|
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. Pre- and Post-Operative Care of the Gdv Patient Introduction Gastric dilatation-volvulus (GDV) is a common, life-threatening emergency in veterinary medicine, and accounts for 0.8% - 2.8% of animals presented to veterinary emergency clinics. In animals with GDV, mortality rates range from 15 - 33%. While GDV can occur in any species, dogs are most commonly affected, although the syndrome has been reported in cats, guinea pigs and primates. The most commonly affected breeds of dogs appear to be giant- and deep-chested. Prompt recognition of clinical signs, rapid triage and assessment of each patient's clinical status, and immediate resuscitative measures are necessary for increasing the chances of a successful outcome. The exact cause of GDV remains unknown, although numerous variables have been implicated to have an underlying role in its development. Etiologies that have been proposed include elevated gastrin levels, altered myoelectric function, decreased gastric motility, decreased esophageal motility, dietary risk factors including type of food, and frequency method of feeding, breed, increasing age, hepatogastric ligament laxity, and increased thoracic depth:width ratios. Failure of eructation and delayed/impaired gastric emptying have also been hypothesized to play a role in the development of GDV in some dogs. To date, no one causative factor has been definitively associated with all cases of GDV. A unifying hypothesis has been suggested in which failure of normal eructation and pyloric outflow abnormalities play a role in the development of gastric dilatation with and without volvulus. Pathogenesis and Pathophysiology Malpositioning and rotation of the stomach around its axis causes obstruction to inflow and outflow, resulting in the rapid accumulation of intraluminal fluid and gas. It is thought that the stomach rotates first, then becomes distended with gas. As the patient becomes uncomfortable, aerophagia can result in further gas accumulation within the stomach. Gastric distension results in increased gastric pressure, and compression of the diaphragm and great vessels, including the caudal vena cava. Inadequate venous return to the right heart subsequently decreases cardiac preload, with a decrease in cardiac output. Decreased perfusion to the gastric mucosa and serosa also result in the release of inflammatory cytokines including IL-10, and tumor necrosis factor. Increased levels of urinary 11-dehydro-thromboxane B2, an indicator of oxidative stress, have been documented in animals with naturally-occurring GDV. Further, areas of gastric ischemia have increased anaerobic glycolysis causing lactic acid to accumulate. The engorged stomach may increase portal pressures and result in bacterial translocation. One study did demonstrate the presence of bacteremia in dogs with GDV, but not significantly different from control dogs. Areas of gastric ischemia may proceed to necrosis if rapid intervention is not performed. The net result of acidosis and activation of inflammatory cascade causes depression of cardiac contractility, further reducing cardiac output. As cardiac output declines, so does diastolic and mean arterial blood pressures. Diastolic blood pressure less than 40 mm Hg compromises coronary artery circulation, and may result in areas of myocardial ischemia. Combined with electrolyte imbalances, ventricular dysrhythmias are a common finding in patients presenting with GDV. Cardiac troponins are enzymes that are specifically released from damaged myocardium. Cardiac troponin levels have been shown to be elevated in dogs with GDV and thoracic trauma. Ventricular dysrhythmias with rates greater than 160 beats per minute further compromise cardiac output due to impaired diastolic filling times, and impaired coronary perfusion. Myocardial oxygen demand increases with worsening tachycardia, and myocardial ischemia with myocardial acidosis cause further declines in cardiac output and blood pressure. Without therapeutic intervention, dysrhythmias perpetuate dysrhythmias and contribute to overall morbidity and mortality. Hypoxemia, respiratory acidosis, and ventilation-perfusion impairment can also result from inadequate ventilatory capacity caused by the distended stomach compressing the diaphragm. Treatment, therefore, is directed at correcting the cause of shock. Hyperventilation can potentially cause a respiratory alkalosis. Therefore, increasing venous return to the heart with intravenous fluid therapy, gastric decompression, and treatment of dysrhythmias are of paramount importance in the early treatment of shock in patients with GDV. Triage and Assessment In most cases of GDV, the client's primary complaint is retching or unproductive vomiting. Commonly, the owner describes vomiting white foamy froth. These initial complaints should increase the index of suspicion for GDV in commonly affected breeds, always remembering that GDV can occur in any breed of dog, as well as other domestic species. The most common clinical signs include nonproductive vomiting, gastric distension, ptyalism, restlessness, and straining to defecate. Whenever a client calls ahead that an animal with suspected GDV is en route to your hospital, the triage team should be mobilized and prepared for the patient's arrival. Whenever possible, set-up should include supplies necessary for placement of a possible GDV is en route to the hospital, the triage team is mobilized, setting up for rapid administration of intravenous fluids, gastric decompression through trocarization or placement of an orogastric tube, flow-by oxygen, and blood analyses including a complete blood count, biochemical profile, serum lactate measurement, and coagulation tests. Once a patient arrives at your clinic with suspected GDV, the most important aspect of intervention is to stabilize the patient's cardiovascular status first, prior to taking any abdominal radiographs. This author's preference is to place as large bore a catheter as possible into the cephalic vein initially, to improve fluid flow. A large-bore intravenous catheter should be placed in the most readily accessible vein, often the cephalic vein or jugular vein. In very large dogs (> 30 kg), 14 gauge catheters can be placed in both cephalic veins to allow rapid fluid resuscitation. If necessary, a catheter can also be placed in the lateral saphenous vein; however, compromise of venous return may limit the amount of fluid administered until gastric decompression occurs. Once a patient is more hemodynamically stable, a central venous catheter can be placed for further blood sample collection and possible central venous pressure measurements. Radiographs A right lateral abdominal radiograph is the best view to confirm the presence of GDV. With the right lateral abdominal radiograph, the pylorus is displaced cranially and dorsally to the fundus, and appears as an area of plication or compartmentalization between the two areas of the stomach. Rarely, the stomach turns in a counter-clockwise direction around its axis, and compartmentalization of the pylorus and fundus are only apparent on a left lateral view. The presence of pneumoperitoneum is highly suggestive of gastric rupture, and warrants immediate surgical exploration. The presence of pneumatosis, or air within the gastric wall, is also an indicator of gastric necrosis, or can potentially be present due to therapeutic interventions such as trocarization to decompress the stomach. After decompression, it is also possible that the stomach has untwisted, and radiographic signs of GDV may not be readily apparent. Patients with suspected GDV that has intermittently untwisted should still be taken to surgery, as gastric serosal and mucosal integrity may be compromised, requiring gastric resection. Further, short gastric vessel avulsion or thrombosis, splenic torsion and thrombosis, and recurrence of GDV may also be present, requiring definitive repair. Bloodwork Blood samples for a complete blood count, PCV, total protein, coagulation profile (Prothrombin Time and Activated Partial Thromboplastin Time) or activated clotting time (ACT), serum biochemical profile, lactate, and electrolytes are drawn and measured at the time of catheter placement, before intravenous fluid therapy, whenever possible. Plasma lactate concentration > 6.6 mmol/L have been positively correlated with the presence of gastric necrosis and decreased survival in dogs with naturally occurring GDV. An elevated lactate cannot always be used to predict a definitive prognosis, however. The extent of gastric necrosis and potential for gastric resection must definitively be performed at the time of surgical repair. More recently, elevated serum cardiac troponin I and c levels have been shown to be predictive of myocardial damage and may be suggestive as a negative prognostic indicator in dogs with GDV. Some patients are hypokalemic at the time of presentation. Elevations in alanine transferase (ALT) are common. Thrombocytopenia is often present. Coagulation tests such as PT, APTT, and ACT may be prolonged. The presence of thrombocytopenia with prolonged coagulation tests increases the index of suspicion for disseminated intravascular coagulation (DIC). More definitive tests for DIC include D-dimers and elevations of fibrin degradation products (FDPs) in the absence of hepatic disease. In many cases, however, these tests must be sent to an outside laboratory, and can take hours to days to be returned. In the emergent GDV patient, any suspicion of DIC warrants consideration of therapeutic intervention. Initial Stabilization Flow-by oxygen should be administered as tolerated by the patient. An electrocardiogram should be attached to the patient and monitored, then watched carefully for the presence of dysrhythmias. Blood pressure monitoring by oscillometric or Doppler method should be obtained and measured at least every 5 - 10 minutes during the fluid resuscitation period. Fluid Therapy Once an intravenous catheter has been placed, crystalloid fluids should be administered. This author uses ¼ of the calculated shock volume (90 ml/kg/hour) initially, and gives this volume as rapidly as possible, often through a fluid pump or a pressure bag. Other treatment protocols can include use of hypertonic saline (7% hypertonic saline with dextran-70 5 ml/kg over 15 minutes. Once the intravenous fluid of choice has been administered, the patient's cardiovascular perfusion parameters, including blood pressure, capillary refill time, and heart rate occurs should be reassessed. Hemoglobin based oxygen carriers such as Oxyglobin®, can also be administered to help maintain intravascular colloid oncotic pressure and perfuse ischemic areas. If a patient remains hemodynamically unstable after a shock volume of fluids has been administered, or if hemodilution occurs, a combination of crystalloid plus a synthetic colloid should be considered. If a patient's PCV is less than 30% prior to surgery, Oxyglobin or packed red blood cells can be administered, depending on the degree of anemia. If anemia does not exist, but the patient's blood pressure is unstable, Hetastarch at a dose of 5 - 10 ml/kg bolus, followed by 20 ml/kg/day can be administered along with crystalloid fluids. Crystalloid dose should be decreased by 25 - 50% if a colloid is going to be administered simultaneously, as the colloid will help retain the crystalloid within the vascular space for a much longer period of time. Analgesia and anti-arrhythmic therapy While crystalloid fluids are being administered, pre-emptive intravenous lidocaine (1 - 2 mg/kg IV, then 50 mcg/kg/minute IV CRI) can be started to treat impending reperfusion injury. The lidocaine should be started even if ventricular dysrhythmias are not present at the time of presentation. The lidocaine CRI also has the added benefit of providing some analgesia to the GDV patient. Prior to decompression, an analgesic agent should be administered to alleviate patient stress and discomfort. Buprenorphine (0.005-0.02 mg/kg IM or IV), hydromorphone (0.1 - 0.2 mg/kg IV, IM, SQ Q4 - 6 hours), or fentanyl (2 mcg/kg IV, followed by 3 - 7 mcg/kg/hour IV CRI until anesthetic induction) should be administered prior to gastric decompression. The triage team can then proceed with gastric decompression, then surgical intervention as rapidly as possible. Gastric decompression Methods of decompression include trocarization or placement of an orogastric tube with subsequent orogastric lavage. Controversy currently exists whether passing an orogastric tube should be performed at all, particularly in the awake patient with cardiovascular compromise. Orogastric intubation for gastric decompression has been implicated as a causative role in esophageal perforation in one patient with GDV. Gastric trocarization should be performed. The abdomen is percussed, locating the most tympanic area. In general, the displaced fundus is located in the right lateral abdomen. Clip and aseptically scrub the right lateral abdomen. Gently but briskly push a 14 - 18 gauge over-the-needle catheter through the lateral abdominal wall into the distended, tympanic stomach. If bleeding through the catheter occurs, the spleen may have inadvertently been tapped, and repeat the procedure in a different location. Once the catheter is in the stomach, push it off of its stylette to allow the gas to escape. Advantages of gastric trocarization are that minimal personnel are required, the procedure is less stressful for the patient than orogastric intubation, and risk of stomach perforation is decreased. Disadvantages of the procedure are that gas accumulation may recur, requiring further trocarization, and gastric laceration or splenic trocarization can occur. Passing an orogastric tube is stressful in the awake patient, and runs the inherent risk of esophageal or gastric rupture or inducing a vagal response. To pass an orogastric tube, premeasure a large tube from the last rib rostrally to the tip of the mouth. Mark that spot on the tube with white tape. Lubricate the tip of the tube with warm water or sterile lubricant. Place a roll of 1 or 2 inch white tape into the patient's mouth and secure it caudal to the canine teeth. Tape the tape around the muzzle to minimize displacement of the roll of tape during placement of the orogastric tube. Place the tip of the tube through the center of the roll of tape, and gently but firmly pass the tube to the level of the tape marker on the tube. It is important to not force the tube if there is any resistance, as esophageal or gastric perforation can occur. In some cases, changing the position of the patient, such as standing the patient on its hind limbs with the forelimbs elevated, can assist in passing the tube by decreasing compression of the gastroesophageal angle. The ease of passing a stomach tube, or the mere success of passing the tube does not mean that volvulus is not present. Once the tube is in place, the stomach should be emptied of gas, then lavaged with warmed tap water using a lavage pump. The presence of gastric mucosa or blood in the gavage fluid is a negative prognostic sign, and is strongly suggestive of gastric mucosal necrosis. If no fluid is returned in the efflux, and the abdomen is becoming more tympanic despite successfully passing the orogastric tube, an important differential diagnosis is that the tube has perforated the stomach, warranting immediate surgical intervention. If this occurs, it certainly increases patient morbidity and risk of mortality. Anti-inflammatory and antioxidant drugs The empiric use of anti-inflammatory drugs in the patient with GDV remains controversial. Plasma endotoxin and other mediators of inflammation (thromboxane A2 metabolites) have been found to be increased in dogs with gastric dilatation-volvulus. Experimentally, allopurinol and deferoxamine, and dimethylsulfoxide have improved survival, but the benefits have not been duplicated in clinical patients with GDV. The use of prostaglandin synthesis inhibitors such as flunixin meglumine have been shown to decrease inflammatory cytokines such as prostacyclin, but have not been proven to be beneficial in improving outcome. Until there is evidence that anti-inflammatory drugs definitively improve outcome with GDV, the routine empiric use of steroids in the GDV patient is not warranted. Anesthesia Anesthetic management of the patient with GDV is often challenging. Premedications should be given to relieve anxiety, and to decrease the total dose of induction agents and inhalant anesthetics required to maintain general anesthesia without compromising cardiac output and arterial blood pressure. Pre-medications including buprenorphine (0.005-0.02 mg/kg IM,SQ, IV), hydromorphone (0.1 - 0.2 mg/kg IV, SQ, IM Q4 - 6 hours), or fentanyl (2 mcg/kg IV bolus) are appropriate, as they have minimal adverse effects on the cardiovascular system. Morphine should be avoided, whenever possible, due to its potent emetic effects. Phenothiazine tranquilizers such as acepromazine should be avoided, as their alpha-blockade effects may predispose the patient to vasodilation and hypotension. Induction agents that cause cardiovascular and respiratory depression should also be avoided. Propofol, although rapidly acting, can cause vasodilation and compromise cardiorespiratory status in a dose-dependent manner. Appropriate combinations of induction agents include an opioid with a benzodiazepine (Fentanyl (5-10 mcg/kg IV) + Diazepam (0.2-0.6 mg/kg IV), thiobarbiturates (Thiopental 13.2-26.4 mg/kg IV), or in extremely critical patients Etomidate (0.5-1.0 mg/kg IV) + Diazepam (0.2-0.6 mg/kg IV). Once anesthesia is induced and the patient is intubated, routine anesthetic monitoring including ECG, blood pressure, esophageal stethoscope, pulse oximetry, and end-tidal capnography should be performed. Until definitive decompression of the stomach occurs, tidal volume may be compromised by gastric compression of the diaphragm. Further, drugs that cause respiratory depression can exacerbate the situation by decreasing minute volume. Mechanical ventilation may be required to maintain adequate oxygenation and ventilation. Treatment of Cardiac Dysrhythmias Cardiac arrhythmias also are a concern during the pre-operative, perianesthetic, intraoperative, and post-operative time periods. The presence of pre-operative dysrhythmias are associated with an increased risk of mortality. Most commonly, arrhythmias are ventricular in origin, with uniform or multiform ventricular tachycardia, or R-on-T phenomenon. Often, clinicians wonder when to treat a ventricular dysrhythmia. Slow idioventricular rhythm with ventricular rates less than 130 beat per minute do not necessarily need antiarrhythmic therapy if the beats are unifocal in origin, return to isoelectric shelf in between beats (i.e. no R on T phenomenon), and if the blood pressure remains normal. In the awake patient, treatment of ventricular tachycardia is based on the following criteria: if premature ventricular beats are sustained at a rate greater or equal to 160 - 180 beats per minute, are sustained for more than 2 minutes, are multiform in nature, display a lack of return to baseline, (that is, no visible isoelectric shelf between beats) or the rhythm is compromising blood pressure. In the anesthetized patient, however, mechanisms to compensate for cardiac dysrhythmias are impaired, and the patient may not tolerate even a few abnormal beats if the dysrhythmia becomes sustained. The constant rate infusion of lidocaine (50 mcg/kg/minute) can be titrated up to 100 mcg/kg/minute as necessary to help control malignant cardiac dysrhythmias. Other causative factors for ventricular dysrhythmias include decreased apparent circulating blood volume. Crystalloid fluid boluses of 5 - 10 ml/kg can be administered to the anesthetized animal. Additionally, increased circulating catecholamines can predispose an irritated myocardium to ectopic beats. Although the animal may appear anesthetized, pain perception under anesthesia can occur, causing the release of catecholamines. If the animal's blood pressure is stable, with a mean equal to or greater than 80 mm Hg, you can also try increasing the anesthetic depth, in the inadvertent chance that patient's pain perception, although anesthetized, is contributing to ventricular dysrhythmias. Management of Hypotension Other important factors for consideration during the perianesthetic period include maintaining adequate cardiac output and sustaining a mean arterial blood pressure of 80 mm Hg. Inhalant anesthetic agents negatively affect the cardiovascular system in a dose-dependent manner. The use of a constant rate infusion of fentanyl (5-30 mcg/kg/hour) during the intra-operative period can allow the clinician to decrease inhalant anesthetic depth and improve blood pressure. At doses required to augment general anesthesia, fentanyl causes respiratory depression, and therefore mechanical or assisted ventilation should be performed when using this drug as a constant rate infusion during perianesthetic periods. Maintenance of adequate circulating volume with 5 - 10 ml/kg/hour intravenous crystalloid fluids should also assist in maintaining adequate cardiac preload. If excessive blood loss or hemodilution has occurred or is anticipated (for example with rupture of splenic or short gastric vessels), red blood cell products or Oxyglobin can also be administered to improve oxygen carrying capacity and oxygen delivery. If decreasing gas anesthetic depth and improving cardiac preload with intravenous fluid boluses do not improve blood pressure, the clinician should be prompted to start pressors and inotropic agents to improve cardiac contractility, Dobutamine (5 - 20 mcg/kg/minute) and/or dopamine (5 - 10 mcg/kg/minute) as constant rate infusions should be started. Ephedrine, a synthetic sympathomimetic, can also be administered as a bolus (0.1 - 0.25 mg/kg IV) to improve cardiac contractility. Finally, if inotropic support alone does not improve blood pressure, a pressor such as epinephrine (0.05-0.4 mcg/kg/min) or norepinephrine (0.05-0.4 mcg/kg/min) should be reserved for patients who fail to respond to other supportive measures to improve blood pressure. Surgical Intervention Definitive surgical repair first requires rapid decompression and derotation of the stomach, then evaluation of the extent of vascular compromise to the stomach and the spleen. Following routine ventral midline approach to the abdomen, the greater omentum will be visible over the stomach. The stomach should be lifted and gently but firmly rotated to its original position. A large bore stomach tube can then be passed for gastric lavage by the anesthetist, to help prevent further gas accumulation during surgery. The short gastric vessels should be carefully evaluated for thrombosis or rupture, as both commonly occur. Next, the spleen should be carefully evaluated for evidence of thrombosis or twisting around the pedicle. If splenic torsion is present, the spleen should be removed without returning it to its original position, to prevent the release of proinflammatory cytokines into circulation. The entire abdominal cavity should then be systematically explored prior to definitive gastropexy. This approach allows the stomach to become reperfused, and allows the clinician a more accurate assessment of the degree of gastric serosal and mucosal compromise which may necessitate partial gastrectomy. Gastric necrosis and partial gastrectomy, with or without the need for splenectomy, is associated with an increased risk of mortality. The entire serosal surface of the stomach should be evaluated. The surgeon should feel carefully for all tissue layers. Any areas of black or dark brown-red tissue should be removed. The area on the greater curvature near the esophageal hiatus is a common place for necrosis. Although invagination of the affected area has been suggested and used in the past, any area of necrotic tissue can be an inciting cause for disseminated intravascular coagulation or gastric ulceration and hemorrhage and therefore, this technique should be avoided. Definitive gastropexy should then be performed, and the abdomen closed routinely. Several techniques for partial gastrectomy and gastropexy have been described, and are beyond the scope of this monograph. The use of ventral midline incisional gastropexy has been described, but increases the risk of gastric perforation if subsequent abdominal surgeries are performed, and thus, are contraindicated. Post-operative Care In the post-operative period, cardiac dysrhythmias are common. Continuous ECG, and blood pressure monitoring become necessary. The pre-emptive treatment with lidocaine (50 - 100 mcg/kg/minute IV CRI) is beneficial in preventing arrhythmias, providing an analgesic effect, and promoting gastrointestinal motility. Post-operative pain management is essential. Fentanyl as a constant rate infusion (3 - 7 mcg/kg/hour) is a potent method of providing analgesia with minimal untoward side effects. Other appropriate analgesic agents for use in the post-operative period include Buprenorphine (0.01-0.015 mg/kg IM or IV), morphine sulfate (0.5-2.0 mg/kg IM or SQ), and hydromorphone (0.1 - 0.2 mg/kg IV, SQ, IM). Opioids, particularly morphine sulfate may predispose the patient to ileus. Therefore, promotility agents such as metoclopramide (1-2 mg/kg/day) can be administered as a constant rate infusion to help prevent ileus, however, the constant rate infusion of lidocaine is often effective at treating post-operative ileus associated with surgery and narcotic administration. If a post-operative GDV patient is actively vomiting or regurgitating, antiemetics such as metoclopramide (1 - 2 mg/kg/day IV CRI), dolasetron (Anzemet 0.6 mg/kg IV once daily) or ondansetron (0.22 mg/kg IV Q8 - 12h) should be administered. Reflux esophagitis can occur, and warrant the use of a histamine receptor blocker such as famotidine (0.5 - 1 mg/kg IV once to twice daily). Proton pump inhibitors such as omeprazole (0.5 - 1.0 mg/kg PO once daily), can also be used in an actively vomiting or regurgitating patient. The question of when and how to feed the post-operative GDV patient remains controversial, and is largely based on individual clinician preference. Enterocytes will undergo atrophy within 24 - 48 hours of lack of luminal nutritional support. As such, feeding should begin as soon as possible. In most instances, a simple routine case of GDV without evidence of gastric necrosis can be fed with 12 - 24 hours of anesthetic recovery. If gastric resection is necessary, or if severe gastric atony is present at the time of surgery, a feeding tube can be placed to allow provision of adequate nutrients in the post-operative recovery period. Disseminated intravascular coagulation (DIC) sometimes occurs in animals with GDV. Daily activated clotting times, coagulation profiles (PT and APTT), and platelet counts should be performed in house. It is important to remember that an animal can be in DIC even with platelet counts within a normal reference range. We often do not know what the animal's platelet count was prior to the onset of GDV and subsequent surgery. For this reason, the platelet count may have decreased significantly, but still be within the normal reference range. Measuring trends in platelet numbers can help lead to a suspicion of DIC. Definitive testing of D-dimers and fibrin degradation products (FDPs) can also be performed. If there is any question of DIC, the patient should be given transfusions of fresh frozen plasma to replace clotting factors and antithrombin. Currently, the use of heparin in the treatment of DIC is controversial, and this debate is beyond the scope of this monograph. Crystalloid fluids at a maintenance rate of (30 x Body weigh in kg + 70) should be administered for maintenance fluid requirements until the animal is eating and drinking normally. Antibiotics such as cefazolin (22 mg/kg IV TID - QID) should be administered if gastric resection has been performed, but are unnecessary in the absence of gastric resection. Empiric use of famotidine (1 mg/kg IV BID) is recommended due to the potential for gastroesophageal reflux. In conclusion, gastric dilatation-volvulus is a common emergency in veterinary medicine. Being prepared, anticipating the worst, and treating aggressively from the start in a systematic manner can allow many successful outcomes for this challenging disease entity in your emergency room. References available upon request. 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. Emergency Management of Congestive Heart Failure Congestive heart failure (CHF) is unfortunately a common problem that presents to the veterinary small animal practitioner. In some cases, a patient presents to you with acute exacerbation of previously diagnosed and treated cardiac disease. Other animals, however, may present to you with vague and nonspecific clinical signs in a previously healthy animal. Clinical signs may include weakness and exercise intolerance, cough, lethargy, inappetance, vomiting, diarrhea, and syncope or collapse. Depending on the primary cause and severity of the cardiac disease, clinical signs can vary from patient to patient, and by no means are pathognomonic for cardiovascular disease at all. A presumptive diagnosis often is made on the patient's primary presenting complaints, signalment, a thorough history, and physical examination findings. One of the most important concepts to remember in the diagnosis and management of any patient with CHF is to minimize patient stress and do no harm. PHYSICAL EXAMINATION A careful physical examination is essential in the diagnosis and management of the patient in CHF. In some cases, the patient should be placed in an oxygen cage or receive flow-by oxygen supplementation, and observed from a distance. The restraint of handling for physical examination and diagnostics can sometimes push the most stressed patients over the edge. Observe the patient from afar. What is the respiratory rate and effort? Is there any fluid from the nares or mouth? Does the abdomen look distended? Is the patient able to stand or are they weak? Next, approach the patient, and perform a systematic examination starting from head to toe. What are the mucous membrane color and capillary refill time? Are the mucous membranes pale pink or do they appear cyanotic? Is the capillary refill time prolonged? Next, look carefully at the thoracic inlet and jugular groove. Is there jugular venous distension or a jugular pulse? Auscult the heart for the presence of murmurs or cardiac dysrhythmias. Is the heart difficult to hear and are the heart sounds muffled? Simultaneously palpate the inguinal region for a femoral pulse. Are the pulses strong or are they weak? Are they synchronous or dysynchronous with the heart rate? Are the pulses absent in a patient with acute onset of respiratory distress and hind- or forelimb paralysis? Auscult all lung fields for the presence of pulmonary crackles or wheezes. Palpate the abdomen for hepatomegaly and the presence of a ballotable fluid wave. Palpate the distal extremities. Are they warm to the touch, or do they feel cold due to poor peripheral circulation? Finally, perform a rectal examination and observe whether bloody feces is present. Patients with fulminant pulmonary edema from left sided CHF may have blood-tinged fluid coming from the nares and mouth and have concomitant pulmonary crackles and a rapid restrictive respiratory pattern. A cardiac murmur is often present in cases of severe mitral insufficiency, but in some cases, the heart may be difficult to hear beyond harsh pulmonary crackles. Cardiac dysrhythmias may or may not be present. Pulse quality may be supportive of low output cardiac failure. Pulses may be absent in cases of severe low output failure, or in cases of arterial embolism. Jugular venous distension and jugular pulses may be visible in cases of right-sided heart failure. Heart sounds may be muffled to absent in cases of pleural or pericardial effusion. Hepatomegaly and a fluid wave may be present on abdominal palpation in cases of right-sided heart failure. Distal extremity coolness and hematochezia on rectal examination may be present due to low cardiac output. DIAGNOSTIC TESTS ECG An electrocardiogram should be considered in all patients with clinical signs of CHF. A lead II ECG may reveal signs of cardiomegaly or dysrhythmia, but in some cases, may simply display a sinus tachycardia. A six-lead ECG may reveal axis deviation in cases of right-sided cardiomegaly. A characteristic ECG abnormality sometimes observed in cases of pericardial effusion is electrical alternans where the ECG complexes alternate from large to small as the heart floats to and fro within the fluid in the pericardial sac. Supraventricular and ventricular tachyarrhythmia and atrial fibrillation are common rhythm disturbances in cases of dilative cardiomyopathy. Radiograph Interpretation In most cases, thoracic radiographs are one of the most important diagnostic tools in making a diagnosis of CHF. Lateral and dorso-ventral radiographs should be performed once the patient is clinically stable. Increased perihilar interstitial to alveolar infiltrates are characteristic of pulmonary edema. Left atrial enlargement may be observed as a "back-pack" sign at the caudal cardiac waist. Right-or left-sided cardiomegaly may also be present in cases of valvular insufficiency. In cats, increased sternal contact and a classic valentine-shaped heart may be observed in cases of hypertrophic cardiomyopathy. A vertebral heart sum/score can be calculated to determine the degree of cardiomegaly in dogs and cats. The vertebral heart sum can be calculated by performing the following steps:
Echocardiogram In emergent patients with CHF, an emergency echocardiogram is often not warranted, particularly if there is radiographic evidence of left atrial enlargement and perihilar pulmonary edema. Echocardiography is often helpful, however, in distinguishing between pericardial effusion and dilative cardiomyopathy, if radiographic changes are equivocal. M-mode echocardiography is useful in calculating the left ventricular chamber size dimensions during systole and diastole. The calculated fractional shortening is a useful loose indicator of cardiac contractile function in the patient with CHF. Blood Pressure Arterial blood pressure can be measured through direct or indirect methods. The gold standard of arterial blood pressure measurement is through cannulation of an artery with a catheter connected to a pressure transducer. In the emergent patient with CHF, however, it is relatively contraindicated to restrain the patient for placement of the arterial catheter until the patient is more stable. Indirect measurements using Doppler or Oscillometric techniques, therefore, should be used to monitor blood pressure in the critical patient. Mean arterial blood pressure should remain above 60 mm Hg at all times. Mean arterial blood pressure is a function of cardiac output and systemic vascular resistance. Cardiac output is influenced by preload, afterload and contractility. Depending on the type of heart failure present, cardiac output can be adversely affected for a number of reasons, leading to hypotension, poor tissue perfusion, and impaired oxygen delivery. Cardiac preload can be decreased in patients with right ventricular failure or pericardial effusion. Afterload can be increased in patients due to peripheral vasoconstriction. Contractility can be impaired in cases of dilative cardiomyopathy or chronic myocardial ischemia. Knowledge of a patient's blood pressure is necessary in order to provide therapeutic intervention to improve preload, decrease afterload, and improve cardiac contractility. Oxygen saturation Edema fluid can cause severe pulmonary diffusion impairment and lead to hypoxia in the patient with CHF. Oxygen saturation can be measured using an arterial blood sample, or by non-invasive pulse-oximetry. The gold standard of measuring a patient's oxygenation status is through arterial blood sampling. In many cases in the emergent patient, however, the restraint required to obtain an arterial blood sample is absolutely contraindicated. Therefore pulse oximetry can be attempted. In some patients with severe hypotension, peripheral vasoconstriction, and patient movement secondary to respiratory distress, an accurate pulse oximetry reading may be extremely difficult to obtain. A rule of thumb is to attempt to obtain the reading if it can be done without causing undue stress to the patient. When in doubt, always place the patient in oxygen and gauge oxygenation status by changes in the patient's respiratory rate and effort and the clearing or pulmonary crackles on thoracic auscultation. Oxygen saturation by arterial blood sampling or pulse oximetry can be attempted when the patient is clinically more stable. EMERGENCY THERAPY Emergency management of the patient in CHF consists improving systemic oxygen delivery and minimizing patient stress. Oxygen delivery is a function of both oxygen uptake by the respiratory system, cardiac output, and hemoglobin concentration. The mainstay of therapy for treatment of congestive heart failure is to provide supplemental oxygen and decrease fluid buildup within the lungs. Oxygen Flow-by oxygen should be administered to patients with congestive heart failure as a physical examination is taking place. Flow-by oxygen is well-tolerated, and requires minimal physical restraint. Because flow-by is a relatively inefficient method of providing an increase in the fraction of inspired oxygen, other methods including oxygen hoods, oxygen cages, nasal, nasopharyngeal and tracheal oxygen insufflation should be used for long-term therapy. Oxygen hoods are available commercially, or can be manufactured in hospital using a firm Elizabethan collar, white tape, and saran wrap. Most patients tolerate oxygen hoods readily; however, panting, increased condensation, and iatrogenic hyperthermia can develop, so the patient needs to be monitored carefully. Nasal or nasopharyngeal oxygen supplementation are well-tolerated for long-term oxygen supplementation. A red rubber (5 - 8 French) catheter or Argyle infant feeding tube can me measured from the ramus of the mandible (nasopharyngeal) or from the medial canthus of the eye (nasal). The tube should be marked, and the tip lubricated with lidocaine jelly. The tube should be inserted ventrally and medially, directing the nasal philtrum dorsally to facilitate passing of the tube either to the level of the medial canthus of the eye or into the nasopharynx. Humidified oxygen flow rates can be administered at 50 - 100 ml/kg/minute. Severe cases of congestive heart failure with severe fulminant pulmonary edema may benefit from endotracheal intubation and some form of artificial ventilation with positive end expiratory pressure (PEEP). Diuretics Aside from supplemental oxygen supplementation, furosemide is one of the most important therapies for management of the patient with congestive heart failure and pulmonary edema. Furosemide can be administered as a bolus (4 - 8 mg/kg IV or IM), or as a constant rate infusion (0.66 - 1 mg/kg/hour IV) to promote diuresis and decrease pulmonary vascular overload and pulmonary edema. The goal of diuretic treatment is to repeat the therapy every 30 - 60 minutes until the patient's body weight has decreased by 5 - 7%. Once the patient's respiratory rate and effort has normalized, oral furosemide can be started. Serum electrolytes can become deranged with repeated administration of loop diuretics. Closely monitor the patient's serum potassium and sodium concentrations. Nitric Oxide Donors Nitric oxide donors should be initiated as a primary initial therapy in any patient with fulminant congestive heart failure. Nitric oxide donors cause dilation of the pulmonary vasculature and a relative decrease in pulmonary vascular pressures. Nitroglycerine paste is not absorbed across the skin as was once thought, and has fallen out of favor for use in veterinary patients. In patients with refractory pulmonary edema that is not responding to traditional diuretic therapy, sodium nitroprusside should be considered, as long as the patient is not hypotensive. Sodium nitroprusside is a balanced arteriolar and venous dilator that decreases both pulmonary and systemic vascular resistance. The drug is administered as a constant rate infusion (2 - 10 mcg/kg/minute IV, titrated to effect). Because of its potent hypotensive effects, arterial blood pressure must be monitored closely throughout the infusion. Morphine Morphine is an opioid agonist that is useful in patients with congestive heart failure. In dogs, low dose (0.025 - 0.05 mg/kg IV) morphine dilates the splanchnic vasculature and increases venous capacitance, allowing drainage of fluid from the pulmonary parenchyma. Morphine provides the additional benefits of allowing slower, deeper respirations, and decreasing anxiety in patients with congestive heart failure. Positive Inotropes Dobutamine is a synthetic beta-adrenergic agonist that is sometimes useful improving inotropic activity of the myocardium in severe cases of CHF, specifically in patients with dilative cardiomyopathy. At lower doses, dobutamine improves cardiac contractility with minimal effects on chronotropy or heart rate. This improves contractile function with minimal effects on myocardial oxygen demand. At higher, doses, however, dobutamine can be pro-arrhythmogenic, and therefore, the patient's ECG should be monitored carefully during the constant rate infusion. Dobutamine can be administered at a dose of 2 - 20 mcg/kg/minute. Potential side effects include tachyarrhythmias (at higher doses), facial twitching, and seizures. Pimobendan is a newer drug that has been used with some success in Europe and Canada in dogs with CHF secondary to DCM and mitral valve insufficiency. Pimobendan is a phosphodiesterase-III inhibitor that sensitizes the myocardium to calcium, and improves inotropic activity in addition to causing arteriolar and venous dilation. The drug is available under special license in the United States. Conclusions Irrespective of the underlying cause, patients with CHF must be managed carefully and aggressively following initial diagnosis. Supplemental oxygen, potent diuretics, and nitric oxide donors continue to be the mainstay of therapy in both cats and dogs during the initial management of CHF. Patients that do not respond to standard therapies may require additional drug protocols, including positive inotropic and intravenous vasodilatory drugs. Careful monitoring of the patient's heart rate and rhythm, arterial blood pressure, respiratory rate and effort, and pulse oximetry or arterial oxygen saturation should be performed to evaluate the patient's response to therapy. References available upon request. Albumin Therapy in the Critically Ill Patient Albumin is a protein that is synthesized by a normally functioning liver, and inarguably, is one of the most important proteins in the body. Approximately 60 -70% of total body albumin is located within the extravascular, interstitial space, and the remaining 30- 40% is located within the intravascular space. The interstitial pool provides a large storage vat from which to draw during states of albumin loss or decreased albumin synthesis in order to maintain colloid oncotic pressure of the serum. and serves a key role in the maintenance of colloid oncotic pressure, free-radical scavenging, mediator of coagulation, transport of exogenous and endogenous substrates, buffering of serum, and contributor to wound healing. The consequences of hypoalbuminemia are dramatic, and include decreased colloid oncotic pressure, increased endothelial permeability, delayed wound healing, and edema formation in tissues. During states of health, albumin contributes approximately 50% to the serum total protein and 80% to the serum colloid oncotic pressure. Once significant hypoalbuminemia ([albumin] < 2.0 g/dL) develops, the intravascular hydrostatic pressure can exceed intravascular colloid oncotic pressure, and lead to efflux of fluid from the intravascular space into the interstitium and overwhelm the lymphatic drainage system and lead to pulmonary and other organ system edema. The consequences of edema include decreased tissue perfusion and oxygen delivery, tissue ischemia, and tissue hypoxia. Although the physical manifestations of edema can be obvious as subcutaneous swelling and edema in the face, extremities, and ventral thorax and abdomen, globally and more importantly, edema can result in organ dysfunction in the cerebrum, lungs, and gastrointestinal tract. In animals and humans with hypoalbuminemia, gastrointestinal manifestations include ileus, delayed gastric emptying, enteral feeding intolerance, decreased nutrient absorption, gastrointestinal edema, and bacterial translocation. Both humans and animals with hypoalbuminemia < 2.0 g/dL have increased morbidity and mortality. A wide variety of critical illnesses can result in, and become exacerbated by hypoalbuminemia. Such illnesses include pancreatitis, heat-induced illness, pneumonia, parvoviral enteritis, sepsis, pancreatitis, burn injury, crush injury, prostatitis, and pyometra. Maintenance of organ perfusion and oxygen delivery through use of crystalloid fluids, synthetic colloid fluids, and inotropes and pressors are currently the mainstay of therapy in the treatment of any illness that can result in systemic inflammatory response syndrome (SIRS). Until recently, replenishment of albumin was only in the form of administration of fresh frozen plasma. Fresh frozen plasma is a largely ineffective and inefficient method of replenishing albumin during states of hypoalbuminemia, particularly when there is ongoing loss. A total volume of 20 - 30 ml/kg of fresh frozen plasma will increase serum albumin by only 0.5 g/dL, provided that no ongoing losses are present. In humans, the use of albumin supplementation in hypoalbuminemic patients is a matter of controversy. In 1998, the Cochrane meta-analysis was published, and concluded that there was no documented benefit of albumin supplementation, and its use may actually increase the risk of morbidity and mortality. A criticism of this study is that the authors compiled data from heterogeneous patient populations, and had no pre-determined end-point of resuscitation or specific outcome. For this reason, other researchers concluded that more research must be performed before a conclusion about albumin could be reached. The Saline versus Albumin Fluid Evaluation (SAFE) Trial investigated the use of 0.9% (normal) saline versus 4% albumin in the resuscitation of patients admitted to a critical care unit. The researchers concluded that the use of albumin did not increase patient morbidity or mortality (a result totally different that that found with the Cochrane meta-analysis), and that there was no significant difference in total days in CCU, total days in hospital, or days on renal replacement therapy. Although the study did not demonstrate a significant benefit in the use of albumin over 0.9% saline, its use did not worsen outcome, either. Concentrated human albumin solutions are now available for use in veterinary patients. Most recently, concentrated human albumin solutions have been used in dogs for a number of reasons, including treatment of hypoalbuminemia and decreased colloid oncotic pressure, and as a potent colloid in the treatment of hypotension. Although albumin is structurally homologous across species, human albumin and canine albumin differs in approximately 20% of its amino acid sequence, and can result in the development of anti-albumin antibodies following its use. In one study, 50 grams of human albumin in 25% solution was administered to 9 purpose-bred mixed breed dogs as a rapid bolus over 1 hour. Both immediate and delayed rare hypersensitivity reactions occurred that include fever, vomiting, acute anaphylaxis, urticaria, angioneurotic edema, and delayed vasculitis and polyarthopathies. All dogs developed anti-human albumin antibodies after infusion. Limitations of this study were that all experimental dogs were normoalbuminemic and had much higher than recommended doses of albumin infused over a much more rapid time period than what has been recommended in the past. The authors acknowledged that immunocompetence in normoalbuminemic dogs differed from critically ill animals, and may put the normoalbuminemic animals at a particular risk of developing anti-human albumin antibodies and reactions to albumin infusion. Early reactions occurred during albumin infusion, while delayed reactions occurred approximately 14 days later. Other researchers demonstrated the development of anti-human albumin antibodies in both healthy dogs as well as critically ill dogs following administration of concentrated (25% human albumin). Additionally, several control dogs which did not receive albumin infusions also had positive antibody titers, suggesting either a lack of specificity of the assay for antibody against human albumin, or that the dogs had prior albumin exposure that resulted in the prior development of anti-human albumin antibodies. The authors surmised that canine vaccination protocols involve use of vaccines produced in bovine albumin cultures, and can result in prior sensitization of dogs to non-homologous albumin. Although there are studies which have demonstrated adverse reactions and the development of anti-human albumin antibodies after concentrated human albumin infusion in dogs, there also have been studies which have documented improved clinical outcome when concentrated human albumin was infused into critically ill animals that were refractory to other more mainstream therapies, including pressors, synthetic colloids, and fresh frozen plasma transfusions. In one study, 71% of patients survived after receiving a mean dose of 1.5 g/kg concentrated human albumin. Following infusion, there was a significant increase in total protein concentration, serum albumin concentration, and blood pressure. Minimal and very minor reactions were reported. More recently, researchers documented positive effect of infusion of concentrated human albumin in critically ill dogs, with minimal complications, although some minor delayed reactions were observed that resolved with minimal treatment. Albumin infusion should be considered in any patient with refractory hypoalbuminemia (< 2.0 g/dL) or hypotension unresponsive to other synthetic colloids, pressors, and inotropes. The perceived benefits of albumin infusion and risks of not infusing albumin must be weighed against the potential risks of its administration. Clinically, this author has seen delayed hypersensitivity reactions in two patients which were severely hypoalbuminemic secondary to septic peritonitis from perforated gastrointestinal foreign bodies. Albumin was infused to help prevent delayed wound healing from the intestinal resection and anastomosis sites. Exactly 14 days post-albumin infusion, the patients returned with primary complaint of urticaria and polyarthropathies that resolved with tapering doses of prednisone (1 mg/kg PO ID x 14 days, then once daily x 7 days, then every other day for 7 doses). Clients must be aware of the potential risks of complications, however, two studies have documented marked benefit and improved survival in animals that were poorly responsive to other more conventional therapies in the intensive care units. Recommendations for albumin infusion include administration of diphenhydramine (0.5 - 1 mg/kg IM or SQ) 15 minutes prior to albumin administration. A small test dose of 0.25 mL/kg of 25% albumin should be administered slowly over 15 minutes. The patient should be monitored for clinical signs of urticaria, vomiting, angioneurotic edema, hypotension , heart and respiratory rates, and temperature, as with the administration of any blood product infusion. A recommended dose of 5 ml/kg should be administered over a period of 4 hours, or more quickly if the animal is hypotensive. The albumin infused will replenish interstitial pools before a rise in serum albumin is observed. Constant rate infusions of 0.1 to 1.7 ml/kg/hour of 25% human albumin have been recommended to maintain serum albumin at low normal values. The ideal is to raise serum albumin to a level of 2.0 g/dL with concentrated human albumin. Fresh frozen plasma can be administered, too, to replenish clotting factors and anti-proteases. Finally, synthetic colloids can be administered to maintain colloid oncotic pressure. Albumin is a very important substance in the body, and any condition that is associated with hypoalbuminemia warrants the consideration of albumin therapy. However, its use is not completely innocuous, and the benefits must outweigh the potential risks of its use, as we strive to improve outcome, not contribute to increased morbidity and mortality, in our most critically ill patients. Suggested Reading: Mazzaferro EM, Rudloff E, Kirby R: Role of Albumin Replacement in the Critically Ill Veterinary Patient. J Vet Emerg Crit Care 12(2): 113-124, 2002. Mathews KA, Barry M. The use of 25% human serum albumin: outcome and efficacy in raising serum albumin and systemic blood pressure in critically ill dogs and cats. J Vet Emerg Crit Care 15(2):110-118, 2005. Cohn LA, Kerl ME, Lenox CE, Livingston RS, Dodam JR. Response of healthy dogs to infusions of human serum albumin. Am J Vet Res 68:657-663, 2007. Martin LG, Luther TY, Alperin DC, Gay JM, Hines SA. Serum antibodies against human albumin in critically ill and healthy dogs. J Am Vet Med Assoc 232:1004-1009, 2008. Mathews KA. The therapeutic use of 25% human serum albumin in critically ill dogs and cats. Vet Clin N Amer Sm Anim 38:595-605, 2008. Trow AV, Rozanski EA, deLaforcade AM, Chan DL. Evaluation of use of human albumin in critically ill dogs: 73 cases (2003 - 2006). J Am Vet Med Assoc 233(4):607-612, 2008. |
