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Emergency Medical / Critical Care Elisa M. Mazzaferro, MS, DVM, PhD, Diplomate ACVECC Wheat Ridge, Colorado Cardiopulmonary Cerebral Resuscitation Cessation of effective circulating blood flow and ventilation constitutes cardiopulmonary arrest. Cardiopulmonary arrest is typically associated with loss of consciousness, collapse, lack of a palpable pulse, pale or cyanotic mucous membranes, lack of effective respirations, and lack of measurable blood pressure. At the time of cardiac arrest, a wide variety of cardiac dysrhythmias may be present on electrocardiogram. The dysrhythmias that occur in our canine and feline patients at the time of arrest dramatically differ from dysrhythmias that result in cardiac arrest in human. Only in rare cases can one anticipate that cardiopulmonary arrest is about to occur. Most cases that require cardiopulmonary cerebral resuscitation (CPCR) unfortunately present to you after cardiovascular collapse and pulmonary arrest have already occurred. Nonetheless, prompt recognition and rapid treatment are paramount in reestablishing both cerebral and coronary blood flow in order to have the greatest chance at a positive outcome. In one retrospective study that investigated the outcome of cardiopulmonary arrest and CPCR in 304 dogs and 95 cats, overall outcome was less than 5% survival to discharge from hospital. Of animals successfully resuscitated, 68% of dogs and 38% of cats re-arrested within 4 hours of the initial episode. A slightly more favorable outcome may occur if cardiopulmonary arrest occurs during an anesthetic episode, most likely because the animals already have vascular access and are intubated receiving 100% inspired oxygen. Although overall outcome may not be very favorable, considerations must be made when asking clients whether they want CPCR to be performed at all in the event of an arrest. In many cases, unless the underlying cause of the arrest can successfully be treated at the time of the event (i.e. hyperkalemia secondary to urethral obstruction, tension pneumothorax secondary to trauma), the outcome is not likely to be favorable. Ethically, unless a client requests "Do Not Resuscitate" orders, attempts at resuscitation must be performed unless otherwise directed. Cardiopulmonary-cerebral resuscitation refers to re-establishing blood flow to the cerebral and coronary systems in the event of cardiopulmonary arrest. The process by which oxygenated blood flow is re-established involves performing manual cardiac and thoracic compressions and manual ventilation until spontaneous circulation and ventilation occurs. There are typically three phases to CPCR. Phase 1 consists of Basic Life Support (BLS). Basic life support involves manual cardiac and thoracic compression to re-establish circulation, and intubation with supplemental oxygen and artificial ventilation. Controversy exists whether to perform the "ABC's" of CPCR versus "CAB's" in CPCR. ABCs refers to "Airway", "Breathing" and "Circulation". Cardiac compressions begin after the patient is intubated and manual ventilation has begun. More recent evidence in a dog model of ventricular fibrillation has demonstrated that the oxygen content of blood in circulation is often adequate to start delivering oxygen to tissues and the coronary sinus if cardiac compression is started. Thus, more recent techniques implement the use of "CABs" of CPR, that is, starting manual external cardiac compressions before endotracheal intubation and ventilation. Additionally, external compression of the thoracic cage causes the animal to artificially breathe. In performing the CABs of CPCR, external thoracic compression occurs usually simultaneously while a second person is intubating the patient and establishing an airway. After successful intubation and securing a patent airway, supplemental 100% oxygen is delivered, and cardiac compressions are continued. Compressions should be performed at 80 - 120 beats per minute. A simultaneous synchronized artificial breath should be performed for every chest compression. This method further increases intrathoracic pressure, generating more effective blood flow upon thoracic relaxation. Peak airway pressure should never be greater than 20 cm H2O, to prevent iatrogenic barotrauma. Effective circulation in CPCR occurs by two mechanisms. The first is called the cardiac pump theory, in which direct compression of the heart from apex to base results in forward flow of blood. Unless internal cardiac massage occurs, in most cases the animal is too large for effective direct compression of the heart to occur. Even with open-chest CPCR and direct cardiac massage, cardiac output achieved is usually only 50% of normal. In animals larger than 7 kg, the "thoracic pump theory" is more effective in causing forward flow of blood. External pressure on the thoracic cage creates increased intrathoracic pressure such that the change in pressure in between external compressions causes forward blood flow through passive mechanisms. Additionally, recent evidence has shown some improvement in circulation with synchronous thoracic compression with synchronous ventilation. Ventilating at the same time as external thoracic compression causes a greater change in intrathoracic pressure, and greater passive filling of great vessels upon relaxation. Generally, cardiac compressions, either direct or external, should be performed at a rate of 80 - 120 compressions per minute. The thorax should be compressed 25 - 30% of its circumference to generate the most effective change in intrathoracic pressure. Compression and thus artificial systole should be the same length as artificial diastole or relaxation. Artificial ventilation should be synchronized at the same rate. Patients should be positioned in dorsal recumbancy if greater than 20 kg, or in lateral recumbancy if less than 20 kg. Interposed abdominal compression is also now advocated during CPCR as an adjunctive therapy to increased cardiac output as well as coronary and cerebral blood flow. In this strategy, the abdomen is compressed during the period of time that the thorax is relaxed, driving forward blood flow from the abdomen toward the heart. One of the most important considerations is that if positioning and external cardiac compression is not generating a femoral pulse, the animal's position should be changed or internal cardiac massage considered. In patients with conditions that prevent a dynamic change in intrathoracic pressure such as obesity, pneumothorax, hemothorax, flail chest or rib fractures, diaphragmatic hernia, or open chest wounds, open-chest CPCR should be initiated immediately, without starting closed-chest CPCR at all. Internal cardiac massage generates twice as much blood flow as external thoracic compressions. However, the overall rate of discharge from the hospital largely remains unchanged at this time in veterinary medicine. If an animal arrests under general anesthesia and is having thoracic or abdominal surgery, immediate open-chest CPCR should be performed. However, if an animal presents to you after experiencing cardiopulmonary arrest, careful consideration should be weighed before opening the chest. For how long has the animal been arrested? If it has been greater than 15 - 20 minutes, the likelihood of having a successful outcome is dismal. Are you able to correct the underlying problem or problems? If not, perhaps it is not in the animal's best interest to pursue open-chest CPCR. However, if the event was witness and not long ago, or if there is an underlying problem that makes closed-chest CPCR ineffective, don't delay in initiating open chest CPCR. Time is of the absolute essence. To perform open chest CPCR, following intubation and initiation of breathing and thoracic compressions, the patient should be placed in right lateral recumbancy and the fur over the left sixth intercostal space quickly clipped. The skin should be incised using a scalpel blade over the intercostal muscles, through the underlying fascia and fat, to the level of the intercostals muscles. A blunt stab incision should be made with a Mayo scissors into the pleural space, making sure that the assistant performing ventilation does not inflate the lungs during the stab incision to prevent iatrogenic lung injury. Once the stab incision has been made, the intercostals muscles are incised dorsally and ventrally to the level of the sternum, using care to avoid the internal thoracic artery and the intercostals vessels located at the caudal edge of each rib. Force the ribs open and visualize the pericardial sac. Visualize the phrenic nerve and incise the pericardial sac ventral to the phrenic nerve. Exteriorize the heart from the pericardial sac and squeeze the heart from apex to base, gently avoiding placing too much tension or torque on the heart to prevent ripping the heart from the great vessels. Handling the heart during open-chest CPCR allows the first-responder to directly visualize and feel the extent of cardiac filling and thus cardiac preload during resuscitation. In many cases, intravenous fluid therapy is not necessary unless hemorrhage, severe hypovolemia secondary to vomiting or diarrhea, or vasodilation secondary to anesthetic agents or sepsis have resulted in the animal's cardiopulmonary arrest. A common misconception is that all patients with cardiopulmonary arrest require large volumes of intravenous fluids. A large amount of time is usually wasted while someone attempts to secure an intravenous or intraosseous catheter. Additionally, increased diastolic filling pressures may actually decrease blood flow to the coronary sinus, thus impairing myocardial blood flow. Diastolic filling can be improved by cross-clamping the aorta during cardiopulmonary cerebral resuscitation. Once either closed-chest or open-chest CPCR and basic life support consisting of airway intubation, artificial ventilation, and artificial cardiac compression (either open or closed), Phase II of CPCR, or Advanced Life Support (ALS) consisting of ECG monitoring and interpretation, electrical defibrillation, and specific drug therapy should be performed. Advanced Life Support strategies can improve the chance of having a successful outcome. Following BLS (if possible, these are performed simultaneously with a well-trained CPCR team), attach an electrocardiograph monitor to the patient to determine the cardiac rhythm. Early and rapid defibrillation can be paramount to a successful outcome. Further, drugs should be administered based on a particular cardiac rhythm and timing during CPCR. If a patient with a witnessed cardiopulmonary arrest is on any medication that is a potential cardiac or respiratory depressant, the offending drug must -be immediately reversed. For example, many post-operative or post-trauma patients are treated with parenteral opioid agents. Reversal with naloxone (0.02 - 0.04 mg/kg IV) should be immediately performed when initiating ALS. If the ECG rhythm indicated fine ventricular fibrillation, epinephrine (0.01 - 0.02 mg/kg IV) should be administered in an attempt to convert fine v-fib to coarse v-fib, a rhythm that may be easier to treat. Immediate electrical defibrillation (3 - 5 joules/kg externally, or 0.5 - 1.0 joule/kg internally) should also occur with a series of three shocks occurring in rapid succession. If external or internal electric defibrillation is unsuccessful, or if an electrical defibrillator is not available, chemical defibrillators can also be used, including magnesium chloride (25 - 40 mg/kg IV), or amiodarone (5 - 10 mg/kg IV, IO) If asystole or so-called "flat-line" is diagnosed, first check the leads on the ECG. If attached to the patient properly, administer both atropine (0.04 mg/kg IV) and epinephrine (0.01 - 0.02 mg/kg IV). Electrical-mechanical dissociation (EMD), also known as Pulseless Electrical Activity (PEA) is a very difficulty rhythm to treat, and has been associated with tremendously increased vagal tone. Electrical-mechanical dissociation is treated with naloxone (0.02 - 0.04 mg/kg IV) and high dose atropine (0.4 mg/kg IV). All drugs except for sodium bicarbonate that can be administered intravenously can also be administered via intratracheal route of administration, but at a higher dose. A table of drug doses and route of administration is provided for you at the end of this monograph. The use of sodium bicarbonate during CPCR is very controversial, due to risk of causing hypotension, paradoxical cerebral acidosis, hyperosmolality, and hypernatremia. Sodium bicarbonate (0.5 - 1 mEq/kg IV)) should only be administered when treating severe hyperkalemia or acidosis, or when cardiac arrest and subsequent CPCR attempts have been unsuccessful after 10 minutes. Phase III of CPCR consists of post-resuscitation care, including protecting the heart and brain from the adverse effects of cardiopulmonary arrest, providing perfusion to vital organ systems, and treating any underlying condition that caused cardiopulmonary arrest in the first place. This is often a very large and difficult responsibility. A spontaneous rhythm usually is generated before the patient has spontaneous respirations. Intravenous antiarrhythmic therapy in the form of lidocaine (50 - 100 mcg/kg/minute IV CRI) should be administered to prevent arrhythmias from developing. Additionally, mannitol (0.5 - 1.0 gram/kg IV over 20 minute, followed by 1 mg/kg IV furosemide 20 minutes after the mannitol) should be administered to decrease cerebral edema secondary to decreased cerebral perfusion and cerebral hypoxia. Intravenous fluids can be administered at a maintenance rate (30 x BW in kg) + 70 = ml/day. This volume can be titrated or increased in patients with hypovolemia or vasodilation. Supplemental oxygen in the form of nasal insufflation, tracheal insufflation, or oxygen cage can be administered for supportive care. Electrocardiogram, Blood pressure, urine output should also be closely monitored, with appropriate pressor or inotropic therapy to maintain normotension and organ perfusion. Dobutamine (3 - 10 mcg/kg/min), primarily a beta-1 agonist, can be administered as a positive inotrope to improve cardiac contractility and cardiac output without compromising organ perfusion. At the lower doses suggested, few negative side effects occur with this drug. At higher doses, tachycardia is a potential complication that should be avoided. Dopamine, with primarily dopaminergic and beta-1 effects at lower doses, can be titrated to higher doses for alpha-adrenergic pressure effects, in the event that dobutamine alone is not successful. Epinephrine, phenylephrine, ephedrine, can also be used for pressor effects. Clearly, there is no specific way to perform successful CPCR. Each case must be handled on an individual basis, taking into careful consideration patient's underlying condition and therapy, client wishes, chance for a successful outcome, and personnel available to perform CPCR. Every clinic should have a designated portable crash-cart that remains fully stocked at all times. A quick reference table listing name of drug, drug dose, and dose in ml for IV and IT administration can be easily made for a wide range of body weights, then kept available near the crash cart for easy access. An emergency drug card containing the information just listed can also be made for each patient, should CPCR become necessary. Team drills can be performed on cadavers or stuffed animals to help insure a practiced team approach. All of these suggestions can decrease the disorganized feeling that sometimes occurs during the chaos of an arrest! While successes are few, knowledge of what to do and practice of how to do it during an arrest can be life saving in some veterinary patients. On the Horizon Techniques using a inspiratory impedance threshold device have been shown to improve initial outcome after CPCR. An inspiratory impedance threshold device (ResQPOD® Circulatory Enhancer) causes a larger amount of negative pressure (small vacuum) to accumulate in the thorax during inspiration, and effectively pulls more blood into the heart, and this increases cardiac preload. Initial studies have been favorable in human and animals, however, the device is not routinely used in small animals at this time. Table of Drugs used during and after CPCR
References available upon request. Fluid Therapy: It's More Than Just LRS These Days Total body water constitutes approximately 60% of a patient's body weight in normal individuals, although this value can vary slightly with age, gender, and obesity. Approximately 67% of total body water is located intracellularly. The remaining 33% of total body water is located extracellularly, in the intravascular and interstitial extravascular spaces. A very small amount of fluid, known as transcellular fluid, is located in the compartments of the gastrointestinal tract, within synovial fluid of joints, and the cerebrospinal tract. Within the body, all fluid is in a constant state of flux in between compartments. The movement of fluids from space to space is largely governed by the concentration of electrolytes, proteins, and other osmotically active particles relative to the amount of fluid within each compartment. The balance of fluids and electrolytes are absolutely necessary for normal body functioning and cellular processes. Normally, fluid intake is in the form or drink and foodstuffs. Water is also produced during the oxidation of food materials. Fluid can be lost during excessive panting, vomiting, diarrhea, and urination. Sensible fluid losses in the form of urine, vomit, and feces can be measured, and constitute approximately 2/3 of the body's daily maintenance fluid requirements. Insensible fluid loss is largely estimated from evaporation from the respiratory tract. Insensible losses can be excessive in situations of excessive panting, salivation, or from evaporation or hemorrhage from surgical sites. In normal individuals, fluid intake and excretion are kept in balance by the activity of sodium and chloride and serum osmolality. Osmoreceptors in the hypothalamus sense sodium and chloride concentration in the vascular space. As serum sodium rises due to increased sodium intake or fluid loss in excess of solute, serum osmolality rises. An increase in serum osmolality stimulates the release of arginine vasopressin (antidiuretic hormone) to be released from the hypothalamus. Antidiuretic hormone stimulates the opening of water channels in the collecting duct of the renal tubules, and thus stimulates water reabsorption. Once water is retained in the vascular space, sodium, urea, and glucose, the major contributors of serum osmolality, are diluted, and serum osmolality decreases. Hypothalamic excretion of ADH ceases once serum osmolality returns to normal. During a state of equilibrium, a patient's daily water intake equals water loss, creating no net loss or gain of fluid under normal conditions. Daily fluid requirements are based on the metabolic water requirements of a patient in a state of equilibrium. For each kilocalorie of energy metabolized, 1 ml of water is consumed. Metabolic energy requirements are calculated based on the linear formula: Kcal/day = [(30 x body weightkg) +70]
By substituting Kcal for 1 mL H2O, the following formula can be used to estimate a patient's daily metabolic water requirements: ml/day = [(30 x body weightkg) + 70]
Recent studies have indicated that metabolic energy requirements rarely increase during states of critical illness except in cases of sepsis. Because our patient frequently pant and may have excessive evaporative losses or sensible fluid losses in the form of vomiting, diarrhea, wound exudates, body cavity effusions, daily fluid requirements may be greater than that calculated above. The formula should be used as a guideline, and careful assessment and measurement of ongoing losses should be added to the patient's daily fluid therapy as needed, to prevent further dehydration. The degree of interstitial dehydration can subjectively estimated based on a patient's body weight, mucous membrane dryness, skin turgor, degree of sunkeness of the eyes, and mentation. Subjectively, if a patient has a history of fluid loss in the form of vomiting or diarrhea, but no external evidence of mucous membrane dryness of skin tenting, dehydration estimate is less than 5%. A patient is said to be 5% dehydrated when mild skin tenting and mucous membrane dryness is present. Clinically, 7% dehydration is manifested as increased skin tenting, dry oral mucous membranes, and mild tachycardia with normal pulse quality. A patient is 10% dehydrated with increased skin tenting, dry oral mucous membranes, tachycardia and decreased pulse pressure is present. Finally, a patient is said to be 12% dehydrated when skin tenting and mucous membrane dryness is markedly increased, the eyes appear dry and sunken, and alteration of consciousness is observed. The parameters are largely subjective, because they can also be affected by loss of body fat and increased age. The later stages of dehydration are also accompanied by parameters consistent with hypovolemic shock. Other factors, including hemorrhage and third spacing of body fluids can also result in a decrease in intravascular circulating volume, resulting in signs of hypovolemia. With severe hypovolemia of more than 15% of circulating volume, transcompartmental fluid shift from the interstitial to intravascular compartments occurs within one hour of fluid loss. When fluid loss is so severe that intravascular fluid volume is affected, hypovolemia can result in clinical signs of tachycardia, prolonged capillary refill time, decreased urine output, and hypotension. The vascular space is very sensitive to changes in the amount of circulating volume. During states of normovolemia, the degree of wall tension is sensed by baroreceptors in the carotid body and aortic arch, sending a pulsatile continuous feedback via vagal afferent stimuli to decrease heart rate. In the early stages of hypovolemic shock, a decrease in vascular wall stretch or tension is sensed by baroreceptors in the carotid body and aortic arch, causing blunting of tonic vagal stimulation, and allows sympathetic tone to increase heart rate and contractility to normalize cardiac output in the face of decreased circulating volume. Later, decreased blood flow and delivery of sodium to receptors in the juxtaglomerular apparatus of the kidneys cause activation of the renin-angiotensin-aldosterone axis, stimulating sodium and fluid retention to replenish intravascular volume. Fluid replacement rate and volume When clinical signs of hypovolemic shock are present, intravascular fluids must be replaced in an emergency phase of fluid resuscitation. Calculated shock volumes of fluids are 90 ml/kg/hour for dogs, and 44 ml/kg/hour for cats. A simple guideline to follow is to replace ¼ of the calculated shock volume as rapidly as possible, the reassess perfusion parameters including heart rate, blood pressure, capillary refill time, and urine output. In dogs, a simple method to calculate ¼ shock volume in dogs is to take the animal's weight in pounds and add a zero, giving you the amount of fluid in mls to administer as a bolus as quickly as possible. Approximately 80% of the volume of crystalloid fluid infused will re- equilibrate and leave the intravascular space within 1 hour of its administration. A constant rate infusion of crystalloid is recommended to provide continuous fluid support in patients that are dehydrated and have ongoing losses. In some cases, the fluid required to restore intravascular and interstitial volume can cause hemodilution and dilution of oncotically active plasma proteins, resulting in interstitial edema formation. In such cases, a combination of a crystalloid fluid along with a colloid containing fluid can help restore colloid oncotic pressure and prevent interstitial edema. Once immediate life-threatening fluid deficits are replaced, additional fluid is provided based on the estimated percent dehydration and maintenance needs. Basic dehydration estimates can be calculated based on the fact that 1 ml of water weighs approximately 1 gram. Dehydration estimates in liters can then be calculated by the formula: Body weight in kg x estimated percent dehydration x 1000 ml/liter. This provides you with the number of liters deficit. A frequent mistake when replenishing fluid deficits is to arbitrarily multiply a patient's daily water requirement by a factor of 2 or 3 to replenish intravascular and interstitial deficits. This practice frequently underestimates the patient's actual fluid needs, and does little to treat volume depletion and interstitial dehydration. Instead, it is better to perform the calculation and add this to daily maintenance fluid requirements and ongoing losses, to maintain hydration in your hospitalized patients. Eighty per cent of the calculated fluid deficit can be replaced in the first 24 hours. After successful treatment of hypovolemic shock and replacement of estimated dehydration volumes, maintenance fluids can be supplemented, provided that no signs of dehydration or ongoing fluid loss are present. An objective way of assessing whether fluids volume is adequate is to assess body weight in a regular basis throughout the day. Acute losses in body weight are commonly associated with fluid losses, and can be used to determine whether the patient is at risk of once again becoming dehydrated. Isotonic Fluids, Hypotonic Fluids, and Hypertonic Fluids
There is a wide variety of fluids are available for use by the veterinary practitioner. A crystalloid fluid contains crystals or salts that are dissolved in solution. Specific crystalloid fluids are indicated in certain disease states, and may be contraindicated in others. Therefore, whenever a crystalloid fluid is used, one must carefully consider it to be another drug in the armamentarium, and justify its use or potential disuse in each patient. Basic categories of crystalloid fluids include isotonic, hypotonic, and hypertonic solutions, depending on the concentration and type of solute present relative to normal body plasma. Isotonic fluids have tonicity, or solute relative to water, similar to that of plasma. Examples of isotonic fluids include 0.9% (normal) saline, Lactated Ringer's solution, Normosol-R, and Plasmalyte-A. Isotonic fluids are indicated to restore fluid deficits, correct electrolyte abnormalities, and provide maintenance fluid requirements. Hypotonic solutions are fluids whose tonicity is less than that of serum. Examples of hypotonic fluid solutions include 0.45% saline, 0.45%NaCl + 2.5% dextrose, and 5% dextrose in water (D5W). Hypotonic fluids are indicated when treating a patient with diseases processes that cause sodium and water retention, namely, congestive heart failure and hepatic disease. Infusion of hypotonic fluids is also indicated when severe hypernatremia exists and you need to slowly correct a free water deficit. To calculate a patient's free water deficit, use the following formula: Free water deficit = 0.4 x lean body weight x [patient serum Na/140 - 1] The free water deficit should be corrected slowly, to not cause iatrogenic cerebral edema. Ideally, the patient's sodium should not decrease by more than 15 mEq/L during a 24 hour period. Hypertonic solutions act to draw fluid from the interstitial fluid compartment into the intravascular space to correct hypovolemia. Their use is absolutely contraindicated if interstitial dehydration is present. Hypertonic solutions such as 3% or 7% saline have solute in excess of fluid relative to plasma. Hypertonic saline should be administered in bolus increments of 3 - 7 ml/kg as a rapid infusion. Because the net effect of hypertonic saline solution lasts only approximately 20 minutes, hypertonic saline must always be infused along with a crystalloid solution to prevent further interstitial dehydration. Electrolyte Composition (mEq/L) of Commonly Used Isotonic and Hypotonic Crystalloid Fluids
Colloids
A colloid solution contains negatively charged large molecular weight particles that are osmotically active, drawing sodium around their core structures. Wherever sodium is, water follows. By drawing sodium around the particle, water is thus held within the vascular space. Colloids replace intravascular fluid deficits only. Therefore, colloids are always administered along with crystalloids, to restore both intravascular and interstitial fluid volume. Examples of artificial colloids include Hetastarch, Dextran 40, Dextran 70, and Oxyglobin . Whenever a colloid is administered along with a crystalloid, calculated crystalloid fluid requirements should be decreased by 25% - 50%, in order to avoid volume overload. Natural colloid solutions include whole blood, packed red blood cells, and plasma. Fresh whole blood is indicated when loss of both red blood cells and plasma has occurred. The Rule of Ones states that one ml of fresh blood infused per one pound body weight will increase the patient's packed cell volume by one per cent, provided that no ongoing losses are present. Packed red blood cells can be administered when anemia is present in sufficient quantity to cause clinical signs of anemia, including lethargy, inappetance, tachycardia and tachypnea. Fresh frozen plasma can be administered at 10 - 20 ml/kg/day to replenish clotting factors and provide antiproteinase activity in states of inflammation, including pancreatitis. Fresh frozen plasma can be used to replace small amounts of albumin, in cases of hypoalbuminemia, however, is not efficient as administering purified concentrated 25% human albumin (2 ml/kg IV in dogs over 4 hours; pre-treat with 1 mg/kg diphenhydramine IV). 20 ml/kg plasma needs to be infused for every 0.5 g/dL increase in plasma albumin, provided that no ongoing losses are present. The goal of albumin administration is to raise the patient's serum albumin to 2.0 g/dL, then provide the remainder of colloidal support with synthetic colloids. Hetastarch is a polymer of amylopectin suspended in a lactated ringer's solution. The average molecular weight of Hetastarch is 69,000 Daltons. Larger particles are broken down by serum amylase, and last in circulation for approximately 36 hours. Because Hetastarch can bind with von Willebrand's factor, mild prolongation of a patient's APTT and ACT may be observed, but do not contribute to or cause clinical bleeding. Hetastarch should be administered in incremental boluses of 5 - 10 ml/kg in dogs, and 5 ml/kg in cats. Because rapid administration of hetastarch can cause histamine release and vomiting in cats, the bolus should be administered slowly over a period of 15 - 20 minutes. Many author's recommend that the total daily dose of hetastarch should not exceed 20 - 30 ml/kg/day. Following the administration of hetastarch boluses, it should be administered as a constant rate infusion (20 - 30 ml/kg/day IV) until the patient is able to maintain its albumin and colloidal support on its own. Dextran solutions contain polymers of glucose with average molecular weights of 40 and 70 Daltons. Dextran 40 is largely unused these days, favoring the larger particles of Dextran-70 in contributing to water holding capacity of blood. The smaller particles of Dextran 40 last in circulation approximately 4 hours before being cleared by the kidneys. The larger particles of Dextran-70 last approximately 9 hours in circulation. Both Dextran-40 and Dextran-70 coat platelets and red blood cells and can impair coagulation and interfere with cross-match procedures. Adverse side-effects of anaphylaxis and renal failure have been reported in humans that received Dextran-40. For this reason, Dextrans are going to become no longer available, as other safer products are being used. Oxyglobin is a solution that contains bovine stroma-free hemoglobin that acts both as a potent colloid and as a carrier of oxygen in the face of thrombosis or anemia. Recommended doses of Oxyglobin are 20 - 30 ml/kg/day. Oxyglobin can be administered as a bolus of 3 - 7 ml/kg. Caution must be exercised when infusing oxyglobin in normovolemic patients and those with congestive heart failure, due to the risk of causing iatrogenic volume overload. References available upon request. Emergency and Critical Care Procedures Procedures such as abdomino- and thoracocentesis, thoracostomy and tracheostomy tube placement, urethral catheterization, and intravenous catheterization can be life-saving in the veterinary emergency room. A thorough knowledge of supplies required allows the procedures to be performed with efficiency. Many of the procedures that will be discussed can also decrease an animal's normal defense mechanisms and make the patient more susceptible to infection. Proper care and maintenance of thoracostomy tubes, urinary catheters, tracheostomy tubes, and intravenous catheters will be discussed. Abdominocentesis Abdominal paracentesis (abdominocentesis) is a useful and inexpensive technique to identify abdominal effusion, particularly in patients with clinical signs of acute abdominal pain or unexplained fever. Evaluation of any fluid obtained often aids in the diagnosis and helps guide treatment. Abdominal effusion can be classified according to its cellularity and protein content as transudates, modified transudates, and exudates. Causes of modified transudates and exudates include neoplasia, septic and non-septic inflammation, and hemorrhage. Additionally, biochemical evaluation of the fluid for blood urea nitrogen, creatinine, potassium, amylase, lipase, bilirubin, lactate and glucose can aid in the diagnosis of various conditions, including uroabdomen, pancreatitis, bile peritonitis, and septic peritonitis. Limitations of this technique are if small (< 6 ml/kg) amounts of abdominal effusion are present, a false negative abdominocentesis may occur. The equipment needed to perform an abdominocentesis includes: 20 - 22 gauge 1 - 1 ½ inch needles, latex gloves, sterile EDTA and red top tubes for sample collection, clippers and fresh blades, antimicrobial scrub and 70% ethyl alcohol. To perform abdominocentesis, the patient should be placed in lateral recumbancy, and the ventral abdomen clipped on midline at the level of the umbilicus, laterally, and cranially and caudally to obtain approximately 10 cm x 10 cm clipped area. Following aseptic scrub of the clipped area, needles should be placed in four quadrants: cranial and left, cranial and right, caudal and left, and caudal and right of the umbilicus. Each needle should gently but quickly be inserted into each site, twisting slightly as the needle is pushed in, to push any intestines away from the tip of the needle. Any fluid that flows freely should be collected and saved for cytological, biochemical, and microbial analysis/susceptibility, as indicated. If no fluid flows freely, a 3 ml syringe can gently be attached to each needle and gently suctioned with negative pressure, repeating for all four quadrants, as necessary. Thoracocentesis Thoracocentesis should be considered in any patient with respiratory distress and a short, choppy restrictive respiratory pattern caused by various causes of pleural effusion or pneumothorax. Thoracic auscultation will reveal dull muffled heart and lung sounds. Other causes of a restrictive respiratory pattern such as pain from fractured ribs, flail chest, pulmonary contusions, pulmonary edema, and lower airway disease should be considered prior to thoracocentesis, or if thoracocentesis is unrewarding. The equipment required for emergency thoracocentesis includes: 20 - 22 gauge 1 inch needles, 3-way stopcock, IV extension tubing, 60 ml syringe, clippers and blades, nonsterile gloves, aseptic scrub, collection basin for fluid, EDTA and red topped tubes, sterile culturettes, and Port-a-cul for bacterial culture. To perform thoracocentesis, the patient should be restrained in sternal recumbancy or in a standing position. The entire thorax should be visualized as a box, and a 10 cm x 10 cm area clipped in the center of the box on both sides of the chest. The clipped areas should be aseptically scrubbed. Wearing gloves assemble the needle, IV extension tubing, 3-way stopcock, and 60 ml syringe. In the center of the box 6th - 9th intercostal space), palpate the intercostal area and carefully insert the needle into the pleural space. Avoid the arterial blood supply and the nerves at the caudal portion of each rib. The bevel of the needle should be directed internally. Once the needle has entered the pleural space, the entire needle should be placed parallel to the body wall, to avoid iatrogenic lung laceration/puncture. The bevel of the needle can be directed dorsally if air is present, and ventrally if fluid is present. Often, it is necessary to sweep the needle in a circular motion (always making sure that the length of the needle is parallel with the thoracic wall), to aspirate air or fluid that is in pockets within the thorax. In some cases, multiple areas will need to be tapped. Any fluid collected should be saved in EDTA and red-topped tubes for cytological and bacterial analyses. BOTH sides of the thorax should always be aspirated, as the mediastinum does not always communicate, and pockets of air or fluid may be trapped on either side of the thorax, causing respiratory distress. Once the thorax has been evacuated of air or fluid and a more normal respiratory pattern has resumed, the needle can be removed. If negative pressure cannot be obtained, or if air re-accumulates rapidly due to an ongoing leak, a thoracostomy tube should be placed. Thoracostomy Tube Placement A thoracostomy tube (or tubes) should be placed when ongoing accumulation of air or fluid causes continued respiratory distress, or if thoracic lavage is indicated (i.e. in cases of pyothorax). Whenever the thorax is entered during surgery, a chest tube is placed in order to evaluate the pleural space of air post-operatively. Once a chest tube is placed, continuous suction can be used to control ongoing accumulation of air (pneumothorax), or fluid such as in cases of chylothorax. The equipment required for thoracostomy tube placement includes: Clippers and blades, antimicrobial scrub, 2% lidocaine, 3 ml syringe, 22 gauge needle, sterile surgical pack including field towels, towel clamps, scalpel handle and number 20 scalpel blade, needle holders, thumb forceps, hemostats, Mayo scissors, gauze 4 x 4s, Trocar-type chest tube (Argyle), 2-0 nylon suture, bandage material, sterile gloves, 3-way stopcock, Christmas tree adapter, wire, wire cutters, antimicrobial ointment. To place a thoracostomy tube, the animal should be placed and restrained in lateral recumbancy and the entire lateral portion of the thorax shaved. Sedation may be necessary in some patients. The clipped area should be scrubbed aseptically, and draped with sterile field towels secured with towel clamps. Infuse lidocaine at the level of the 10th intercostals space and tunnel the needle cranially and insert at approximately the 7th intercostal space where the trocar will enter the thorax. While the lidocaine is taking effect, cut the widened end of the thoracic drain with a scissors, and assemble the IV extension tubing, 3-way stopcock, Christmas tree adapter, and 60 ml syringe. Make a very small (1 cm) stab incision (just large enough to accommodate the size of the thoracic drain but no larger) at the level of the 10th intercostal space dorsally. Have an assistant pull the thoracic skin cranially and ventrally. This technique will help make a larger skin tunnel. Tunnel the trocar cranially and once over the 7th intercostal space, direct the trocar perpendicular to the thoracic wall. Grasp the trocar at the level of the skin firmly, and using the palm of your hand, push the trocar through the intercostal space into the thorax. Once the trocar has entered the thorax, push the tube off of the trocar cranially and ventrally, and have the assistant release the skin. Immediately secure the Christmas-tree adapter set-up, and have an assistant evaluate the thorax while you are securing the tube in place. Place a purse-string suture around the point of entry at the level of the skin, leaving the ends of the suture long in order to make a finger-trap suture. Place a horizontal mattress suture cranially to the purse-string suture, around the tube. Use care to not puncture the tube, and don't make the suture so tight to occlude blood flow and cause skin damage. Secure the finger-trap suture against the tube, puckering the tube with each knot. Place a piece of 1-inch tape around the tube, and suture the piece of tape to the skin to prevent movement as the skin moves. Secure the 3-way stop-cock, Christmas tree adapter to the tube with wire. Place a piece of gauze 4 x 4 with antimicrobial ointment over the chest tube point of entry into the skin, and secure to the thorax with bandage material. It is very important to make sure that all connections remain secure, and that there are no leaks in the system in order to maintain negative pressure. The use of three-way stopcocks secured to the system with surgical wire can help to prevent introduction of air into the system. Wear gloves at all times when changing bandage dressing or performing manual aspiration of the tube, as bacterial contamination of the system can occur from the hands of personnel. Thoraseal collection devices are available on-line, and from medical supply stores, for continuous suction. Nasal and nasopharyngeal oxygen catheter placement Placement of a nasal oxygen insufflation catheter is a quick and simple means to provide supplemental oxygen to the hypoxic patient. Nasal oxygen insufflation catheters are well-tolerated, require minimal equipment, and are easy to maintain. Their use should not be considered in patients with laryngeal obstruction, nasal or facial trauma, nasal obstruction (foreign bodies or mass lesions including fungal infections or neoplasia), or bleeding disorders. Additionally, since sneezing sometimes occurs during placement, their use is relatively contraindicated in patients with risk of increased intracranial pressure including intracranial neoplasia. The equipment required for a nasal or nasopharyngeal oxygen catheter includes: Argyle feeding tube or red rubber catheter, surgical staples or 3-0 nylon suture, 2% lidocaine or 0.5% proparacaine hydrochloride, sterile lubricant, permanent marker, 1 ml syringe case, flexible extension tubing, oxygen source, bubble for humidification, rigid Elizabethan collar The patient's nostril should be anesthetized with 0.5 - 1 ml of dilute 2% lidocaine or several drops of 0.5% proparacaine, tilting the head back to assure coating of the nasal mucosa with the topical anesthetic. In the case of nasal oxygen catheter placement, the tip of the tube is placed at the medial canthus of the eye, and the portion adjacent to the tip of the nose marked with a permanent marker. In the case of nasopharyngeal oxygen catheter placement, the tip of the tube is measured from the ramus of the mandible to the tip of the nose, and marked accordingly. The tip of the tube is lubricated, and the tube held just adjacent and in front of the nostril, as close to the nostril as possible. The patient's muzzle is held with the other hand, for ease of placement. The tube is directed ventrally and medially to the level of the mark on the tube. In the case of nasopharyngeal catheter placement, the nostril is pushed dorsally and the lateral portion of the nostril pushed medially at the same time, directing the catheter into the ventral nasal meatus. Once the tube is in place, it is secured using surgical staples or nylon suture material, avoiding the whiskers. We usually secure it over the top of the nasal planum in between the eyes, to the top of the head, and immediately place a rigid Elizabethan collar. Oxygen flow rates of 50 - 100 ml/kg/minute are usually well-tolerated, as long as the oxygen source is humidified to prevent drying of the nasal and airway mucosa. Topical anesthetic (0.5% proparacaine) can be instilled as necessary for patient comfort. Central Venous Catheter Placement A jugular central venous catheter can be useful for large and small volume intravenous fluid, blood product, or drug administration, central venous pressure measurement, and frequent collection of blood samples. A jugular catheter often well-tolerated by the patient, and can be maintained for many days. Additionally, jugular catheters tend to stay cleaner and dryer than catheters placed in other areas of the body. Jugular catheters are contraindicated in patients with various forms of coagulopathies, and in hypercoagulable patients (i.e. hyperadrenocorticism, DIC, IMHA). Sedation may be necessary in some patients. The equipment required to place a central venous catheter includes: Clippers and blade, antimicrobial scrub, sterile or nonsterile gloves, 1 inch white tape, Kling and other bandaging material, antimicrobial ointment, 14, 16, or 18 gauge Venocath catheter, 3 ml syringe with heparinized saline to use as flush, t-port, gauze 4 x 4s, To place a jugular catheter, restrain the patient in lateral recumbancy. Clip the lateral cervical area from the ventral ramus of the mandible caudally to the thoracic inlet and dorsally and ventrally to midline. Extend the head and neck and have the restrainer pull the front legs caudally. Occlude the jugular vein and visualize. Aseptically prepare clipped area. Wearing gloves, tent the skin over the jugular vein. Insert the needle carefully and briskly though the skin. Do not try to immediately enter the vein. Once the needle is inserted under the skin, occlude the vein and "strum" the vein with the needle. Isolate the vein under the needle and insert the needle in a smooth motion. Once the needle is inserted into the vein, a flash of blood should appear in the catheter. Insert the needle a small amount into the vein, and then push the catheter into the vein, not letting go of the needle. Once the catheter is secured in the hub of the needle/catheter assembly, remove the needle from the vein and push down the wings over the needle and place clean 4 x 4s over the point of entry at the level of the skin to decrease bleeding from the venipuncture site. Make a small loop or half-loop in the catheter approximately the size of a quarter, and tape the shaft of the needle assembly with a piece of white tape, securing the white catheter hub to the blue piece. Continue the wrap around the neck. Attach one of two more pieces of white tape around the neck and gauze 4 x 4s in the direction opposite than the first piece of white tape. Secure the bandage with 2 inch Kling, going in the same direction as the last two pieces of white tape. Secure the Kling with Elasticon or white tape, and label the bandage with the date of catheter placement, catheter type and gauge, and person who placed the catheter. Central venous catheters can also be placed in the lateral and medial saphenous veins. The steps involved are identical as jugular catheter placement, with the exception of the anatomic site. The site of both peripheral and central venous catheter placement should be selected based on an animal's needs and clinical signs. For example, peripheral cephalic catheterization is ideal for a patient with diarrhea, but is not ideal for a vomiting patient, as vomitus can potentially contaminate the catheter site. Cephalic and jugular catheterization should be avoided in an animal with seizures, due to the increased risk of personnel being bitten while administering anticonvulsant drugs during a seizure episode. Lateral and medial saphenous catheter placement should be avoided in a patient with urinary incontinence or diarrhea, because of the risks of contamination. All catheters should be placed after washing your hands and wearing gloves. Latex gloves can decrease the incidence of bacterial contamination of intravenous catheters, and should be worn whenever changing a catheter bandage or fluid line. The catheter bandage should be changed whenever visible contamination occurs. The catheter site itself should be evaluated at least once a day for evidence of thrombophlebitis, inflammation and pain upon injection. Intravenous catheters should be removed and replaced, with bacterial culture of the catheter tip, in any patient with an unexplained fever. Seldinger Over-the-Wire Catheter Placement The Seldinger, or "over-the-wire" technique for central venous catheter placement is easy and simple to perform, with practice. Over-the-wire catheters are available with single or multi-lumen systems. Multi-lumen systems are advantageous when a patient requires the infusion of multiple fluids and drug products, including parenteral nutrition. Surgivet, Abbott, and Arrow all make over-the-wire catheter kits that contain all supplies necessary, including local anesthetic, number 11 scalpel blade, sterile gauze squares, intravenous catheter, vascular dilator, long wire in introducer, and long central catheter. Sterile gloves and aseptic technique are absolutely necessary when placing an over-the-wire catheter into a central vein. Surgical suture is required to secure the catheter hub in place. To place an over-the-wire catheter, the patient should be restrained in an identical manner as that described for placement of a jugular catheter. The patient's lateral cervical area should be clipped from dorsal to ventral midline, from the ramus of the mandible to the thoracic inlet. The clipped area should be aseptically scrubbed, then draped with sterile field towels. An assistant should occlude the jugular vein to enhance visualization of the vessel. The skin is tented over the proposed site of catheter placement, and a small amount of lidocaine injected into the skin, taking care to avoid intravenous injection. While the lidocaine is taking effect, the ports of the long catheter should be flushed with heparinized saline and clamped. Next, insert an 18 - 20 gauge over-the-needle catheter into the jugular vein, watching for a flash of blood in the stylette. Push the catheter off of the stylette, then remove the stylette. Next, insert the long wire through the catheter into the jugular vein. Never let go of the wire. Remove the over-the-needle catheter from the vein, again, never letting go of the wire. Insert the vascular dilator over the wire into the vessel in a blunt twisting motion to create a larger hole in the vessel. Remove the vascular dilator off of the wire. At this point, the vessel will bleed, so be ready to insert the long catheter over the wire very quickly, to close off the hole in the vessel. Once the catheter has been inserted to its hub, secure it to the skin with suture. The catheter can be bandaged as with other types of jugular catheters. Different catheter ports can be designated for specific purposes, like parenteral nutrition. Over-the-wire catheters can also be placed in the lateral and medial saphenous veins, when necessary. Intraosseous catheter Intraosseous catheters are an excellent means of infusing large volumes of crystalloid and colloid fluids, blood products, and drugs to a patient in which intravenous access is difficult or impossible due to extreme hypovolemia, hypotension, small patient size or exotic species. Uptake of fluids and other products from the intraosseous space is as rapid as intravenous infusion. Placement of an intraosseous catheter is simple and well-tolerated in most patients, and can be life-saving when valuable time is sometimes wasted in procuring vascular access. The equipment required for placement of an intraosseous catheter includes: Clippers and blades, antimicrobial scrub, 16 - 18 gauge bone marrow needle or spinal needle with stylette, 16 - 18 gauge needle, 2% lidocaine, 22 - 25 gauge needle, Heparinized saline flush, antimicrobial ointment, T-port connector, ½ - 1 inch white tape, 3-0 nylon suture Tracheostomy tube placement A temporary tracheostomy tube should be placed in cases of severe upper airway obstruction, trauma, laryngeal or pharyngeal collapse, or if long-term positive pressure ventilation is going to be performed. Equipment required for tracheostomy tube placement and maintenance includes: sterile surgical pack including sterile field towels, towel clamps, number 10 scalpel blade, scalpel handle, small gelpi retractors, sterile mettzenbaum scissors, curved hemostats, gauze 4 x 4s, nylon suture, number 11 scalpel blade, various sized Shiley tracheostomy tubes, umbilical tape, hydrogen peroxide, sterile bowls, sterile pipe cleaners, sterile bottle brush, and sterile long cotton swabs. To place a tracheostomy tube, the procedure is performed with the patient under general anesthesia. The patient's ventral neck is clipped from the ramus of the mandible caudally to the thoracic inlet and laterally to the dorsal cervical region. The patient is positioned in dorsal recumbancy, making sure that the head and neck are perfectly straight. The ventral cervical region is aseptically scrubbed and draped with sterile field towels secured with towel clamps. The larynx is palpated carefully, and a skin incision made with a number 10 scalpel blade caudally on ventral cervical midline for several centimeters. The subcutaneous tissue, underlying fascia and sternohyoideus muscles are visualized and bluntly dissected using curved hemostats and mettzenbaum scissors, using care to dissect through tissue/muscle planes and not cause any damage or hemorrhage. Hemorrhage should carefully be controlled to allow best visualization. The lateral edges of the skin incision and the underlying tissue should be carefully retracted using Gelpi retractors to allow best visualization. A horizontal incision should be made with Number 11 scalpel blade in between the 4th and 5th or 5th and 6th tracheal rings, using care to not cut more than 50% of the circumference of the trachea. A suture should be placed around the tracheal ring at the cranial and caudal edges of the incision to allow retraction of the incision to hold the incision open and place the tracheostomy tube. The sutures should be left long and tied as stay sutures. The stay sutures are retracted to pull the incision in the trachea open, and the appropriate sized Shiley catheter placed into the trachea. The tracheostomy tube can be secured with umbilical tape and a light wrap. Once no longer needed, the tracheostomy tube can be removed. The stay sutures should be left in place until you are sure that the patient no longer requires tracheostomy tube. Once the stay sutures are removed, the sutures can be cut and simply removed. The wound is left to heal by second intention. A tracheostomy tube bypasses the body's normal upper airway defense mechanisms, and can increase the risk of airway infection and pneumonia. A patient with a tracheostomy tube should be monitored 24 hours a day. Strict aseptic technique should be maintained at all times whenever handling the tracheostomy tube. Shiley tracheostomy tubes are preferred because they contain an inner cannula that can be removed and cleaned on a regular basis, without disrupting the outer cannula in the patient's trachea. Wear gloves, and remove the inner cannula whenever necessary, place it in a sterile bowl with hydrogen peroxide, and clean the cannula with sterile cotton swabs, sterile bottle brush, or sterile pipe cleaners, to remove the excessive mucus and debris. Rinse the cannula with sterile water or saline before replacing it into the patient's airway. Intermittently, small amounts of sterile saline can be introduced into the tracheostomy tube and suctioned with a small sterile red rubber catheter if large amounts of debris obstruct the patient's airway. Triage Stat! Emergency Approach to the Trauma Patient Introduction
"Triage STAT to the front!" Trauma is invariably one of the most common emergencies seen in small animal practice, and is a leading cause of death in our small animal patients. Your staff must be prepared, be organized, and be able to effectively perform the art of triage. The word "triage" is French, and means "to sort" or "to cull". Patients are assessed and categorized according to the nature and severity of injuries, treating the most life-threatening problems first. Once the patients have been categorized, a rapid history and physical examination can be performed. An organized and aggressive approach to rapid assessment and treatment of the traumatized patient is necessary in order to have the best chance of a positive outcome. Initial Assessment and Stabilization: Remember the "ABC's"
One of the most important concepts to remember when approaching any critically ill patient is to routinely perform a rapid primary survey, keeping in mind the ABC's of evaluation and resuscitation. "A": Airway and Arterial Bleeding. Observe the patient from a distance. Take note of the patient's respiratory rate and character. Rapid, shallow, restrictive respirations can be associated with a variety of conditions of the thoracic cage, pulmonary parenchyma, or pleural space, including the pain associated with rib fractures, flail chest, pulmonary contusions, diaphragmatic hernia, pneumothorax, or hemothorax. Any arterial bleeding should have a compression bandage or rapid ligature placed to prevent exsanguination. Definitive repair of lacerations can occur once the patient's overall status has been assessed and the clinical condition is determined to be stable. "B": Breathing: What is the color of the mucous membranes? Watch the character of the patient's respirations. Slow deep respiration with inspiratory stridor is often associated with an upper airway obstruction. Careful auscultation of the upper airways and thorax can aid in the diagnosis of the primary problem. Harsh sounds that are the loudest over the arytenoid area is likely associated with an upper airway obstruction, whereas, harsh pulmonary crackles after a traumatic event are most likely associated with pulmonary contusions. Decreased lung sounds dorsally with a restrictive respiratory pattern may be associated with pneumothorax or the presence of a diaphragmatic hernia. Decreased lung sounds more ventrally may be associated with pleural effusion including hemothorax or a diaphragmatic hernia, depending on the location of the rent in the diaphragm, and the abdominal contents now within the pleural space. "C": Circulation Assess the patient's perfusion status. What is the heart rate and rhythm? What is the ECG? What is the blood pressure? What is the pulse quality? What is the capillary refill time? Is there any evidence of external hemorrhage, or do you suspect internal bleeding? When clinical signs of hypovolemic shock are present, fluids must be replaced in an emergency phase of fluid resuscitation. "D": Disability Is the patient ambulatory? What is the patient's mental status? Is it the same as on presentation or is the patient becoming more mentally dull or obtunded. Are the pupils equal in size or is there any anisocoria? Is the patient laterally recumbent with rigid forelimbs and flaccid paralyzed hind limbs suggestive of a Schiff-Sherrington with a spinal cord lesion somewhere between T3 to L3? If so, that patient should be placed immediately on a backboard to prevent further neurologic injury. Does the patient have evidence of fractures? Are there any open wounds that should be covered to prevent infection with nosocomial organisms? If there is blood on the patient, always wear gloves, as sometimes human caretakers get bitten during the process of transporting the injured animal. You might not be sure whether the blood on the animal is human or non-human animal in origin. Treatment of Shock
Shock is defined as inadequate circulating blood flow such that oxygen delivery is insufficient to meet cellular energy and substrate demands. After sustaining a traumatic injury, shock is usually associated with some form of hypovolemia and inadequate circulating blood volume secondary to internal or external hemorrhage. Shock is characterized according to stage and the body's physiologic response. Rapid assessment and aggressive therapy are necessary to improve oxygen delivery to the tissues. Early compensatory shock is characterized by hyperemic mucous membrane color, tachycardia, rapid capillary refill time, and normal to increased mean arterial blood pressure. Early decompensatory shock is characterized by pale pink mucous membranes, tachycardia, prolonged capillary refill time, and normal to decreased mean arterial blood pressure. Late decompensatory shock is characterized by pale gray mucous membranes, prolonged capillary refill time, normal to decreased heart rate, weak pulse quality, decreased mean arterial blood pressure, and hypothermia. Treatment of shock largely consists of re-establishing adequate circulating blood volume without exacerbating further hemorrhage. Ideally, the administration of isotonic crystalloids fluids and natural and synthetic colloids during the treatment of hypovolemic shock should be based on constant assessment and reassessment of the patient's cardiovascular status and perfusion parameters. In dogs, shock volume of fluid is related to the patient's intravascular blood volume, 90 ml/kg. In cats, shock volume of fluid is calculated at 44 - 45 ml/kg. Typically, I start with administering ¼ of the calculated shock volume as rapidly as possible, then reassess the patient to evaluate if heart rate is decreasing, if blood pressure is rising, and if the patient's capillary refill time and mucous membrane color is improving. Fluid resuscitation to reach supraphysiologic blood pressures should be avoided. First, hypertension can cause clots that have formed to become unplugged, exacerbating further hemorrhage. Secondly, overzealous fluid administration of isotonic crystalloid fluids can contribute to the diffusion impairment and interstitial and alveolar flooding observed with pulmonary contusions. Finally, dilutional coagulopathies can occur with fluid replacement without administration of coagulation factors. Ideally, fluid therapy should be titrated to a systolic blood pressure of 100 mm Hg, diastolic blood pressure above 40 mm Hg, and mean arterial blood pressure above 60 mm Hg. Pulse pressure and quality alone are poor methods of assessing an accurate blood pressure in the traumatized patient, and thus, direct or indirect methods should be obtained, whenever available. To avoid iatrogenic worsening of pulmonary edema and dilutional coagulopathies, administration of synthetic colloids such as Hetastarch (5 ml/kg IV) or Oxyglobin (3 - 7 ml/kg IV) can be administered as a bolus. By administering a colloid in combination with a crystalloid, the total volume of crystalloid that is required for volume resuscitation is reduced. The colloid particle serves to attract the crystalloid fluid around the colloid's core structure, thus preventing the crystalloid from leaving the vascular space. When crystalloid fluids are administered in the absence of a colloid, 80% of the crystalloid fluid volume infused will leave the vascular space and travel into the interstitium within 1 hour of infusion. Although some authors feel that administration of a colloid to a patient with pulmonary contusions can worsen pulmonary pathology and diffusion impairment, the risks of colloid administration are largely outweighed by the benefits of small volume resuscitation and decreased alveolar flooding with isotonic fluids. Hypertonic saline (7.5%) can be administered as a bolus (5 - 7 ml/kg IV in dogs, 2 - 4 ml/kg IV in cats) along with a colloid (5 - 10 ml/kg IV) such as dextran-70 in a hypovolemic traumatized patient. Hypertonic saline draws fluid from the intracellular and interstitial spaces into the intravascular compartment to restore circulating fluid volume and oxygen delivery. The effect of hypertonic saline is short-lived, and lasts just 20 - 30 minutes without further colloid or crystalloid administration. Finally, in some cases, shock remains unresponsive to fluid administration due to continued patient pain and discomfort. The judicious and appropriate use of analgesic drugs is absolutely necessary as one of the most important treatments of any trauma patient. Analgesia for the Traumatized Patient No patient should ever be painful. Depending on the nature of the patient's injuries, however, analgesic choices should be considered carefully in order to prevent iatrogenic exacerbation of injuries and impaired oxygen delivery. In cases of head or ocular injury, for example, ketamine should be avoided due to the risk of increasing intracranial and intraocular pressure. No patient should receive any -2 receptor agonist due to the inherent properties of decreased cardiac output, and increased systemic vascular resistance even at minutely small doses. Instead, the best drugs available for veterinarians to use are opioids that cause minimal cardiovascular and respiratory depression and can readily be reversed with naloxone if difficulty arises. Opioids are classified based on their potency relative to morphine. Fentanyl (2 mcg/kg as an IV bolus, followed by 2 - 7 mcg/kg/hour IV CRI) is the most potent drug we have available in our analgesic armamentarium. Fentanyl has a potency 100 times that of morphine, and is extremely safe to use in patients with severe trauma. Hydromorphone, too, is a safe and potent alternative (0.1 - 0.2 mg/kg IV, SQ, IM). Partial agonists such as buprenorphine, or agonist-antagonist drugs such as butorphanol can never reach the same efficacy of analgesia as the pure mu-agonists, and therefore, are not ideal to use in any painful patient. Both buprenorphine and butorphanol bind avidly to opioid receptors. Because of this pharmacokinetic property, it may be difficult to reverse any adverse side effects that may occur, and they may also inhibit the efficacy of more potent analgesics used later. In specific circumstances such as rib fractures and flail chest, local anesthetic blocks can greatly assist in pain management and improve ventilatory function. These techniques will be discussed in more detail later. Thoracic Trauma Many patients with thoracic trauma and associated injuries have a rapid, shallow, restrictive respiratory pattern, often with a pronounced expiratory effort. Trauma to the thorax is first characterized as open versus closed thoracic trauma. Injuries can occur that involve the pleural space, pulmonary parenchyma, thoracic wall, and tracheobronchial tree. Finally, injuries to the thorax can also damage or irritate the underlying myocardium and lead to cardiac dysrhythmias and impaired cardiac output. The four most common injuries associated with trauma to the thoracic cage include pulmonary contusions, pneumothorax, rib fractures or flail chest, and a diaphragmatic hernia. In many cases of thoracic trauma, any or all of these injuries may be observed, depending on the severity of the trauma. Thoracic radiographs should be performed only after initial stabilization with oxygen, therapeutic (relieve respiratory distress) and diagnostic (confirm pneumothorax) thoracocentesis and alleviation of respiratory distress. PULMONARY CONTUSIONS A pulmonary contusion is a bruise of the pulmonary parenchyma that is characterized by increased vascular permeability, edema fluid and hemorrhage that accumulates in the interstitial and alveolar space accumulation in the alveolar space, and atelectasis. The degree of diffusion impairment and ventilation-perfusion mismatch contribute to patient hypoxemia. Radiographically, contusions may be apparent on initial survey films, or may lag behind the appearance of clinical signs, leading to a false sense of security that the patient is stable. Pulmonary crackles may be heard on thoracic auscultation. Clinically, the patient develops a rapid, choppy, restrictive respiratory pattern, that may progress to open-mouthed breathing, severe orthopnea, cyanosis, and bloody froth emitting from the nose or mouth. Even in the most stable patients, pulmonary contusions can develop over a period of 24 - 36 hours after the initial traumatic insult. The treatment of pulmonary contusions is largely supportive in nature, with oxygen supplementation and careful titration of intravenous fluids to avoid overhydration and exacerbation of pulmonary interstitial and alveolar fluid. In the most severe cases, sedation and mechanical ventilation may become necessary until the pulmonary parenchyma heals. PNEUMOTHORAX Pneumothorax, or the accumulation of free air in the pleural space, can be categorized into one of three types. A simple pneumothorax is usually associated with non-penetrating trauma and involves damage to the pulmonary parenchyma that results in the leakage of air into the pleural cavity. In most cases, the leak is self-limiting and can be managed conservatively with thoracocentesis alone. An open pneumothorax results from penetrating injuries to the chest wall that allows communication of the pleural space and the atmosphere. If the wound is small relative to the size of the glottis, adequate ventilation can be maintained. If the wound is large relative to the size of the glottis, however, severe hypoventilation results. Open wounds should be managed with immediate coverage, insertion of a thoracic drain, and aspiration of the pleural space with intermittent or continuous thoracic suction. Finally, a tension pneumothorax occurs when intrapleural pressure exceeds atmospheric pressure resulting from a one-way flap valve in either an airway (bronchopleural fistula) or the chest wall (pleurocutaneous fistula). When a patient presents with a tension pneumothorax, immediate alleviation of the intrapleural pressure via therapeutic thoracocentesis is necessary. This is best accomplished by quickly clipping a small area on the thoracic wall, aseptically scrubbing the area, and inserting a 20 - 22 gauge needle or catheter between the 7th - 9th intercostal spaces. The needle or catheter should continually be suctioned while preparing and placing a chest tube. Rib Fractures and Flail Chest The pain associated with rib fractures can greatly impede respiratory excursions and lead to hypoventilation and hypoxia. Frequently, the administration of analgesia improves pulmonary function to such an extent that hypoxemia resolves with analgesia and administration of supplemental oxygen. A flail chest occurs when two or more adjacent (contiguous) ribs have been fractured in two or more places, resulting in chest wall instability. The "flail" segment causes paradoxical chest wall motion in which the segment moves inward during inspiration and outward during expiration. The pain associated with the flail segment significantly diminishes the ventilatory capacity of the animal. Previous treatments for flail chest included external or surgical stabilization of the flail segment. However, external stabilization severely restricts respiration, and surgical stabilization using metal fixators can be prone to breakdown or osteomyelitis. Intercostal nerve blocks involve the administration of local anesthesia dorsal and ventral to each fracture, and blocking the ribs cranial and caudal to the flail segment markedly improves respiratory function by alleviating pain associated with the injury. A total of 0.75 mg/kg in cats and a total of 1.5 mg/kg in dogs of 2% lidocaine or bupivicaine can be infused up to three times daily. Diaphragmatic hernia Forceful impact of the abdomen while the glottis is open is associated with diaphragmatic hernia. Radiographic signs of diaphragmatic hernia include loss of diaphragmatic line, absence of the caudal heart border, increased soft tissue density within the thorax, and the presence of gas-filled bowel loops within the thorax. Herniation of the abdominal organs into the thoracic cavity and gastric tympany compress the thoracic viscera and cause pulmonary atelectasis. Atelectasis and pleural effusion result in a loss of functional lung capacity. Additionally concurrent injuries all contribute to hypoxemia, impaired venous return to the right heart, and decreased cardiac output. The net result is impaired oxygen delivery to vital organs. In most cases, stabilization of the patient can be accomplished before surgery is required to repair the diaphragmatic hernia. However, in some cases, a diaphragmatic hernia is a surgical emergency. If a gas-filled viscera such as the stomach is entrapped, venous return to the heart will be impeded. Organ entrapment such as the liver or spleen can also cause tissue necrosis, and unresponsive shock. If the stomach is within the thorax, the patient is unresponsive to initial stabilization with oxygen support and intravenous fluid therapy, surgical exploration of the thorax is a surgical emergency and should not be delayed. Ventilatory support via mechanical ventilation will be necessary during surgery, and may be required post-operatively in severe cases with severe pulmonary contusions are present. Penetrating bite wounds to the thorax should be explored, carefully debrided and lavaged thoroughly once the patient is stabilized. Broad spectrum antibiotics should immediately be administered to decrease the risk of pyothorax. Open wounds, penetrating foreign bodies, persistent severe hemorrhage into the pleural space, massive hemoptysis, recurrent cardiac tamponade, or persistent rapid accumulation of air in the pleural space refractory to negative suctioning are reasons to consider exploratory thoracotomy. Abdominal Trauma Any penetrating traumatic injury to the abdomen requires surgical exploration. A negative exploratory laparotomy is much better than waiting for septic peritonitis to manifest itself as leakage from bowel or biliary perforation occurs. In some cases, injuries such as hemo- or uroabdomen are obvious at the time of initial injury. In other cases, however, mesenteric thrombosis or bile peritonitis may take days to weeks to become apparent. Diagnosis of abdominal trauma is usually based on index of suspicion, abdominal radiographs, ultrasonography, and abdominal paracentesis or diagnostic peritoneal lavage. In the past, it was commonplace even in human medicine to perform an exploratory laparotomy on any patient with a traumatic hemoabdomen. A more conservative approach has been adopted by veterinarians in more than 99% of cases of traumatic hemoabdomen. Placing an abdominal compression bandage around the patient's abdomen with careful titration of intravenous fluid support is usually sufficient to tamponade any hemorrhage. Most recently, human trauma surgeons and criticalists have learned from what veterinary criticalists have known for years, and are becoming more conservative in their approach, as well. Uroabdomen Ruptured urinary bladder, avulsed kidneys, avulsed ureters, and traumatic injury to the urethra can cause life-threatening metabolic complications, but are rarely a surgical emergency, provided that aggressive fluid and medical management are performed. Abdominal fluid creatinine should be compared with peripheral creatinine to rule out a uroabdomen in any case of traumatic injury to the abdomen. If abdominal fluid creatinine is greater than that in the periphery, a diagnosis of uroabdomen is made. If creatinine is not available on an emergent basis, a simple azostick comparison or potassium will also suffice. The urea nitrogen and potassium in the abdominal fluid will be greater than that in the periphery if urine is present. Placement of a drainage catheter into the abdominal cavity under local anesthesia, then connecting the drainage catheter to a closed collection system is usually sufficient to remove urine from the abdominal cavity until the patient can be stabilized medically and become a more suitable candidate for anesthesia and definitive surgical repair of the urinary tract trauma. In such cases, the presence of an inappropriate bradycardia can signify atrial standstill secondary to hyperkalemia. Every effort should be made to decrease serum potassium to less than 7 mmol/L before any anesthesia is induced. Treatment protocols include administering calcium gluconate (0.5 - 1.0 ml/kg 10% solution IV), regular insulin (0.25 units/kg IV) with dextrose (2 gm dextrose IV per unit of insulin, followed by 2.5 - 5% dextrose CRI to prevent hypoglycemia), or intravenous sodium bicarbonate (0.25 - 1.0 mEq/kg). Neurologic Trauma The patient should be assessed carefully for mentation, the presence of nystagmus, miosis, stupor, coma, seizures, or abnormal postures such as Schiff-Sherrington. Worsening mentation or coma after a head injury should rapidly be treated with mannitol (0.5 - 1 g/kg IV) followed 20 minutes later by furosemide (1 mg/kg IV). Although there is a potential risk of worsening intracranial hemorrhage, patient's that are dying before your eyes can benefit from this aggressive therapy. If spinal trauma is suspected, the patient should be stabilized immediately on a flat stable surface to prevent worsening of a potentially correctable injury. The absence of deep pain perception indicates a very poor prognosis for return to function. It is important to attempt to elicit some degree of conscious perception of a painful stimulus, rather than a local withdrawl reflex alone, when making the decision to pursue further aggressive therapy in cases of spinal trauma. If concurrent cerebral injuries are present, it may be difficult to accurately assess spinal cord function until the patient is more alert. The administration of glucocorticosteroids in the treatment of head trauma or any other form of shock is not indicated unless the patient has severe head injuries that is causing swelling of the oropharynx and obstruction to adequate ventilation. Glucocorticosteroids have not been shown to definitively improve neurologic outcome in cases of head injury. Additionally, Glucocorticosteroids influence negative nitrogen balance, delay wound healing, impair glucose homeostasis, and suppress immune function. Hyperglycemia and decreased cerebral oxygen delivery can contribute to intracranial and intracellular acidosis that can worsen neurologic outcome. In cases of spinal trauma, however, corticosteroids such as Soludelta-cortef (30 mg/kg IV, then 15 mg/kg 2 and 4 hours later) may or may not anecdotally improve outcome. References available upon request. Management of Peri-Anesthetic Hypotension General anesthesia involves the careful and judicious use of compounds that induce sensory deprivation to noxious stimuli, muscle relaxation, and in most cases, unconsciousness. In critically ill patients, there often is a delicate balance between loss of consciousness and cardiovascular and respiratory compromise, requiring careful monitoring techniques to ensure patient safety. Fortunately, many animals that present to you in an emergency setting will be young, healthy animals that may require anesthesia to repair minor trauma. Other cases, however, will present to you with potentially life-threatening critical illnesses, making anesthesia more challenging and somewhat risky. Many anesthetic agents induce some degree of cardiovascular and respiratory depression. The goal of this presentation is to describe anesthetic protocols for both healthy and unhealthy animals. The Physical Examination The physical examination is one of the most important aspects of preparation prior to inducing anesthesia. In critically ill patients, a careful physical examination should be performed just prior to inducing anesthesia, as clinical status may have changed dramatically since initial presentation, often changing your choice of anesthetic protocols. Questions to ask yourself include: Is the patient's airway patent? Does the animal require mechanical or assisted ventilation? Is the animal morbidly obese or have an intraabdominal mass that will change efficacy of ventilation once the patient is placed in dorsal recumbancy? Does the animal have a sucking chest wound, rib fractures, pleural effusion, or potential for pneumothorax? Are there pulmonary contusions that may be affected by large volumes of intravenous fluids? Are the animal's respirations effective or ineffective? Is the animal in a state of circulatory shock? Is there a normal circulating blood volume? Is the heart beating efficiently, or is there a cardiac murmur or dysrhythmia? What is the clinical status of the animal? Is there an adequate blood pressure? Is there any sign of ongoing hemorrhage or severe electrolyte loss? In most cases, the answers to these questions can be obtained from a thorough and systematic physical examination, starting with the basic ABC's of emergency medicine. The animal must have a patent Airway, to deliver oxygen into the lungs while Breathing, and the oxygen can be delivered to tissues during the process of normal Cardiac function and Circulation. Once the ABC's have been evaluated and stabilized, other diagnostics can then be performed. Preanesthetic Agents There are several rationales for using pre-anesthetic medications. First, some forms of pre-medication provide both sedation and analgesia for the patient. Others maintain normal heart rate and rhythm while decreasing respiratory secretions. One of the most important reasons for using premedications is to decrease the total amount of anesthesia required to induce and maintain general anesthesia. The use of a balanced anesthetic approach provides many benefits for the patient, particularly those that are critically ill. Anticholinergic drugs such as atropine and glycopyrollate increase heart rate by inhibiting vagal stimulation. Glycopyrollate though, has less of a chance of inducing tachyarrhythmias. Atropine reduces respiratory secretions and can cause second-degree heart block. Atropine crosses the blood-brain and placental barriers, while glycopyrollate does not. This has important implications when providing anesthesia for the periparturient dam in need of a C-section, anesthesia that can potentially affect the outcome of the neonates. Opioids, used in combination with a phenothiazine tranquilizer such as acepromazine, provide neuroleptanalgesia. Morphine provides excellent analgesia without inducing severe cardiovascular compromise. Potential complications of morphine and other opiate drugs include bradycardia (which can be reversed or prevented by using a anticholinergic agent), and hypoventilation. Morphine administration can also induce vomiting and ileus in ambulatory patients. In recumbent patients, though, the use of morphine is justified by decreasing doses of induction agents and inhalant drugs required to maintain general anesthesia. Butorphanol, a mu antagonist, kappa agonist, also can be used as a premedication when used in combination with a phenothiazine tranquilizer such as acepromazine. Used alone, however, butorphanol's sedative effects are fairly unreliable and short-lived. Additionally, due to its receptor affinity, using butorphanol early in the course of anesthesia may prevent more potent drugs such as morphine and fentanyl from providing adequate analgesia in the early post-operative time period, depending on the length of surgery. For these reasons, this author does not routinely use butorphanol, favoring more potent and more reliable opioids such as morphine and fentanyl. Fentanyl, a pure opioid agonist, is potent opioid with a very short duration of action. It should be used in very critical patients for analgesia, then as part of an induction protocol. When used as a premedication, induction of general anesthesia should occur shortly thereafter, within approximately 20 minutes, or the drug should be given as a constant rate infusion until general anesthesia is induced. Phenothiazine tranquilizers, namely acepromazine, should be given to healthy animals as part of the premedication protocol. Acepromazine's antagonism of alpha-adrenergic activity can potentially induce vasodilation with subsequent hypotension, so should be used with caution. Other untoward side effects that have been reported include reduction of seizure threshold in predisposed animals. Thus, its use is relatively contraindicated in such patients. A potentially beneficial side effect of acepromazine is decreasing catecholamine-induced dysrhythmias. Alpha-2 agonists such as xylazine and medetomidine induce intense peripheral vasoconstriction, AV nodal block, bradycardia, and decrease in cardiac output. For these reasons, alpha-2 agonists should never be administered to emergency and critical care patients for absolutely any reason. The alpha-2 agonists may have their place in healthy animals, but should never be used in emergent settings. Anesthetic Induction Anesthetic induction should occur rapidly. The most critically ill patients often will benefit from pre-oxygenation prior to induction. An intravenous catheter should be in place prior to induction, for maintenance of vascular access. Benzodiazepene tranquilizers such as diazepam (0.3 - 0.5 mg/kg IV) or midazolam can be used. Diazepam induces more reliable tranquilization and is less expensive than the more costly midazolam. If given alone, diazepam can potentially induce excitement; therefore, this drug is often used in combination with dissociative agents such as ketamine (5.5 mg/kg IV, 10 - 30 mg/kg IM), opioids such as fentanyl (10 mcg/kg IV), or in combination with etomidate (0.5 - 1.5 mg/kg IV). Ketamine is a dissociative anesthetic agent that will initially cause a catecholamine-induced increase in cardiac output. In critically ill patients that have maximized sympathetic tone, however, ketamine can decrease cardiac contractility; therefore its use is relatively contraindicated. Ketamine, when used pre-intra- and post-operative, can decrease activation of NMDA receptor-mediated "wind-up" and decrease post-operative pain even days after surgery. Its use in combination with other analgesic agents is therefore beneficial, especially in controlling post-operative orthopedic pain. Propofol (4 - 7 mg/kg IV) is another drug that can be used to induce general anesthesia. Unrelated to other pharmacologic agents, propofol induces rapid anesthesia. Recovery from Propofol is also very rapid in most cases. Potential untoward effects of this drug include vasodilation and hypotension, and apnea. In cats, Propofol should not be used on consecutive days due to the potential for development of Heinz body anemia. In the most critically ill patients, Etomidate can be administered along with Diazepam with minimal effects on cardiovascular status. Anesthetic Maintenance and Monitoring Immediately after successful induction of anesthesia, anesthesia should be maintained with an appropriate gas anesthetic agent. For short procedures in cardiovascularly stable patients, Propofol can be administered as a constant rate infusion (6 - 20 mg/kg/hour). It must be remembered, however, that Propofol has no analgesic properties; therefore, if a painful procedure is to be performed, appropriate analgesia should be administered prior to recovery from anesthesia. Proper anesthetic monitoring including pulse oximetry, electrocardiogram, temperature, capnography, and blood pressure should be performed and recorded for even "apparently routine" procedures. In many critical patients, pre-, intra- and post- anesthetic hypotension is a potential hazard that should be carefully addressed. First, the level of gas anesthesia should be decreased. Secondly, a fluid bolus (5 - 10 ml/kg) can be administered IV. All patients under general anesthesia should have vascular access. If a patient is hypotensive and hemodilution or true anemia is a concern, synthetic colloids such as Hetastarch or Oxyglobin can be administered as an IV bolus (5 ml/kg). Alternatively, component blood products such as whole blood, packed red blood cells, or fresh frozen plasma can be administered depending on the primary problems at hand. If decreasing anesthetic depth and fluid bolus does not sufficiently increase blood pressure, use of a positive inotrope such as dobutamine (2 - 20 mcg/kg/min IV CRI) can be administered. Dopamine at lower doses (2 - 10 mcg/kg/min IV CRI) stimulates cardiac contractility through beta-adrenergic stimulation. Dobutamine, primarily a beta- agonist, stimulates cardiac contractility and as such, indirectly increases blood pressure. Dobutamine increases blood pressure more reliably than dopamine. Ephedrine is a synthetic sympathomimetic drug that stimulates both alpha- and beta-adrenergic receptors to stimulate catecholamine release. Bolus injection of ephedrine (0.1 - 0.25 mg/kg IV) has a longer duration of action than dobutamine, thus does not require administration as a constant rate infusion. If none of the above options are successful, vasopressor agents such as dopamine (> 10 mcg/kg/minute IV CRI), epinephrine (0.05 - 0.4 mcg/kg/min IV CRI), and norepinephrine (0.05 - 0.4 mcg/kg/min IV CRI) can also be administered. It is important to remember that agents that induce peripheral vasoconstriction may increase blood pressure but not necessarily improve renal, cerebral, and coronary blood flow. Management of Perianesthetic Hypotension In many critical patients, pre-, intra- and post- anesthetic hypotension is a potential hazard that should be carefully addressed. First, the level of gas anesthesia should be decreased. Secondly, a fluid bolus (5 - 10 ml/kg) can be administered IV. All patients under general anesthesia should have vascular access. If a patient is hypotensive and hemodilution or true anemia is a concern, synthetic colloids such as Hetastarch or Oxyglobin can be administered as an IV bolus (5 ml/kg). Alternatively, component blood products such as whole blood, packed red blood cells, or fresh frozen plasma can be administered depending on the primary problems at hand. If decreasing anesthetic depth and fluid bolus does not sufficiently increase blood pressure, use of a positive inotrope such as dobutamine (2 - 20 mcg/kg/min IV CRI) can be administered. Dopamine at lower doses (2 - 10 mcg/kg/min IV CRI) stimulates cardiac contractility through beta-adrenergic stimulation. Dobutamine, primarily a beta- agonist, stimulates cardiac contractility and as such, indirectly increases blood pressure. Dobutamine increases blood pressure more reliably than dopamine. Ephedrine is a synthetic sympathomimetic drug that stimulates both alpha- and beta-adrenergic receptors to stimulate catecholamine release. Bolus injection of ephedrine (0.1 - 0.25 mg/kg IV) has a longer duration of action than dobutamine, thus does not require administration as a constant rate infusion. If none of the above options are successful, vasopressor agents such as dopamine (1 - 10 mcg/kg/minute IV CRI), epinephrine (0.05 - 0.4 mcg/kg/min IV CRI), and norepinephrine (0.05 - 0.4 mcg/kg/min IV CRI) can also be administered. It is important to remember that agents that induce peripheral vasoconstriction may increase blood pressure but not necessarily improve renal, cerebral, and coronary blood flow or oxygen delivery. In any patient with tachy- or bradyarrhythmias such as AV block, bradycardia, or sinus or ventricular tachycardia, attempts should be made to treat the dysrhythmia. Anticholinergic drugs such as atropine or glycopyrollate should be administered to treat cardiovascularly unstable bradyarrhythmias. In some cases, if the heart rate is 50, and the animal's blood pressure is stable and normal, treatment may not be necessary, However, if the animal is bradycardic and hypotensive, interventions should be implemented. Sinus tachycardia can adversely affect blood pressure by decreasing the amount of time the heart has to fill. Decrease in diastolic filling will result in a decreased cardiac wall stretch available for rebound, the force necessary for normal myocardial contraction. Therefore, filling the cardiovascular space with fluids, and in some cases, INCREASING anesthetic depth if the animal is actually feeling the procedure, may be necessary to decrease heart rate. Ventricular dysrhythmias should be treated with a combination of crystalloid/colloid therapy, oxygen, and drugs such as lidocaine (2 mg/kg IV bolus, followed by 50 - 100 mcg/kg/minute IV CRI) or procainamide. Procainamide can contribute to refractory hypotension, and is not the antiarrhythmic of choice in a patient with hypotension. Conclusions: "What's the Bottom Line?" In the emergent situation, there may not be enough time to take a "wait and see if this works" kind of approach. One of the most important things to remember is that gas is poison. Many animals, particularly those that are critically ill, are exquisitely sensitive to the cardiorespiratory effects of inhalant anesthetic gases. For this reason, when an animal is hypotensive, one of the first things to consider is turning down the anesthetic vaporizer. If there is concern about an animal waking up during the anesthesia and surgery, balanced anesthesia with constant rate infusions of fentanyl or fentanyl and ketamine can be administered, to decrease the total amount of anesthetic gas required to maintain an adequate plane of anesthesia without causing hypotension and cardiovascular compromise. Next, (or sometimes simultaneously), a crystalloid (10 ml/kg) or colloid (5 ml/kg) fluid bolus can be administered, to fill up the vasodilated vascular beds. When a blood vessel dilates, a state of relative hypovolemia occurs, in which there is inadequate circulating volume to maintain vascular tone and cardiac preload. If there is insufficient myocardial stretch, the force of contraction is limited, and thus, can result in impaired cardiac output and a decrease in systemic blood pressure. Many anesthetic agents render the cardiovascular system incapable of compensatory changes such as vasoconstriction, so blood pressure and thus tissue perfusion and oxygen delivery become compromised. If decreasing the anesthetic depth and administration of fluids does not cause an increase in blood pressure, then positive inotropes (dobutamine and/or ephedrine) and vasopressors (dopamine) can be administered. Having an "anesthetic book" that contains charts of all of the necessary drugs, instructions on how to dilute each drug, resulting concentration, and volume of the diluted drug to administer to each patient based on body weight can save a lot of time and quick arithmetic in an emergent situation. |
