and Abdominal Binding

Whenongoing abdominal hemorrhage is suspected from trauma, hindlimb and abdominal counterpressure can improve perfusion. This procedure compresses the arteries and arterioles within the bound regions, increasing regional vascular resistance and producing abdominal tamponade, thereby effectively slowing or arresting hemorrhage and redirecting blood flow from the venous capacitance vessels in the caudal half of the body to the more central (core) circulation. It may be used when damage control surgery must be delayed or is not possible.

Hindlimb and abdominal counterpressure can be performed by first placing a small rolled towel or rolled cotton between the hindlimbs and along the ventral midline of the abdomen. This prevents the wrap from impairing ventilation or fracturing the spleen or liver. If time permits, a urinary catheter is placed. The hind limbs and abdomen are then firmly wrapped with padded bandage material or towels, beginning at the toes of the hind limb and moving cranially toward the xiphoid, taking care not to impede respiration. The bandage should be secured with tape or stretch bandage material wrapped in a spiral pattern starting caudally and moving cranially. Abdominal binding should be avoided in cases of intrathoracic or intracranial hemorrhage.

Once perfusion has stabilized for several hours, the wrap is removed slowly by sections (releasing one section every 15 minutes), starting at the most cranial portion and moving caudally. Any signs of decompensation warrant rapid rebinding of the region last unwrapped. If the patient is going to surgery, unwrapping, aseptic preparation, and entry into the abdomen must occur quickly.

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