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Primary Survey (Triage) and Resuscitation in Animals

By

Andrew Linklater

, DVM, DACVECC, Lakeshore Veterinary Specialists, Glendale, Wisconsin;


Annie Chih

, DVM, DACVECC, Animal Medical Center of Seattle, Shoreline, WA

Last full review/revision Nov 2020 | Content last modified Nov 2020
Topic Resources

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

  • 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
icon

Parameters to Evaluate During Triage

Parameter

Evaluation

Significance

Mucous membrane color

Pink

Normal PCV and adequate perfusion

Pale or white

Anemia or shock

Cyanotic or muddy

Severe hypoxemia or decompensatory shock

Yellow

Increased serum bilirubin due to hepatic disease or hemolysis

Capillary refill time

1–2 seconds

Normal perfusion and rapidity with which capillaries refill with blood

>2 seconds

Poor perfusion or peripheral vasoconstriction

<1 second

Hyperdynamic states; could be associated with fever, heat stroke, distributive shock, or early compensatory stage of hypovolemic shock

Heart rate

70–120 bpm (small dogs)

60–120 bpm (large dogs)

120–200 bpm (cats)

Normal heart rates; indicate that at least one component of cardiac output is normal

Bradycardia

Decreased cardiac output and subsequent poor perfusion; cats in particular develop bradycardia (<120 bpm) in shock; an irregular, slow heart beat can be associated with imminent cardiac arrest, severe arrhythmias, or metabolic derangements ( hyperkalemia, hypocalcemia, etc.)

Tachycardia (dogs >180 bpm, cats >220 bpm)

Compromised diastolic filling; sinus tachycardia often results from hypovolemic shock, pain, or primary cardiac disease; tachycardia that is irregular or associated with pulse deficits usually indicates an arrhythmia, and an ECG is indicated

Pulse rate and quality

Strong and synchronous with each heart beat

Normal; both femoral and digital pulses should be palpated

Irregular

Usually indicative of a cardiac arrhythmia

Bounding

Hyperdynamic (compensatory) state of shock; indicates an increase in pulse pressure (ie, an increase in systolic pressure, decrease in diastolic pressure, or both)

Weak or absent

Decreased cardiac output (including cardiopulmonary arrest), peripheral vasoconstriction, decreased pulse pressure, or thrombosis

Level of consciousness

Alert and responsive to surroundings

Normal overall neurologic and metabolic state

Depressed or obtunded (less responsive to visual and tactile stimuli, sleepy appearance but still arousable)

Can be caused by any illness or decreased perfusion; may be mild, moderate, or severe

Stupor (arousable only with painful stimuli)

Severe neurologic or metabolic derangements, including toxin ingestion

Comatose (unarousable with any stimuli) or seizures (usually associated with whole body convulsions, salivation, facial tremors, possibly involuntary urination and defecation)

Abnormal cerebral electrical activity from primary neurologic disease or secondary to metabolic derangements seen in diseases such as diabetes, hepatic encephalopathy, hypoglycemia, or toxin exposure; accurate history or prior health problems, current medications, and possible toxin exposure important

Level of pain

Vocalization, changes in behavior (avoidance, aggression), or physical changes (tachycardia, dilated pupils, etc)

Clinical signs can be similar to those seen in compensatory stage of shock; pain delays healing and must be treated.

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

  • 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

  • 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.

Establishment of an Airway in Complete Airway Obstruction

Unconscious, apneic animals require immediate tracheal intubation. The clinician should be practiced in orotracheal intubation of animals in dorsal, lateral, and sternal recumbency. If an obstruction is present, it must be immediately relieved (with suction, manual removal, or the Heimlich maneuver) or bypassed via emergency tracheotomy. Once an airway is established, confirmed, and secured, ventilation is initiated with 100% oxygen via a bag-valve-mask. Should auscultation during ventilation detect absent or muffled lung sounds indicative of pleural fluid or air, immediate thoracocentesis is warranted. Heart sounds and pulses are checked and, when absent, cardiopulmonary resuscitation is initiated.

Treatment for Partial Large Airway Obstruction

With partial large airway obstruction, flow-by oxygen is delivered through oxygen tubing at a high flow rate aimed at the open, panting mouth until an airway is secured or, if appropriate, a transtracheal or nasotracheal oxygen line is placed. Heavy sedation using a narcotic or tranquilizer (eg, butorphanol 0.2–0.4 mg/kg with or without acepromazine 0.01–0.05 mg/kg) may be used to relieve anxiety. When tracheal intubation is necessary, general anesthesia should be induced using rapid-acting IV anesthetics, as noted below. During or immediately before intubation, the ability of the laryngeal cartilages to abduct during inspiration should be assessed and a full oropharyngeal examination performed when time allows. A tracheotomy is necessary when pharyngeal, laryngeal, or tracheal pathology prevents orotracheal intubation or when prolonged intubation is anticipated.

A transtracheal catheter can be used to provide oxygen support during stabilization. When the airway pathology lies within the thoracic cavity, airway patency must be established down to the bifurcation of the trachea. Once the airway is established, it should be secured with a tie and inflation of the cuff mechanism to a maximum of 20 mmHg.

Once the airway is secured, intubation should be confirmed with at least two of the following methods:

  • palpation of the tube within the trachea (only one "tube" palpated in cervical region)

  • bilateral auscultation of the lungs

  • visualization of chest wall movement with manual ventilation

  • visualization of the tube entering the airway

  • placement of end-tidal CO2 monitor (normal is 35–45 mmHg)

  • radiographs

Options for IV medications for rapid sequence induction/intubation include:

  • etomidate (0.5–3 mg/kg)

  • ketamine (5–20 mg/kg) in combination with a benzodiazepine (ie, diazepam, 0.2–0.4 mg/kg)

  • propofol (8 mg/kg, to effect)

  • alfaxolone (1–2 mg/kg)

Clinicians should choose medications that they are familiar with.

Therapy for Small Airway Obstructive Disease

Cyanosis from small airway obstructive disease is treated by providing oxygen by flow-by, hood, or nasal cannula and sedation with a narcotic/tranquilizer combination. Epinephrine is given for its bronchodilatory effects both in anaphylaxis (0.01–0.02 mg/kg, IV) and in life-threatening asthma (0.02 mg/kg, IM). Corticosteroids (prednisone sodium succinate, 15 mg/kg, IV, or dexamethasone sodium phosphate, 0.1–0.2 mg/kg, IM or IV) are given for allergic bronchitis, asthma, or severe swelling of the larynx or pharyngeal tissues. Other bronchodilators, such as aminophylline or terbutaline, are given IM, or albuterol can be given by nebulization in the case of an animal in crisis. Diphenhydramine (1–2 mg/kg, IM) is given for allergic reactions. Also see the calculator on this page for various emergency drug dosages for dogs and cats.

Breathing

Diagnosis

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

Respiratory Patterns

Compromised breathing manifests with an increased respiratory rate and effort, immediately followed by a change in the respiratory pattern. Clinical evaluation should first focus on the distant and close physical examination before imaging and other diagnostic tests. Postural changes (orthopnea) follow; dogs stand with the elbows abducted and the back arched or high on the rear haunches, with the head and neck extended, whereas cats may sit crouched on all four limbs with the sternum slightly elevated. Obvious labored, open-mouth breathing, and changes in mucous membrane color (gray, dark pink, and/or blue [cyanosis]) develop last and indicate significant loss of pulmonary function and impending pulmonary arrest.

Location of Pathology

The location of the pathology—pleural space or parenchymal disease—can be determined at presentation by careful observation of the breathing pattern and auscultation of the thorax. This will direct therapeutic efforts. Stressful diagnostic procedures such as radiographs can lead to rapid decompensation.

Pleural space disease causes asynchronous breathing. The chest expands on inspiration as the abdomen is pulled inward, then the chest moves inward on expiration as the abdomen expands. In cats, breathing is slower and more deliberate than in dogs. The respiratory pattern is the same whether air, fluid, or abdominal contents are in the pleural space. Thoracic auscultation reveals muffled lung sounds over the affected regions. Grunting during expiration may be present.

Lung parenchymal disease causes quiet or loud breathing, with the chest and abdominal wall moving in the same direction (synchronous). Inspiration and expiration are equally labored unless concurrent small-airway edema or constriction adds an expiratory push. Thoracic auscultation reveals louder-than-normal lung sounds in early phases. As disease progresses, harsh lung sounds with moist crackles and rales are heard over the affected lungs. Pulmonary edema, when secondary to cardiac disease, is often accompanied by a murmur, gallop, or arrhythmia and mild hypothermia. Note that a lack of murmur in a cat does not rule out underlying cardiac disease.

Differential diagnoses for pulmonary parenchymal disease include:

  • pneumonia (viral, parasitic, fungal, bacterial, aspiration)

  • acute respiratory distress syndrome or acute lung injury; inflammatory fluid secondary to systemic illness

  • congestive heart failure (cardiogenic pulmonary edema)

  • pulmonary contusions or hemorrhage (trauma or coagulopathy)

  • noncardiogenic pulmonary edema (secondary to seizures, electrocution or acute airway obstruction: choking or near-drowning) or re-expansion pulmonary edema

  • lung lobe torsion

  • neoplasia

  • pulmonary hypertension

  • thermal or chemical injury to the lung

Differential diagnoses for respiratory disease look-alikes include:

  • central and peripheral neurologic disease

  • severe acidemia

  • anemia or altered hemoglobin

  • nasal occlusion

  • hyperthermia

  • opioid administration

  • cardiac disease

  • diaphragmatic hernia

  • orofacial disease (dental malocclusion or mandibular dislocation or fracture)

  • other systemic illness (hyperadrenocorticism, hypoglycemia, hypocalcemia, hyperthyroidism)

  • pain, stress, or anxiety

Imaging

Thoracic radiography should be performed only when the animal is able to tolerate the procedure. Radiographs can help differentiate many of these diseases; however, imaging should not delay therapy. Some animals may be more tolerant of ultrasonography. The thoracic-focused assessment with sonography (TFAST) technique may be used to identify pleural fluid or air and signs of "wet lung," examining both hemithoraces at a minimum of 4 points. A pneumothorax may be present when the "glide sign" is absent; this is a linear movement noted between the visceral and parietal pleura and requires practice to identify. Examination with CT often provides additional information.

Treatment

Treatment with Oxygen

Oxygen is administered immediately via flow-by, mask, hood, nasally, or oxygen cage techniques:

  • Longterm continuous supplemental oxygen is best provided by a nasal oxygen catheter.

  • The intranasal oxygen catheter is placed after topical anesthetic has been instilled into the nostril where the tube is to be inserted.

  • Humidified nasal oxygen flow rates of 50–100 mL/kg/minute deliver 40%–60% inspired oxygen while allowing the animal to be examined and the underlying disease treated.

  • Nasopharyngeal or nasotracheal catheters or bilateral nasal cannulas may provide higher percentages of inspired oxygen.

  • Patients placed in oxygen cages must have the following monitored: environmental O2 and CO2 levels, humidity, and temperature. It is common for any of these parameters to be significantly altered and be detrimental to patients in an oxygen cage.

  • Sedation with a narcotic/tranquilizer combination (butorphanol 0.2–0.4 mg/kg, IV or IM, with or without acepromazine, 0.05 mg/kg, IV or IM) can relieve struggling and anxiety.

  • If cyanosis and decompensation persist or work of breathing is profound, with concern for respiratory fatigue, intubation and positive-pressure manual ventilation or mechanical ventilation with 100% oxygen is necessary.

Treatment for Pleural Space Disease

Catastrophic pleural space disease with rapid cardiovascular decompensation, absent lung sounds throughout the thorax, and a barrel-shaped thorax suggests tension pneumothorax. A routine thoracocentesis is often inadequate for these animals, so an intercostal incision or placement of a large-bore catheter is necessary: the area is quickly clipped free of hair and prepared in an aseptic fashion, lidocaine is injected for local anesthesia, a small skin incision is made between ribs (at the seventh to eighth intercostal space), and hemostats are used to enter the pleural space, relieving the tension. This allows cardiovascular filling and lung re-expansion. The open pneumothorax is then managed by placing an indwelling thoracostomy tube and closing the intercostal incision.

Pleural air or fluid without tension pneumothorax should be drained by thoracocentesis. Sedation is often administered as noted above, along with a local lidocaine block. The intended site is clipped and aseptically prepared. If fluid is expected, ultrasound guidance can be used to identify a pocket of fluid. Alternatively, the needle can be inserted ventrally between the sternum and costochondral junction, cranial or caudal to the heart. When air is to be recovered, the needle is inserted into the dorsal half of the thorax, above the costochondral junction.

Usually, an 18- or 20-gauge needle is slowly inserted perpendicular to the thoracic wall, on the cranial aspect of the rib at the selected location. An evacuation apparatus (IV extension set, 3-way stopcock, and syringe) is attached, and aspiration begins as soon as the pleural space is entered. The needle is then directed so that it lies within the fluid/air or against the parietal pleura. This prevents laceration of the lung by the needle as the lung re-expands. In animals in which the pleural space cannot be emptied (eg, due to tension or continuous pneumothorax, ongoing hemorrhage) or when repeated chest taps are required within minutes to hours, an indwelling thoracostomy tube should be placed.

Treatment for Lung Parenchymal Disease

Lung parenchymal disease is primarily treated using oxygen supplementation and sedation to relieve anxiety, as noted above; specific therapy is directed at the underlying cause. After initial stabilization, further diagnostic procedures (eg, thoracic imaging and echocardiography) help determine the cause and specific therapy. Sampling of the lungs (direct lung aspirate, tracheal wash, etc) will help determine infectious or inflammatory etiologies but may be contraindicated in patients with severe respiratory compromise.

Cardiogenic pulmonary edema is usually associated with a gallop, murmur, arrhythmia, and/or mild hypothermia and responds well to furosemide administration (1–4 mg/kg, IV, every 1–2 hours or delivered as a constant-rate infusion of 1–2 mg/kg/hour) until improvement in respiratory rate or effort improves. Cardiogenic pulmonary edema may also respond to venodilation from nitroglycerin ointment (1/4 in. for cats and 1/2 in. for larger dogs) applied topically to a shaved area of the abdomen, inguinal region, or directly to a mucous membrane; severely affected animals with normal blood pressure may benefit from a balanced vasodilator (nitroprusside, 0.5–10 mcg/kg/minute or hydralazine, 0.2–0.5 mg/kg), These medications are tapered up slowly while monitoring blood pressure continuously to keep the mean arterial pressure >85 mmHg.

Animals with proteinaceous fluid (such as occurs with noncardiogenic pulmonary edema, respiratory distress syndrome, pneumonia, hemorrhage, etc) will not respond to diuretic therapy. Treatment should be directed at the underlying cause (antimicrobials for infectious pneumonia, correction of coagulopathy for hemorrhage, etc).

If oxygen supplementation does not maintain PaO2 >60 mmHg (pulse oximetry or SpO2 >90%), if PaCO2 ≥60 mmHg, if there is moderate to severe increases in work of breathing despite oxygen therapy, or respiratory failure is imminent, then intubation and manual (with a manual bag-valve-mask) or mechanical positive-pressure ventilation with 100% oxygen is required while the underlying disease is being treated. Suction should be available to help clear the airway. Physical maneuvers may help to clear the lungs or airway for fulminant disease: elevated or postural pulmonary parenchymal evacuation (EPPE) can be performed with two or more people elevating the pet vertically, head down, while guarding the endotracheal tube. The thoracic cavity is manually compressed to assist airway and lung fluid drainage. Manual ventilation with 100% oxygen and suction of the airway should be performed between EPPE efforts. Occasionally, surgical procedures may be necessary to alleviate hypoxemia (example, lobectomy for consolidation or lung lobe torsion or repair of a diaphragmatic hernia).

Circulation

Diagnosis

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

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, initially at 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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