Critical care- Ettinger Flashcards

Question

The respiratory system provides ......... ......................, changing with the onset of a metabolic disorder in ...........Metabolic compensation occurs ................, taking ........before becoming maximally effective. With either system, compensatory mechanisms should slow as the pH approaches normal, and compensation should .................... the pH.

Answer 1

The respiratory system provides rapid compensation, changing with the onset of a metabolic disorder in minutes. Metabolic compensation occurs more slowly, taking days before becoming maximally effective. With either system, compensatory mechanisms should slow as the pH approaches normal, and compensation should never completely normalize the pH.

Answer 2

Base excess, which is expressed in milliequivalents per liter (mEq/L), is the amount of base above or below the normal buffer base, a value calculated by taking into account the expected change in HCO3− secondary to acute changes in PCO2.

Answer 3

The general rule of thumb is that the HCO3− concentration rises about 1 to 2 mEq/L for each acute 10 mm Hg increase in PaCO2 above 40 mm Hg to a maximum increase of 4 mEq/L, and that the HCO3− concentration falls 1 to 2 mEq for each acute 10 mm Hg decrease in PaCO2 below 40, to a maximum decrease of 6 mEq/L. This negative base excess may be referred to as a base deficit.

Answer 4

By convention, a simple acid-base disorder is limited to the ............. disorder and the appropriate .............. response. A mixed disorder is one in which at least two separate abnormalities occur simultaneously. These abnormalities may both result in acidosis (i.e., metabolic acidosis and respiratory acidosis), may both result in alkalosis (i.e., metabolic alkalosis and respiratory alkalosis), or may be a combination of acidosis and alkalosis (e.g., metabolic acidosis and respiratory alkalosis). It takes cautious examination of a patient and blood gas results to avoid attributing the latter scenario to simple compensation.

Answer 5

Normal values at sea level for venous blood gas interpretation are: pH, 7.35 to 7.45; PCO2, 40 to 45 mm Hg; HCO3−, 19 to 24 mEq/L. Base excess normally should be −5 to 5 mEq/L.

Answer 6

An algorithm for interpretation of blood gas values is provided in Figure 124-2

Answer 7

Respiratory acidosis results from an increased partial pressure of CO2 in the blood (hypercapnia).

Answer 8

Hypercapnia can be caused by any condition that prevents normal pulmonary gas exchange, including impaired circulation, reduced respiratory rate or effort, circulation of blood to nonventilated portions of the lung, or impaired gas diffusion.

Answer 9

Diffusion impairment is the least likely cause of hypercapnia, because CO2 is approximately 20 times more diffusible than oxygen. Therefore, profound diffusion impairment is necessary before hypercapnia results.

Answer 10

1. Circulatory failure from cardiopulmonary arrest, 2. nervous system disease (central, spinal, or neuromuscular junction), 3. respiratory muscle failure (e.g. severe hypokalemia), 4. physical impairment of ventilation (e.g., pleural space disease, pain, thoracic wall disease, external constriction), or primary pulmonary disease (e.g., alveolar flooding, interstitial disease, pulmonary thromboembolism). 5. Iatrogenic respiratory acidosis results from inadequate ventilatory monitoring and assistance under general anesthesia.

Answer 11

Clinical signs of hypercapnia are consistent with the underlying disorder. Situations that might cause respiratory acidosis must be anticipated since there are no specific clinical signs that would clue the clinician in to its presence. End-tidal CO2 can be monitored noninvasively in animals with endotracheal tubes in place on closed-circuit breathing loops under general anesthesia or on mechanical ventilation. In animals with regular respirations in which alveolar gas exchange is occurring, end-tidal CO2 approximates PaCO2.

Answer 12

1. Correcting the underlying disorder by increasing alveolar ventilation. Chronic respiratory acidosis should be corrected slowly. 2. Increasing the inspired oxygen concentration may be lifesaving; however, with severe hypercapnia, stimulation for respiration becomes driven by hypoxia. In those situations, administration of oxygen therapy and resolution of the hypoxia may result in decreasing the rate of voluntary respiration, which may in turn promote hypercapnia. The hypoxic drive for respiration remains adequate below a dissolved oxygen content of .............blood (PaO2) of ......... mm Hg. It is not necessary to administer supplemental oxygen with a goal of normalization of oxygenation.

Answer 13

Sodium bicarbonate should not be administered to treat respiratory acidosis because this drug exacerbates hypercapnia by donating substrate for the carbonic acid equation.

Answer 14

Respiratory alkalosis results from an increase in ventilation through which more CO2 is eliminated than is produced by normal metabolic function. Hypocapnia develops, and alkalemia ensues.

Answer 15

1. Pulmonary or circulatory abnormalities that result in hyperventilation, 2. Primary pulmonary diseases that stimulate ventilation independent of hypercapnia, 3. Central nervous system disorders, and iatrogenic tachypnea/hyperpnea in animals receiving assisted ventilation. Chronic respiratory alkalosis is usually well compensated.

Answer 16

Primarily aimed at the underlying cause of tachypnea or hyperpnea (e.g., treatment for bacterial pneumonia, resolution of anxiety-associated tachypnea with sedation). As with respiratory acidosis, there are few if any clinical signs suggesting this specific acid-base disorder. Again, oxygen supplementation can be useful in support of these animals while the underlying disease is addressed.

Answer 17

1. Gain of H+ through ingestion of an acid into the body, 2. increased production of an endogenous acid, 3. failure to eliminate an acid load by the renal tubular cells. 4. Metabolic acidosis can also be caused by a loss of HCO3− buffering ability. Differentiating between increased acid gain or loss of HCO3- buffering ability causes (4) of metabolic acidosis is important both for diagnosis of the underlying disorder and for determining correct therapeutic intervention.

Answer 18

Anions are atoms or radicals which are a group of atoms, that have gained electrons. Since they now have more electrons than protons, anions have a negative charge. For example Chloride ions Cl- , Bromide Br- , Iodide I-. These are monovalent anions as it has a combining capacity with only one ion of Hydrogen. Similarly there are bivalent anions, etc. Anions are one of the two types of ions. The other type is called a cation, and these have a positive charge. Ions are atoms that have an electrical charge. Anions are termed so because they get attracted towards the Anode(the positive electrode). All Anions tend to accept a proton H+ thus they are categorized as bases

Answer 19

Dissociation of acid into the H+ ion and the corresponding anion occurs in the circulation. When acid accumulates, HCO3− combines with H+ to buffer the acid load, while the anion remains in solution.

Answer 20

Because electroneutrality must be maintained as anions accumulate following acid dissociation, some other circulating anion must decrease correspondingly. Anion gap (AG), the difference between measured cations and measured anions, is useful in the classification of disorders causing metabolic acidosis.

Answer 21

AG = (Na+ + K+) - (Cl- + HCO3-)

Answer 22

Although ranges for anion gap can vary somewhat based upon the reference ranges of electrolytes for various laboratories, a reference value of 16 ± 4 is typical. When metabolic acidosis exists with an increased anion gap, there has usually been a gain of organic acid.

Answer 23

1. ethylene glycol intoxication, 2. uremia, 3. tissue hypoxia (e.g., lactic acidosis), 4. diabetic ketoacidosis, 5. salicylate intoxication, 6. other unusual intoxications (e.g., drugs, alcohol).

Answer 24

Loss of bicarbonate buffers or a failure to excrete H+ ions, with a corresponding increase in chloride to maintain electroneutrality. This is often referred to as a hyperchloremic metabolic acidosis.

Answer 25

Hyperchloremic metabolic acidosis occurs less commonly than metabolic acidosis with an increased anion gap and is caused by 1. renal tubular acidosis (failure of the renal bicarbonate buffer or hydrogen excretory system) or by 2. severe diarrhea and loss of intestinal bicarbonate. 3. Iatrogenic hyperchloremic metabolic acidosis can also occur with administration of an alkali-free chloride-containing crystalloid solution, such as 0.9% sodium chloride (0.9% NaCl) for intravenous volume replacement.

Answer 26

1. lethargy, 2. decreased cardiac output, 3. decreased blood pressure, and 4. decreased hepatic and renal blood flow. These changes may be referable to the acidemia, to the underlying cause of the acid-base disorder, or both.

Answer 27

Unless the patient has some impairment of normal ventilatory ability, compensatory mechanisms cause an increase in the respiratory rate, which allows the animal to eliminate CO2 generated by carbonic acid formation, mitigating acidosis.

Answer 28

1. should be aimed at correcting the underlying disorder. This might involve improving tissue perfusion (e.g., appropriate intravenous fluid therapy), eliminating ingested toxin, or correcting metabolic, renal, or GI disease. 2. With severe metabolic acidosis (pH of <12 mEq/L), injectable sodium bicarbonate may be administered judiciously.

Answer 29

Bicarbonate dose =0.3 x (body weight (kg)) x base deficit

Answer 30

1. Hyperosmolarity, 2. hypernatremia, 3. hypokalemia. 4. Hypocalcemic tetany may be caused by shifting of calcium from the ionized to the protein-bound form after bicarbonate administration. 5. Paradoxical central nervous system acidosis occurs when CO2 generated following bicarbonate administration crosses the blood-brain barrier and takes part in the carbonic acid equation, essentially fueling acid production in the CNS. 6. Iatrogenic metabolic alkalosis can also occur after administration of bicarbonate.

Answer 31

1. Metabolic alkalosis is generated by loss of chloride in excess of extracellular fluid volume, which often occurs as a result of upper GI fluid loss or sequestration. 2. Additionally, administration of a thiazide diuretic may cause chloride wasting. 3. Rarely, metabolic alkalosis may be caused by overzealous administration of sodium bicarbonate or another organic anion 4. or by hyperaldosteronism (i.e., Conn's syndrome), which causes sodium retention in excess of chloride.

Answer 32

Gastric outflow obstruction.

Answer 33

During gastric outflow obstruction, appropriate renal compensation prevents an acid-base disorder until hypovolemia induced by vomiting results in aldosterone release.

Answer 34

Aldosterone increases renal uptake of sodium. Normally, sodium is reabsorbed with bicarbonate or chloride or is exchanged for potassium. Because gastric fluid has high chloride and potassium concentrations, animals with gastric outflow obstruction become systemically depleted of these electrolytes so that renal reabsorption of sodium can only occur with concurrent bicarbonate uptake.

Answer 35

As with other acid-base disorders, clinical signs of metabolic alkalosis are dictated by the underlying disorder generating the acid-base abnormality. Muscle twitching and seizures have been reported in animals with metabolic alkalosis. Signs associated with concurrent potassium depletion may include weakness, cardiac arrhythmias, renal dysfunction, and GI motility disturbances.

Answer 36

1. Directed at resolving the underlying cause. 2. Intravenous 0.9% NaCl is the fluid of choice to replace volume deficits and normalize chloride concentrations since these patients are often chloride-depleted. Fluids should not contain buffer (e.g., not lactated Ringer's solution). 3. Pyloric outflow obstruction is often addressed surgically, or by removal of an obstructing foreign body. 4. In animals with profuse vomiting unassociated with obstruction, drug therapy to minimize gastric hydrochloric acid (HCl) excretion may be warranted (e.g., famotidine, omeprazole). 5. Because animals with metabolic alkalosis often have concurrent hypokalemia, cautious intravenous potassium chloride supplementation is often indicated.

Answer 37

1. a low concentration of inspired oxygen, 2. hypoventilation, 3. diffusion impairment, 4. ventilation-perfusion mismatch, 5. pulmonary shunting.

Answer 38

Measurement of PaO2 Measurement of peripheral oxygen saturation (SpO2) by pulse oximetry.

Answer 39

A noninvasive device that calculates hemoglobin oxygen saturation by measuring differences in absorption of two wavelengths of light (red and infrared) by oxygenated and deoxygenated hemoglobin. The measured light absorption values are applied to a preset nomogram, and a value for SpO2 is determined. If tissue perfusion is adequate, SpO2 approximates arterial hemoglobin saturation (SaO2).

Answer 40

The advantage of oximetry as a monitoring tool is that it provides continuous, noninvasive determination of hemoglobin oxygen saturation. Technical aspects that help ensure accuracy include placing the probe on nonpigmented, moist skin with adequate perfusion (usually the tongue, the buccal, vaginal, or preputial mucosa, or the ear pinna), avoiding probe movement and light pollution, and monitoring the pulse rate to ensure accurate pulse signal transmittance. In poorly perfused tissues, the SpO2 may be falsely low compared with the SaO2. If inaccuracy of oximetry is suspected, the arterial blood gas PaO2 may be obtained to evaluate oxygenation. In patients with alterations of hemoglobin concentration causing increased carboxyhemoglobin or methemoglobin, oximetry may be normal despite severe patient hypoxemia. Oximetry does not evaluate the PCO2 and cannot be used to determine ventilation status.

Answer 41

The hemoglobin saturation of oxygen and partial pressure of oxygen (PaO2) both contribute to arterial oxygen content (CaO2) (according to a formula)

Answer 42

Therefore, SpO2, which approximates SaO2, provides an estimation of hemoglobin saturation, whereas PaO2 estimates dissolved oxygen in blood.

Answer 43

According to the formula listed, hemoglobin saturation is the biggest determinant of arterial oxygen content. Increasing the PaO2 by increasing the inspired oxygen concentration has a minimal effect, whereas increasing the SaO2 has a greater potential effect.

Answer 44

In an anemic patient, increasing the arterial oxygen content would best be accomplished by increasing hemoglobin by transfusion of a product containing red blood cells or purified hemoglobin.

Answer 45

By the oxyhemoglobin dissociation curve, an SaO2 of 90% corresponds to a PaO2 of 60 mm Hg. This value is clinically important in that small decreases beyond this point in either partial pressure of oxygen or oxygen saturation of hemoglobin may have tremendous clinical consequences for oxygenation.

Answer 46

Use of an oxygen chamber, tent or mask administration, placement of an indwelling nasal oxygen catheter, or mechanical ventilation with an increased fraction of inspired oxygen. Other methods to correct hypoxemia are related to correcting the underlying cause. For instance, hypoxemia in an animal with severe pneumothorax or pleural effusion would be accomplished through thoracic drainage while hypoxemia related to airway obstruction would be addressed by relief of the obstruction.

Answer 47

Definitively diagnosing the cause of acute abdomen can be challenging. The goal of early and aggressive treatment is to minimize the impact of the systemic inflammatory response syndrome (SIRS), sepsis and to avoid multiple organ dysfunction syndrome (MODS). The abdominal pain characteristic of this condition is typically caused by inflammation, especially of the peritoneal lining, stretching of or traction on a hollow viscus such as a gall bladder or loop of intestine, stretching of or traction on the capsule of a solid organ such as the liver, or ischemia. Typically the pain is severe. Patients that present collapsed in a state of hemodynamic shock may not exhibit signs of pain until resuscitation has been instituted. Extraabdominal causes of abdominal pain that need to be ruled out include conditions such as intervertebral disc disease, steatitis and myositis.

Answer 48

Altered levels of consciousness, collapse, tachycardia with weak or absent peripheral pulses, tachypnea, and pale mucous membranes with delayed capillary refill time and cool extremities indicate serious perfusion abnormalities and the need for immediate fluid resuscitation. Findings of fever, tachycardia with bounding pulses, and injected mucous membranes with capillary refill times of less than 1 second are consistent with a hyperdynamic phase of shock. These patients usually have a relative hypovolemia due to decreased systemic vascular resistance and also need immediate fluid resuscitation.

Answer 49

The goal of resuscitation is to reverse the signs of shock and provide effective oxygen delivery to the cells. Efforts should be aimed at maximizing 1. hemoglobin levels (oxygen-carrying capacity), 2. blood volume, and 3. cardiac function. Oxygen and intravenous fluid therapy should be provided. Patients presenting in extremis may require rapid intubation and ventilatory support. Hypoglycemic patients should be treated with dextrose. Antibiotics may not be indicated in all cases

Answer 50

Nonsteroidal antiinflammatory drugs should be avoided due to their negative effects on splanchnic organs. Opioids such as butorphanol, hydromorphone, morphine, and fentanyl are recommended. Pure mu agonists are preferred, although butorphanol can be useful in the cat due to side effects of some of the pure mu agonists in this species. Drugs should be given intravenously since absorption from subcutaneous or intramuscular sites may be unpredictable.

Answer 51

Examination findings Abdominal flid examination: In the dog a blood glucose concentration that is at least 20 mg/dL more than that in the abdominal fluid is strongly supportive of septic peritonitis. A blood-to-fluid lactate difference of less than 2 mmol/L is also suggestive of septic peritonitis in the dog.

Answer 52

Concentrations of abdominal fluid amylase or alkaline phosphatase that are higher than serum suggest pancreatitis or intestinal disease. Concentrations of bilirubin that are higher in the abdominal fluid than serum indicate a disruption of the biliary tract. High potassium concentrations are consistent with urinary tract rupture. Urea nitrogen will equilibrate rapidly between the serum and peritoneum, but in an acute bladder rupture the peritoneal urea concentration will be higher than serum.

Answer 53

Abdominocentesis has a high incidence of false-negative results. Diagnostic peritoneal lavage has an extremely low rate of false results and should be performed if a confirmation of the diagnosis is required

Answer 54

1. Asystole (complete absence of QRS-T complexes), 2. Ventricular fibrillation (chaotic depolarization of the ventricles characterized by a lack of QRS-T complexes with unorganized fibrillation waves), 3. Electromechanical dissociation (little or no myocardial contractile activity with a normal ECG tracing). All these arrhythmias require immediate intervention using standard CPR recommendations. Other potentially lethal arrhythmias include continuous (sustained) or intermittent (paroxysmal) ventricular tachycardia, ventricular flutter, paroxysmal or sustained supraventricular tachycardia, sick sinus syndrome (SSS), complete or high-grade second-degree atrioventricular block, and sinus standstill. Sinus bradycardia frequently precedes CPA in critically ill patients.

Answer 55

Antiarrhythmic therapy should be initiated if treatment of the underlying disorder does not improve the arrhythmia, if hemodynamic impairment is identified, or if the risk of sudden death exists.

Answer 56

HEART FAILURE Heart failure is a clinical syndrome caused by cardiac disease that results in systolic or diastolic cardiac dysfunction or both. Systolic failure describes decreased myocardial performance, and diastolic failure results from abnormal filling of the ventricles during diastole. Decompensated heart failure manifests either as congestion/edema (backward heart failure) or circulatory failure (low-output, forward heart failure). Right-sided congestive heart failure results in systemic venous congestion and may manifest as jugular distention, subcutaneous edema, hepatic congestion, ascites, and/or pleural effusion. Left-sided congestive heart failure presents as pulmonary edema.

Answer 57

The immediate goals of medical therapy in acute congestive heart failure are the reduction of pulmonary venous pressure (use of a diuretic to reduce total blood volume and a vasodilator to redistribute intravascular fluid volume), inotropic support, and adjunct therapy (oxygen, anxiolytics).

Answer 58

Furosemide is the diuretic of choice for relieving acute pulmonary edema and normalizing cardiac filling pressures. High doses of furosemide (up to 4 mg/kg given intravenously or intramuscularly every 2 hours) may be used initially to induce diuresis. Intravenous furosemide acts within 5 minutes, peaks within 30 minutes, and dissipates after 2 to 3 hours. Use of the intravenous route is preferred, but this must be weighed against the potential stress of administration. Lasix can also be given using a constant rate infusion (CRI) (0.5 to 1.0 mg/kg/hr) after an initial loading dose is given.

Answer 59

Intramuscular administration of furosemide is an alternative to the IV route. The dose is highly variable and depends on the response desired. The dose and frequency should be reduced as a clinical response (diuresis, respiratory rate reduction, and respiratory character improvement) is achieved. Cats tend to be more sensitive to furosemide than dogs and respond to lower doses (2 mg/kg).

Answer 60

Nitroglycerin, a venodilator, may further reduce congestion, although information in the veterinary literature is merely anecdotal. Nitroglycerin paste can be applied to the inner surface of the pinna of the ear (¼ to 1 inch every 6 hours in the dog; ⅛to ¼ inch every 6 hours in the cat). Nitroglycerin is typically used for only 48 hours due to the drug tolerance that develops.

Answer 61

Hydralazine, a potent arteriolar dilator, can be used in the emergency management of a normotensive congestive heart failure patient (0.5 to 2.0 mg/kg given orally).

Answer 62

Nitroprusside is both a potent venodilator and a potent arteriolar dilator for use in severe, refractory congestive heart failure (1 to 2 µg/kg/min given intravenously initially). Continual blood pressure monitoring is essential with nitroprusside.

Answer 63

Augmentation of systolic performance is important with acute congestive heart failure due to DCM and severely decompensated mitral regurgitation. The positive inotropic agents most commonly used increase cytosolic cyclic adenosine phosphate (cAMP). As a result, there is enhanced ventricular contraction (a result of increased calcium entry into the cell), ventricular relaxation, and peripheral vasodilatation.

Answer 64

Dobutamine and dopamine are sympathomimetic agents that bind to B1 receptors, thereby increasing production of cAMP.

Answer 65

Dobutamine increases contractility with little effect on heart rate or afterload. It is administered by CRI (5.0 to 15 µg/kg/min).

Answer 66

Dopamine stimulates B1 receptors and at high doses also releases norepinephrine. At low doses (

Answer 67

Amrinone and milrinone are potent positive inotropes with direct-acting arterial vasodilator properties. These bipyridines increase cAMP by phosphodiesterase inhibition. Amrinone and milrinone are available as IV preparations. Unfortunately, both the sympathomimetics and the bipyridines can promote tachycardia and ventricular arrhythmias.

Answer 68

Pimobendan is a benzimidazole-pyridazinone derivative approved for the treatment of congestive heart failure due to DCM and MVI in dogs. Pimobendan is classified as an inodilator (i.e., positive inotrope and arteriovenous dilator). The positive inotropic effects are primarily through sensitization of the cardiac contractile apparatus to intracellular calcium. This is done with little or no increase in myocardial oxygen consumption. There is improved efficiency with limited arrhythmogenic side effects seen with other positive inotropes. The vasodilating properties of pimobendan are due to the phospodiesterase inhibition.

Answer 69

Pimobendan has a rapid onset of action and can be used in the treatment of acute congestive heart failure when a positive oral inotrope is needed. Following oral administration (0.1 to 0.3 mg/kg q12h) peak hemodynamic effects are achieved in 1 hour and last 8 to 12 hours.

Answer 70

A low dose of morphine (0.05 to 0.1 mg/kg given subcutaneously or intramuscularly) can reduce the anxiety associated with pulmonary edema and provide mild venodilatation.* The dose is repeated up to four times a day, as necessary, to achieve the desired effect. The primary adverse consequence of using morphine is respiratory depression; therefore, it must be used with caution in hypoxic animals.

Answer 71

Acepromazine (0.05 to 0.1 mg/kg given subcutaneously) is an anxiolytic that does not depress respiration. Acepromazine is an alpha-adrenergic blocker that decreases peripheral vascular resistance, which may also be beneficial.

Answer 72

Dogs and cats with severe pulmonary edema are hypoxic due to the decreased ability of oxygen to diffuse from the alveoli into the pulmonary capillaries. Supplemental oxygen increases this pressure gradient, resulting in an increase in arterial oxygen tension. Therefore, it is of critical importance that patients with severe edema have supplemental oxygen. This can be achieved using an oxygen cage (40% oxygen) adjusted to maintain a normal temperature (20° to 22° C [68° to 72° F]) and appropriate humidity (45% to 55%). Oxygen cages are generally better tolerated and less stressful than other means of administration. In a larger dog, oxygen can be administered through a nasal cannula. An oxygen mask is an alternative but should not be used if the animal is struggling against the mask.

Answer 73

Endotracheal intubation may be required in animals with extreme respiratory distress and fulminant pulmonary edema to provide controlled ventilation and 100% oxygen administration. In addition, copious amounts of pulmonary edema may be removed physically by suction or postural drainage. Intravenous fluids are rarely indicated in the treatment of acute, cardiogenic pulmonary edema because they often exacerbate the edema.

Answer 74

PERICARDIAL EFFUSION Pericardial effusion is an abnormal accumulation of fluid in the pericardial sac. The hemodynamic effects of pericardial effusion depend on the rate and volume of the fluid accumulation and the compliance of the pericardium itself. If the effusion develops slowly, the pericardium will expand and the intracardiac pressure will not increase enough to compromise cardiac filling. In contrast, acute cardiac tamponade is characterized by rapid accumulation of fluid in the pericardial space, leading to a rise in intrapericardial pressure. The results are restriction of ventricular filling, decreased cardiac output, and arterial hypotension. C

Answer 75

Clinical signs of right-sided congestive heart failure or reduced cardiac output predominate and include anorexia, lethargy, syncope, dyspnea, weakness, exercise intolerance, and abdominal distention (hepatomegaly, ascites). Common physical examination findings are muffled heart sounds, jugular venous distension, sinus tachycardia, and weak femoral pulses. Pulsus paradoxus (an exaggerated decline greater than 10 mm Hg in systemic arterial pressure during inspiration) is a valuable clinical sign that may also be appreciated in cardiac tamponade.

Answer 76

Attempts to lower venous pressures with medical therapy (i.e., diuretics) should be avoided because the patient's cardiac preload depends on these elevated pressures. The result can be a significantly reduced cardiac output, manifested as hypotension or syncope or both.

Answer 77

Neoplasia, sepsis, Cushing's disease, protein-losing nephropathy, or other hypercoagulable states.

Answer 78

Distal aortic embolization (saddle thrombus at the distal aortic trifurcation) occurs in more than 90% of feline cases. Corresponding clinical signs may occur with embolization of other organs, such as the lungs (respiratory distress), kidneys (acute renal failure), brain (central nervous system signs), gastrointestinal tract (bowel ischemia), and right (more commonly than left) brachial artery (pain and paresis).

Answer 79

Paralysis, Pain, Pulselessness (lack of palpable femoral pulses), Pallor (cold, pale distal extremities and pads).

Answer 80

Absence of bleeding from a cut nail on the affected limb may also be seen. Ten to 12 hours after the embolization, the anterior tibial and gastrocnemius muscles often become firm as a result of ischemic myopathy. In most cases these muscles become softer after 24 to 72 hours.

Answer 81

Respiratory distress is commonly associated with systemic thromboembolism in cats because most have concurrent congestive heart failure. Acute aortic blockade by the thromboembolus increases afterload to the left ventricle. The clinician must differentiate the respiratory changes seen with congestive heart failure from those seen with pain.

Answer 82

Although heparin has no effect on established thrombi, it is commonly administered in hopes of limiting thrombus growth.* Heparin can be administered at an initial dose of 220 U/kg given intravenously, followed by a maintenance dose of 70 to 200 U/kg given subcutaneously every 6 hours.

Answer 83

Thrombolytic agents such as streptokinase, urokinase, and tissue plasminogen activator (t-PA) are used extensively in humans and infrequently in cats. These agents are expensive, have not been studied extensively, and are associated with high mortality and poor outcomes. Risks of bleeding complications, death from reperfusion syndrome (hyperkalemia, metabolic acidosis), and rethrombosis are common.

Answer 84

During the initial stages of the disease, most cats experience intense pain. The pain subsides as sensory nervous function is lost. Common choices for pain control include oxymorphone (0.05 to 0.15 mg/kg given intramuscularly or intravenously every 6 hours), butorphanol (0.1 mg/kg given intravenously or 0.02 to 0.4 mg/kg given intramuscularly or subcutaneously every 4 hours), and/or acepromazine (0.05 to 0.1 mg/kg given intravenously). Euthanasia should be considered as an option when severe, unrelenting pain is present

Answer 85

General supportive care consists of maintaining hydration and normal electrolyte status, massaging firm muscles, expressing the bladder as necessary, and preventing self-mutilation. Management of concomitant congestive heart failure is discussed above.

Answer 86

Cardiopulmonary arrest is defined as the cessation of effective ventilation and circulation. Cardiopulmonary resuscitation (CPR) provides artificial ventilation and circulation to restore spontaneous cardiopulmonary function and includes basic life support (BLS), advanced life support (ALS), and prolonged life support (PLS). The term cardiopulmonary cerebral resuscitation was coined in recognition of the severe central nervous system complications of prolonged CPR. CPCR is aimed at restoration of blood flow to the brain, not only the heart and the lungs, to avoid cases in which return of spontaneous circulation (ROSC) results in a poor neurologic outcome such as a vegetative state.

Answer 87

PREPAREDNESS Preparedness includes ascertaining that each patient has a code status upon hospitalization, the presence of a fully equipped crash cart (Table 127-2), a minimum of three people trained in CPCR, a ready area, and a routine plan of action. All hospitalized patients should have one of three code assignments: do not resuscitate (DNR or no code), closed chest code (external compressions only), or open chest code (internal compressions). The code status should be discussed at the time of admission, and owner's wishes should be clearly stated on the chart. The ready area and the crash cart should be inspected and stocked daily.

Answer 88

(1) those who succumb to an underlying terminal or multisystemic illness—a DNR code status may be appropriate for these patients for ethical reasons and since their prognosis is generally grave; (2) those suffering from a severe, but potentially reversible, medical condition such as trauma (e.g., hemorrhage, pneumothorax, diaphragmatic hernia), upper respiratory obstruction, or electrolyte abnormalities—this population has a slightly higher chance for ROSC, assuming the underlying cause can be quickly reversed; and (3) those with anesthetic complications, drug reactions, and accidental drug overdoses. Three retrospective studies published in veterinary medicine concluded that the last group has the highest survival rates as they are usually witnessed arrests and in some cases already have an endotracheal tube in place.[1-3]

Answer 89

Prior to initiation of CPCR, the senior person on the scene should take a few seconds to confirm full CPA. Respiratory arrests alone carry a better prognosis and do not necessitate chest compressions. In addition, the animal may not be pulseless but rather bradycardic, which will alter the order of drugs used during ALS such that atropine is given prior to epinephrine.

Answer 90

bradycardia or other cardiac arrhythmias, hypotension, hypothermia, irregular respiratory pattern, and vagally mediated activities such as vomiting or urination in a critically ill patient.

Answer 91

Basic life support is the foundation of CPCR (class I AHA recommendation) and follows the mnemonic of ABC (airway, breathing, circulation). Endotracheal intubation, ventilation with an Ambu bag or an anesthesia machine connected to 100% oxygen (with the inhalant anesthetic turned off), and external or internal cardiac compressions. Time should be taken to ensure that the endotracheal tube is in place, secured, and inflated. If intubation is not possible due to upper airway obstruction, emergency tracheostomy is performed. The mouth and trachea should be suctioned if secretions are present.

Answer 92

Respiratory rate is aimed at 10 to 24 breaths/min, a tidal volume of 10 to 15 mL/kg, and a peak inflation pressure of 20 cm H2O. Some animals may require a higher respiratory rate, but hyperventilation should be avoided.

Answer 93

The volume delivered should produce a visible chest rise of approximately 25% to 30% of resting state, but should not be too forceful to avoid barotrauma. If an anesthesia machine or Ambu bag is not available, mouth-to-tube or mouth-to-nose ventilation can be performed. For chest compressions, the animal is positioned in right lateral recumbency, and compression rate is aimed for 100 to 120 compressions/min. If the animal is already in dorsal recumbency, such as during a surgical procedure, it may remain this way.

Answer 94

If the first recorded arrest rhythm is ventricular fibrillation (VF), defibrillation should be performed as soon as possible, but BLS should not be delayed. In anesthetic-related incidents, inhalant anesthetics should be turned off immediately, and anesthetics, sedatives, or analgesics should be reversed if possible.

Answer 95

ADVANCED LIFE SUPPORT Advanced life support consists of drug administration, electrocardiography (ECG) interpretation, and electrical defibrillation (D and E). Drug and defibrillation doses are listed in Table 127-3. Drugs given IT (intratracheal) should be diluted with 2-3 mL of water for injection and given at the level of the carina using a red-rubber or polyethylene catheter

Answer 96

Drug Administration and Access Establishing access for drug administration is vital during CPCR. A central line is the preferred route because of short circulation times, but if not already in place, time should not be wasted on establishing a central line during CPCR.[6] Peripheral catheterization using a large-bore catheter should be established as soon as possible, and if not feasible, an intraosseous catheter may be placed (class IIa). Drug administration via a peripheral catheter should be followed by large flush volumes to facilitate drug delivery to the central circulation.[7] If intravenous (IV) access is not possible, drugs can also be given intratracheally (IT). Epinephrine, atropine, lidocaine, naloxone, and vasopressin are all absorbed via the trachea but may result in lower blood concentrations and a less predictable drug delivery and pharmacologic effect than the same dose given IV.[8-16] The optimal endotracheal dose of most drugs is unknown, but typically the dose given is twice the recommended IV dose. Endobronchial administration of epinephrine diluted with water for injection, instead of sterile saline, was shown to achieve the highest blood concentrations.[17] In summary, if IT administration is used, drug doses should be doubled; the drug should be diluted with a few milliliters of water for injection and administered via a red rubber or polypropylene tube that is passed through the endotracheal tube to the level of the carina.[5] Sodium bicarbonate and calcium gluconate should not be given IT.

Answer 97

Epinephrine is the drug of choice for all types of CPA (class IIb). Epinephrine is a potent catecholamine with strong affinity to both α- and β-adrenergic receptors.

Answer 98

Administration causes immediate peripheral vasoconstriction mediated by its alpha effects; however, the β-adrenergic activity may cause significant tachycardia, which will shorten diastole and decrease myocardial perfusion.

Answer 99

Atropine is a parasympatholytic agent that acts to increase heart rate by antagonism of muscarinic receptors. If sinus bradycardia is present on initial auscultation, atropine should be administered before epinephrine (class IIa). Otherwise, atropine is given following epinephrine.

Answer 100

Amiodarone affects sodium, potassium, and calcium channels as well as α- and β-adrenergic blocking properties. It can be considered for the treatment of VF or pulseless VT unresponsive to shock delivery, CPR, and vasopressors (class IIb). Intravenous amiodarone is rarely maintained in most veterinary hospitals, is expensive, and is not a drug that an inexperienced individual should probably use.

Answer 101

Lidocaine, a sodium channel blocker, is an alternative antiarrhythmic with fewer immediate side effects than may be encountered with other antiarrhythmics. Lidocaine, however, has no proven short-term or long-term efficacy in cardiac arrest (class indeterminate). In addition, lidocaine should not be used in cats.

Answer 102

Magnesium can effectively terminate torsades de pointes (irregular/polymorphic VT associated with prolonged QT interval).

Answer 103

Electrocardiography (ECG) Changes in ECG throughout CPCR dictate the type of interventions that should be implemented and serve as a monitoring tool. The three recognized arrest rhythms are asystole, pulseless electrical activity, and VF (Figure 127-1). Asystole is the most common arrest rhythm in companion animals, while VF is more common in humans. Ventricular fibrillation has the highest likelihood of being converted with the aid of defibrillation and CPCR, which is most likely one of the reasons for the higher success rates reported in some human studies.

Answer 104

Figure 127-1 Algorithm for basic and advanced life support. CPCR, Cardiopulmonary cerebral resuscitation; ECG, Electrocardiography; ETCO2, end-tidal carbon dioxide; IO, intraosseous; IV, intravenous; VF, ventricular fibrillation.

Answer 105

Although the most common initial arrest rhythm in companion animals is asystole, this rhythm can often change as CPCR progresses, and defibrillation may be indicated. ECG interpretation should be performed concurrently to auscultation, as pulseless electrical activity can appear as a normal rhythm on the ECG screen with no audible pulse or heart rate. Pulse palpation should also be interpreted with caution, as it is the pulse pressure that determines the blood pressure and not the pulse quality

Answer 106

Fluid Therapy Administration of large fluid boluses during CPCR should not be performed routinely because it may decrease coronary perfusion pressure (CPP), which represents the difference between aortic pressure and right atrial pressure during diastole. Large fluid volumes may decrease CPP as they increase right aortic pressure.

Answer 107

In animals suffering CPA due to congestive heart failure, fluid therapy should be avoided. If the animal is euvolemic, conservative fluid therapy may be considered. However, large fluid volumes should be reserved for those cases suffering CPA due to hypovolemic shock.

Answer 108

MONITORING DURING CPCR Monitoring tools for CPCR include a stethoscope, ECG, Doppler blood pressure monitor, pulse oximeter, and capnograph. ECG monitoring was discussed earlier. A capnograph is one of the most important monitoring tools during CPCR. Higher end-tidal carbon dioxide (ETCO2) levels during CPCR are associated with increased myocardial perfusion pressure and increased success rates in human beings and dog models of CPCR, whereas a low ETCO2 represents ineffective elimination of CO2 due to low flow.[18] Rising levels of ETCO2 during a successful CPCR indicate tissue perfusion and ROSC. However, arterial blood gases should be interpreted cautiously during CPCR, as they may not provide a reliable indicator of the severity of tissue hypoxemia, hypercarbia, or tissue acidosis.

Answer 109

PROLONGED LIFE SUPPORT PLS refers to the time period following ROSC and the measures required to support continued perfusion, maintain adequate circulation and oxygenation, and treat underlying conditions. As the likelihood of recurrence of CPA in an animal that already suffered one is high, intensive monitoring is required in post-CPCR patients. The following parameters should be monitored: pulse rate, rhythm, and character, mental status, ECG, pulse oximetry, body temperature, lung sounds, mucous membrane color, capillary refill time, urine output, electrolytes, blood gases, PCV and total solids, blood glucose concentration, serum lactate concentration, central venous pressure, neurologic function, and patient comfort. Oxygen supplementation should be provided initially. Some patients may need mechanical ventilation to maintain adequate oxygenation. Positive inotropes and vasopressors (e.g., dobutamine, dopamine, or vasopressin) may need to be used to support circulation and maintain blood pressure. Mannitol (0.5 to 1 g/kg over 20 minutes administered via a filter) may be considered in patients with suspected cerebral edema or neurologic dysfunction.

Answer 110

OLD CONTROVERSIES AND NEW RECOMMENDATIONS FOR CPCR Open- versus Closed-Chest CPCR As no prospective randomized studies of open-chest CPCR for resuscitation have been published, performing it remains controversial and largely depends on clinician and owner preference. In humans, open-chest CPCR is considered a class IIa recommendation only for patients with cardiac arrest in the early postoperative period after cardiothoracic surgery and when the chest or abdomen is already open.[5] In addition, several retrospective studies suggest there may be a role for open thoracotomies in patients with penetrating thoracic and cardiac trauma. In veterinary medicine, open-chest CPCR is recommended for patients in which external compressions are unlikely to be effective, such as very large dogs and patients with pleural or pericardial effusion, pneumothorax, diaphragmatic hernia, or thoracic trauma, or if the thoracic or abdominal cavities are already open.

Answer 111

Epinephrine Dosage Although epinephrine has been used universally in resuscitation, there is a paucity of evidence to show that it improves survival in humans. Administration of high dose epinephrine (0.1 to 0.2 mg/kg, IV) has been called into question, as the β-adrenergic properties of epinephrine cause significant tachycardia, decreased diastolic filling, and decreased coronary perfusion and have been associated with decreased survival. Based on several clinical trials, the 2005 AHA guidelines recommend the use of low-dose epinephrine (0.01 to 0.02 mg/kg, IV). For in-hospital witnessed CPA, the author is in favor of using low-dose epinephrine in veterinary patients.

Answer 112

Vasopressin versus Epinephrine Vasopressin is a potent noradrenergic vasopressor, acting through direct stimulation of vasopressin (V1) receptors in vascular smooth muscle. As opposed to catecholamines, its vasoconstrictive effects are not blunted in the presence of acidosis and, following ROSC, there is no increase in myocardial oxygen demand. In a recent human clinical trial comparing IV vasopressin (two doses of 40 IU) with epinephrine (two doses of 1 mg) in 1219 out-of-hospital cardiac arrests, patients with VF, asystole, and pulseless electrical activity did not have survivability differences compared to patients with only VF or pulseless electrical activity; however, vasopressin was superior to epinephrine in asystolic patients.[19] In addition, recovery from CPA has been reported in one case in veterinary medicine using vasopressin with no epinephrine.[20] The single use of vasopressin, at a dose of 0.1 to 0.8 U/kg IV, has otherwise been anecdotally used in veterinary CPCR. A CRI of 0.01 to 0.08 U/kg/hr can be used for the postresuscitation period. The authors have successfully resuscitated patients with vasopressin in conjunction with epinephrine; however, more studies are needed to confirm the role of vasopressin in veterinary CPCR.

Answer 113

Hyperventilation and Interruptions during CPCR An observational study found that emergency medical service personnel consistently hyperventilated human patients in the arrest scene,[21] and several small case series in humans showed that during CPR, health care providers delivered an inadequate number and depth of compressions, interrupted compressions frequently, and provided excessive ventilation.[22-24] The 2005 AHA guidelines stress the importance of early initiation of chest compressions with minimal interruptions and a 50 : 50 compression/relaxation rate to allow diastolic filling of the heart and maximize myocardial perfusion. Although establishing an airway is the first step in CPCR, chest compressions should not be delayed if an airway cannot be captured immediately.

Answer 114

Traumatic Brain Injury PATHOPHYSIOLOGY Primary versus Secondary Injury There are two described phases following TBI: primary and secondary injury. Primary injury refers to pathologic changes that take place at the time that injury is sustained—it is complete at the time of trauma and there is little that can be done to alter its course. Examples of primary injury include direct axonal damage and vascular disruption.

Answer 115

Secondary injury refers to a variety of pathologic processes that occur after the primary insult, resulting in progressive neuronal damage, not only at the initial site of trauma but extending to the brain globally.

Answer 116

Because the brain has high metabolic requirements, decreased cerebral oxygen delivery or hypoglycemia can rapidly result in adenosine triphosphate depletion, cell membrane pump failure, and loss of ion homeostasis. This can lead to excitotoxicity, oxidative stress, cytotoxic and vasogenic cerebral edema, inflammatory mediator release, activation of the coagulation cascade, vasospasm, and cell death.

Answer 117

With ongoing anaerobic metabolism, hyperglycemia has been documented to exacerbate neurologic damage by increasing lactic acid accumulation in the brain, resulting in neuronal and glial cell death.

Answer 118

Systemic hypoxia and hypotension, both of which can be easily recognized and treated clinically.

Answer 119

In the healthy brain, pressure autoregulation ensures that cerebral blood flow (CBF) is maintained within an acceptable range over a wide spectrum of systemic mean arterial blood pressures (50 to 150 mm Hg). In response to changes in blood pressure, parallel changes in cerebral vascular resistance occur to maintain blood flow to the brain. Pressure autoregulation is often impaired (either globally or regionally) in pets with TBI, at which time CBF becomes linearly dependant upon systemic blood pressure.

Answer 120

Intracranial pressure (ICP) is defined as the pressure exerted between the skull and its intracranial contents. The components of ICP are the volume of blood, brain tissue, and cerebrospinal fluid (CSF) within the cranial vault. In TBI, intracranial volume will increase with hemorrhage or edema. Compensatory decreases in CSF production, shunting of CSF into the cisterna magna, or by arterial vasoconstriction to lower blood volume attempt to maintain ICP within a normal range (4 to 12 mm Hg in cats and dogs). ICP increases when changes in intracranial volume exceed the ability for compensatory decreases in the other components.

Answer 121

Cerebral perfusion pressure (CPP) is the primary determinant of CBF in patients with TBI. With intracranial hypertension, CPP is equal to systemic mean arterial blood pressure (MAP) less ICP (CPP = MAP − ICP). Maintaining CPP at or above a 50 to 70 mm Hg is recommended to optimize oxygen and nutrient delivery to the brain.

Answer 122

An altered level of consciousness indicates abnormalities in the cerebral cortex or brainstem (reticular activating system).

Answer 123

alert, depressed/obtunded, stuporous, comatose.

Answer 124

An obtunded animal should still respond to noise or touch. Stupor indicates a severely impaired level of consciousness, with response only to noxious stimuli. A comatose animal exhibits no response to stimuli, including repeated noxious stimuli. It is important to remember that shock (decreased tissue oxygen delivery) can cause moderate alterations in consciousness that should improve with restoration of tissue perfusion.

Answer 125

Brainstem reflex assessment should focus on pupil size, symmetry, and position, pupillary light responses, and physiologic nystagmus.

Answer 126

the brainstem, leaving the oculomotor nerve intact and unopposed from higher centers.

Answer 127

The oculomotor nerve on the side of the injury.

Answer 128

...one side exclusively or more than the other.

Answer 129

In the absence of an underlying ophthalmologic disorder, the lack of a pupillary light response indicates disruption of the oculomotor nerve tracts ipsilateral to the injury.

Answer 130

Physiologic nystagmus refers to the normal tracking movements of the eye in response to turning the head from side to side. The absence of this reflex indicates injury to the central region of the brainstem, as may be seen with hemorrhage or compression caused by swelling or herniation.

Answer 131

Abnormalities in any of these brainstem reflexes can help localize neurologic lesions and grade severity. Pupils that are of normal size but not responsive to light represent significant brainstem dysfunction, and are only one step less severe than a fixed and dilated pupil.

Answer 132

Serial evaluation of these reflexes assists in monitoring of progression or improvement of neurologic function. For example, if midrange or mydriatic pupils without a pupillary light reflex are present on initial examination and no progression is noted, one may suspect brainstem hemorrhage. These signs, in conjunction with a comatose state and loss of physiologic nystagmus, are associated with a grave prognosis. Alternatively, a gradual progression of pupils toward mydriasis or loss of pupillary light response may indicate the development of cerebral edema that may respond to therapy to lower ICP.

Answer 133

Notation of the patient's motor activity and posture may help to localize neurologic lesions. Following TBI, the presence of ataxia, hemiparesis, or tetraparesis may be the result of lesion in the cerebral cortex or brainstem.

Answer 134

The evidence of other cranial nerve abnormalities will help differentiate intracranial from cervical lesions. Decerebrate rigidity (extension of all four limbs and opisthotonus) indicates a rostral brainstem lesion and is often associated with brainstem compression secondary to marked intracranial hypertension and/or herniation.

Answer 135

Decerebellate rigidity (extension of the front legs with hindlimb flexion) indicates a cerebellar lesion, as may be seen with cerebellar herniation.

Answer 136

Patients with decerebrate posturing will have markedly altered levels of consciousness while those with decerebellate posturing are usually alert and aware of their surroundings.

Answer 137

The Cushing (or CNS ischemic) response is a compensatory mechanism that can be seen with markedly elevated ICP. Intracranial hypertension results in decreased CBF. In response to CO2 accumulation from decreased blood flow, the vasomotor center emits a sympathetic discharge, resulting in peripheral vasoconstriction, which elevates MAP to maintain CPP. The increased blood pressure sensed at baroreceptors results in a reflex bradycardia.

Answer 138

The combination of hypertension and bradycardia in a patient with a decreased level of consciousness should alert the clinician to the possibility of increased ICP and prompt aggressive treatment.

Answer 139

THERAPEUTICS AND PATIENT CARE Extracranial Stabilization In patients with TBI, it is essential that extracranial organ systems be assessed and stabilizing therapy be instituted before initiating therapy directed at lowering ICP. The goals of extracranial stabilization should focus on early optimization of systemic oxygenation, ventilation, and tissue perfusion to minimize perpetuation of secondary neurologic injury. Hypoxemia should be avoided with TBI, as desaturation worsens outcome in humans with head trauma. Oxygen supplementation should be provided to maintain a hemoglobin saturation above 97% or a PaO2 >90 mm Hg. When in doubt, supplemental oxygen should be given to avoid any potential adverse consequences. Intranasal and intratracheal routes should be avoided, as they can cause sneezing or coughing, which transiently increases ICP.

Answer 140

Hypoventilation, resulting in an elevated partial pressure of arterial carbon dioxide (PaCO2), can occur with TBI secondary to direct damage to the respiratory center, sedatives, thoracic trauma causing pain or pleural space disease, and mechanical airway obstruction. Acute hypercarbia (respiratory acidosis) is sensed at the central chemoreceptors and results in cerebral vasodilation, increasing CBF and exacerbating elevations in ICP. PaCO2 should be maintained below 40 mm Hg with TBI. If PaCO2 cannot be maintained within a normal range, intubation alone or in combination with mechanical ventilation is required.

Answer 141

The primary goal of fluid therapy with TBI is rapid restoration of tissue perfusion and blood pressure, such that CPP is maintained above 50 mm Hg. Fluid restriction should be avoided, as it will achieve only minimal decreases in ICP and will place the animal at greater risk for hypovolemia and decreased CPP and exacerbate cerebral ischemia.

Answer 142

There are a variety of fluids for intravascular volume replacement in the head trauma patient, including isotonic crystalloids, hypertonic saline, and artificial colloids (see Chapter 129). No one fluid type can be deemed optimal for every situation.

Answer 143

Euvolemia has been restored, as its diuretic effect will contract intravascular volume and potentially worsen CPP.

Answer 144

Hypovolemic animals may respond better if hypertonic saline (7.5%) is used, as this fluid will both restore intravascular volume and exert osmotic effects on the brain.

Answer 145

Corticosteroids are not indicated, as multiple prospective clinical trials in human head trauma patients have shown no benefit. This, in combination with the many adverse effects of corticosteroids (hyperglycemia, immunosuppression, gastric ulceration, delayed wound healing, and exacerbation of a catabolic state), precludes its recommendation for use in animals with TBI.

Answer 146

Elevating the head and neck uniformly 15° to 30° above the rest of the body facilitates venous drainage from the brain, thereby decreasing ICP. Angles higher than 30° and kinking of the neck such that the jugular veins become occluded should be avoided, as arterial inflow and venous outflow can be compromised, respectively

Answer 147

Analgesia and nutrition are important treatment concerns with TBI. Provision of adequate analgesia is essential, utilizing drugs that minimize cardiovascular and respiratory depression, such as butorphanol or hydromorphone

Answer 148

Understanding the difference between perfusion abnormalities and dehydration is extremely important.

Answer 149

DISTRIBUTION OF FLUIDS Approximately 60% to 70% of body weight is water, of which one third is extracellular and two thirds is intracellular. Of the water that is extracellular, 75% to 80% is interstitial and 20% to 25% is intravascular.

Answer 150

The movement of fluid between compartments is dependent upon the permeability of the membranes separating the compartments as well as the osmotically active particles in each compartment. The colloid osmotic pressure (COP), or oncotic pressure, is one of the major forces governing fluid movement. Larger proteins that do not readily move between compartments generate this pressure.

Answer 151

Approximately 80% of the oncotic pressure is produced by albumin. This effect is enhanced by the negative charge of the protein, which attracts cations such as sodium that then attract water.

Answer 152

1. capillary hydrostatic pressure, 2. interstitial hydrostatic pressure, 3. plasma oncotic pressure, 4. interstitial oncotic pressure. Movement of molecules also depends to some extent on the size of the molecule.

Answer 153

The filtration coefficient represents the ability of water and small molecules to pass through membrane.

Answer 154

The reflection coefficient represents the ability of macromolecules (generally plasma proteins) to pass through membranes. Starling's equation on diffusion of fluids across membranes (formula)

Answer 155

Fluid flux varies in the different organs. In general intravascular hydrostatic pressure and plasma oncotic pressure are the key forces in regulating fluid balance, with the net movement of fluid being toward the interstitial space. The remaining fluid is moved back into the circulation via the lymphatics.

Answer 156

The lung is far more permeable to albumin than are other organs. This means that hydrostatic forces play a much larger role in the lung than in other tissue beds and also that the pulmonary lymphatics are extremely effective at preventing accumulation of fluid. This explains why patients with hypoalbuminemia do not regularly develop pulmonary edema, even in the face of peripheral edema, but patients with increased hydrostatic pressure, such as fluid overload, do.

Answer 157

Clinically insignificant changes in extravascular lung fluid have been noted in research animals subjected to significant changes in COP. This is due to the ability of the lymphatics to dramatically increase the fluid uptake (as much as sevenfold).

Answer 158

ALBUMIN Albumin plays a vital role in the body, of which maintaining oncotic pressure is only a part. It plays an important role as a free radical scavenger, it reduces microvascular permeability, and it reduces endothelial cell apoptosis. It is important as a carrier of drugs and other endogenous substances and affects acid-base status and metabolic functions and has anticoagulant effects.

Answer 159

Current recommendations suggest maintaining the albumin concentration at or above 2.0 g/dL in patients with acute hypoalbuminemia. Approximately 60% of the albumin is within the interstitial space, so replenishing albumin levels often requires significant volumes of plasma, especially in large dogs.

Answer 160

POOR PERFUSION (SHOCK) Perfusion is defined as the flow of blood through an organ. Poor perfusion indicates some degree of cellular shock exists associated with inadequate blood supply and delivery of oxygen to the cells. Waste products (primarily CO2) accumulate as well. The combination leads to anaerobic metabolism and acidosis/acidemia. This can lead to a breakdown in the cellular functions and ultimately cell death.

Answer 161

Patients presenting in shock often are hypovolemic from fluid loss (hemorrhage) or decreased vascular resistance (sepsis) leading to decreased venous return, but they may have poor cardiac output (congestive heart failure) poor blood flow due to circulatory disturbances (saddle thrombus).

Answer 162

1. secondary to trauma (e.g., whole blood loss), 2. third spacing of fluids (e.g., vasculitis, idiopathic hemorrhagic gastroenteritis, peritonitis), 3. acute severe dehydration (e.g., severe vomiting and/or diarrhea).

Answer 163

Understanding the cause helps determine the appropriate treatment. Altered levels of consciousness, weakness, tachycardia (not typically seen in the cat) or bradycardia with weak or absent peripheral pulses, tachypnea or severe bradypnea, pale mucous membranes with delayed or absent capillary refill time and cool extremities all indicate a state of poor perfusion or shock.

Answer 164

BLOOD VOLUME Approximately 10% of the blood volume is in the arteries, 20% is in the capillaries, and 70% is in the veins.

Answer 165

If the blood volume is normal, preload and blood pressure should be normal, assuming the animal is healthy. If a healthy animal's blood volume is low, the animal is hypovolemic, although a combination of changes in systemic vascular resistance and shunting of blood from various tissue beds means blood pressure may be normal. This can be misleading, since these patients actually require fluids to expand the intravascular space. Patients with hypervolemic states (e.g., congestive heart failure, advanced liver disease, oliguric renal failure) that require fluid therapy often present a significant challenge since continued expansion of the intravascular space can easily lead to fluid overload.

Answer 166

In clinical terms preload is the volume returning to the right side of the heart.

Answer 167

Preload is assessed most effectively by measuring central venous pressure (CVP) (normal, 1 to 3 cm H2O).

Answer 168

If no central catheter is present, the jugular veins should be clipped and examined for distention and filling. Patients with hypovolemic shock will have flat jugular veins and poor filling when the vein is held off at the thoracic inlet. Patients with diseases that interfere with return of blood to the right side of the heart (e.g., pericardial tamponade, tension pneumothorax) may have distended jugular veins in the face of hypovolemia.

Answer 169

Patients with right-sided heart failure and advanced liver disease generally will have elevated CVP.

Answer 170

Dehydration is caused by inadequate fluid intake for the animal's fluid output leading to a decrease in the fluid level in the interstitial and intracellular spaces. Dehydration is often defined by evaluating clinical parameters such as moistness of mucous membranes, skin turgor, and eye position (Table 129-1); however, these are very subjective and can be difficult to evaluate. At less than 5% dehydrated the patient may not have any physical exam abnormalities. Changes become more evident as dehydration worsens: at 10% to 12% dehydration signs of shock will be evident, and dehydration greater than 15% is associated with impending death.

Answer 171

Laboratory tests may help with the assessment of dehydration as long as the patient was normal initially.[2] For example an elevated total solids often indicates dehydration but can be confounded by the presence of hyperglobulinemia. An elevated blood urea nitrogen is consistent with prerenal azotemia as long as the patient did not have preexisting renal disease or does not have gastrointestinal hemorrhage. A urine specific gravity above the high range of normal for the species and hyperalbuminemia are always consistent with dehydration.

Answer 172

Fluids administered to patients are characterized frequently by their osmolality and are considered hyperosmolar, isosmolar, or hypoosmolar. Fluids are also referred to as being hypertonic, isotonic, and hypotonic to the patient's serum based on the number of effective osmoles in a solution.

Answer 173

Osmolality is the concentration of osmotically active particles in a kilogram of solution. It is dependent solely on the number of particles and is not affected by size, weight, or charge of the particle. Osmolarity is the number of particles per litre of solvent. Normal osmolality for dogs is 290 to 310 mOsm/kg and 308 to 335 mOsm/kg in cats. (osmolality can be calculated from a formula).

Answer 174

Osmoles may be effective or ineffective. Effective osmoles generate osmotic pressure—the ability to cause water to shift from one compartment to another. If the membrane separating the two compartments is permeable to the solute in question, the osmole is ineffective. Urea is an osmole but is generally ineffective since it is permeable across most membranes. Glucose is an effective osmole since it will not pass across most membranes without the addition of insulin. Tonicity refers to the effective osmolality

Answer 175

Crystalloids Crystalloids are aqueous solutions of mineral salts (usually predominantly sodium and chloride) or other water-soluble molecules that are capable of distributing to all fluid compartments. They include replacement fluids, maintenance fluids, and fluids such as 5% dextrose in water.

Answer 176

Crystalloids are generally isosmolar; however, they become hyperosmolar once other medications or supplements are added to the fluids. This may be important to patient therapy.

Answer 177

All of the replacement fluids, except for 0.9% saline, are hypotonic in the cat.

Answer 178

Replacement crystalloids have electrolyte concentrations that resemble the extracellular fluid. Commonly used replacement fluids are 0.9% saline, lactated Ringer's solution, and Normosol-R or Plasmalyte-A (Table 129-2).

Answer 179

Since approximately 75% of extracellular fluid is in the interstitial space, crystalloids will rapidly redistribute, and after as short a period of time as 20 to 60 minutes only approximately 25% of the administered volume will remain in the circulation. This number may be even smaller in the face of increased vascular permeability. The remainder of the fluid will be in the interstitium minus a small amount that will have been lost via the urine. This increase in interstitial fluid can lead to tissue edema, which decreases the ability of oxygen to diffuse to the cells.

Answer 180

Interstitial edema may be extremely detrimental in cases of cerebral edema and pulmonary edema. On a short-term basis crystalloids will expand the intravascular space, but this effect will be temporary. Replacement crystalloids should be thought of as interstitial rehydrators, not intravascular volume expanders.

Answer 181

All of the replacement crystalloids except for 0.9% saline contain a buffer. Buffered solutions usually contain lactate, gluconate, or acetate, which when metabolized produce bicarbonate.

Answer 182

Lactate must be metabolized in the liver. Significant liver dysfunction must be present in order for the lactate in lactated Ringer's solution to cause a clinically significant problem.

Answer 183

Solutions buffered with acetate and gluconate (e.g., Plasmalyte-A, Noromsol-R) have theoretical advantages over lactated Ringer's solution in that muscle can metabolize the acetate and gluconate and the amount of buffer present in these solutions is almost double the amount in lactated Ringer's solution.

Answer 184

Concerns have been raised about the routine use of lactated Ringer's solution due to the adverse effects of the lactate, including neutrophil priming and worsening of cellular apoptosis. Buffered solutions are usually indicated for resuscitating patients in shock as well as routine use in patients that require a replacement fluid.

Answer 185

Due to its acidifying nature, 0.9% saline should generally be reserved for patients with 1. gastric outflow obstructions, 2. patients with hypoadrenocorticism, and 3. patients with hypercalcemia. It is important to note that electrolyte abnormalities cannot be corrected in patients with any of these three conditions without infusion of saline.

Answer 186

Maintenance crystalloids contain electrolyte concentrations designed to match normal daily electrolyte losses in urine and feces. They contain much less sodium (40 to 60 mEq/L) and more potassium (15 to 30 mEq/L) than a replacement crystalloid (see Table 129-2). Maintenance fluids are isotonic in the bag due to the added dextrose; however, the dextrose is rapidly metabolized to free water, making the solution hypotonic.

Answer 187

Maintenance crystalloids should be used in patients who are unable to drink, and, therefore, have a free-water requirement, but only have ongoing electrolyte losses through normal urine and feces production. Maintenance fluids should also be used in those who will not tolerate the sodium load of a replacement fluid such as patients with heart failure, severe liver disease, or oliguric renal failure.

Answer 188

Dextrose 5% in water is a nonelectrolyte fluid and should not be used for fluid resuscitation. It is hypotonic and may cause fluid shifts and red cell lysis. It is typically used to replace free-water deficits or as a diluent for medications that need to be administered via constant rate infusion. It should never be given as a large volume bolus since the rapid decrease in osmolality can lead to life-threatening cerebral edema. Dextrose 5% in water only contains 200 kcal/L and does not contain sufficient energy to keep up with patient caloric requirements.

Answer 189

Hypertonic saline is a hyperosmolar crystalloid fluid. It is usually given as a 7.5% solution (2600 mOsm/L). The hyperosmolarity leads to extremely rapid intravascular volume expansion by drawing fluids from the interstitial and intracellular space into the intravascular space. It can produce an intravascular volume expansion equivalent to that of colloids but at one fourth the volume. Because it is a crystalloid it will rapidly redistribute, similar to all other sodium chloride–based solutions; however, its effects can be prolonged by concurrent administration of a colloid. It also appears to have immunomodulatory effects including decreasing mesenteric lymph production and eliminating neutrophil priming, which decreases susceptibility to sepsis following hemorrhagic shock.[3] It is used in resuscitation of severe hypovolemic shock and is the fluid of choice in patients who are in extremis due to its rapid onset of action as well as efficacy. It should be used with caution in patients with uncontrolled internal hemorrhage

Answer 190

Colloids Colloids are effective intravascular volume expanders. They are fluids containing high–molecular weight substances that generally are not able to pass through capillary membranes. The colloid osmotic pressure they exert is related to the size of the molecule: the smaller the size of the molecule the higher the initial oncotic pressure since more smaller particles fit in a volume of fluid than larger molecules. The larger the molecule, the longer it lasts. Examples include synthetic colloids such as the gelatins, dextrans, hydroxyethyl starches, and hemoglobin-based oxygen-carrying solutions, and natural colloids such as whole blood, plasma, and human serum albumin

Answer 191

Gelatins are hyperosmolar fluids produced from bovine gelatin. Dextrans are polysaccharides produced by the bacterium Leukonostoc in a sucrose media. Hydroxyethyl starch is a molecule made from maize or sorghum that is primarily an amylopectin. Pentastarch is a slightly lower molecular weight hydroxyethyl starch with an average molecular weight of 264,000 Daltons. Synthetic colloids are indicated when the patient is hypovolemic and has a low colloid osmotic pressure. Conditions including acute hemorrhage or loss of albumin (“third-spacing”) due to increased vascular permeability such as SIRS (systemic inflammatory response syndrome) and sepsis frequently lead to low oncotic pressure.

Answer 192

Since most patients in shock require sustained intravascular volume expansion, colloids are indicated frequently during fluid resuscitation. Sequential volumes of 5 mL/kg to a maximum of 20 mL/kg in the dog and 15 mL/kg in the cat are given during resuscitation. Synthetic colloids can be given as a slow intravenous push in dogs but should be given over 15 to 20 minutes in cats because hypotension will worsen temporarily in some cats following a rapid infusion. Patients with SIRS or sepsis with ongoing losses of albumin frequently require constant rate infusions of a synthetic colloid until the inflammation has subsided. During constant rate infusions of colloids crystalloid infusion volumes are decreased by 40% to 60% of what would be calculated if crystalloids alone were being used. If volumes greater than 20 mL/kg/day are infused, the patient should be monitored for the possible onset of a dilutional coagulopathy.

Answer 193

Hemoglobin-Based Oxygen Carriers The only hemoglobin-based oxygen-carrying (HBOC) solution currently approved for use in veterinary medicine is Oxyglobin (Biopure, Cambridge, Mass.), which is a purified, polymerized bovine hemoglobin that is in a modified lactated Ringer's solution. It has many properties that make it a valuable fluid during resuscitation.[11] It is isosmotic and has an average molecular weight of 200,000 Da, making it a very effective colloid, and a pH of 7.8. Its oxygen affinity is dependent upon the chloride ion concentration not the concentration of 2,3-diphosphoglycerate (2,3-DPG). This provides a distinct advantage over canine blood that has been stored longer than 1 week, which may have significantly depleted 2,3-DPG levels lead to increased oxygen binding and decreased oxygen delivery at the tissue level. In addition, the normal oxygen affinity of Oxyglobin is lower than that of normal canine blood, which enhances delivery of oxygen to the tissues. It has a lower viscosity than canine blood, which may improve microvascular flow. Because it is a smaller molecule than red cells, it is able to perfuse vasoconstricted tissue beds that red cells cannot pass through. It has vasconstricting properties that are of benefit in shock; however, concerns have been raised about excessive vasoconstriction in some tissue beds—especially the lung, where pulmonary hypertension may result.

Answer 194

Oxyglobin can be administered via standard intravenous administration sets, and standard intravenous infusion pumps can be used for delivery. Because it contains no antigens, cross-matching is not required and there is no possibility of transfusion reactions. Filters are not required. It can be kept at room temperature and has a 3-year shelf life, which makes it useful for hospitals that cannot keep blood products readily available. Once opened, the bag must be discarded within 24 hours due to the production of methemoglobin.

Answer 195

Oxyglobin is up to 10 times more effective than blood when given during fluid resuscitation to animals in hemorrhagic shock. For this reason, low volumes of Oxyglobin can be used effectively to treat hemorrhagic shock. It has a short half-life (30 to 40 hours); however, the length of clinical benefit is currently unknown. Primary effects last about 24 hours, and 90% of the Oxyglobin is eliminated in 5 to 7 days.

Answer 196

HBOCs are indicated during resuscitation when increased oxygen delivery to tissues is desired. Administration of HBOCs also is indicated in anemic patients but must be used with caution in patients that are euvolemic (e.g., those with immune-mediate hemolytic anemia), and should be used with extreme caution in patients that are hypervolemic (e.g., patients with congestive heart failure or oliguric/anuric renal failure) because of its potent oncotic pressure.

Answer 197

Since cats appear to be more predisposed to rapid onset of pulmonary edema when fluid overload occurs, Oxyglobin should be infused over a minimum of 8 hours in euvolemic cats.

Answer 198

Low-volume resuscitation with Oxyglobin may restore aerobic metabolism, although hypovolemia, hypotension, and low cardiac output persist.

Answer 199

The hemoglobin is dissolved in the plasma, and some is able to diffuse into the interstitium, which makes it a very effective oxygen-carrying solution. Therefore, the amount of Oxyglobin administered should be based on clinical signs rather than a specific target hemoglobin concentration. Doses of Oxyglobin as low as 3 to 5 mL/kg may be effective in improving tissue oxygen delivery in moderate shock, and doses as low as 7 to 8 mL/kg may be all that is indicated in severe hemorrhagic shock.[12] The daily volume administered should not exceed 30 mL/kg/day.

Answer 200

Discoloration of mucous membranes, sclera, and urine, which affects patient monitoring. Measurements of many serum tests are affected for at least 24 to 72 hours after administration of Oxyglobin. A list of which tests are accurate with different analyzers is available. Packed cell volumes do not correlate with hemoglobin; therefore, hemoglobin levels should to be measured directly if an accurate measurement is indicated. Mild gastrointestinal effects have been reported but are very rare.

Answer 201

Human Albumin Human albumin, made from pooled human plasma, is a concentrated source of albumin. At a 25% concentration the COP is 200 mm Hg, making it a very potent colloid that is able to expand the intravascular volume by 4 to 5 times the volume infused. It is also hyperosmolar at 1500 mOsm/L. Because of these combined effects, the risk for fluid overload in a patient that is only mildly hypovolemic or euvolemic is high. It provides all the beneficial effects of albumin (see above).

Answer 202

The fluid infusion should be considered a transfusion with all the potential for both acute reactions such as facial swelling, fever, vomiting and anaphylaxis and delayed immune-mediated reactions such as polyarthritis and vasculitis that may not show up for several weeks. Once patients have been exposed to the human serum albumin, they will develop antibodies and transfusions should never be administered again during the life of the patient (severe allergic reactions may make human albumin a product to be used only if no other options are available).

Answer 203

Natural colloids include whole blood (fresh, stored, or autotransfused), packed red blood cells (although the oncotic pressure of packed red blood cells is very low), and plasma. (The reader is referred to Chapter 142 for further information.) If the patient is acutely anemic, administration of red blood cells may be required. In the critical acutely anemic patient the goal should be to maintain a hematocrit of approximately 30% in the dog and 27% in the cat.

Answer 204

Autotransfused blood is the simplest to give but has a potential for significant side effects. Blood should be collected aseptically into sterile containers and administered with a filter. The need to anticoagulate is somewhat controversial since blood collected from body cavities tends to lack platelets and fibrin and is not able to clot.

Answer 205

If a large volume of autotransfused blood is administered, fresh frozen plasma should be transfused to minimize the likelihood of disseminated intravascular coagulation developing. Ideally blood from the abdomen should not be used until it has been determined that there is no gross contamination (e.g., from a ruptured bowel). In emergency situations only, the blood may have to be used without aseptic collection or knowing whether it is contaminated, and may be delivered without a filter.

Answer 206

Unless the blood type of the recipient and donor are known, all recipients of a red cell–containing transfusion ideally should have a major and minor crossmatch. Dogs who are in danger of dying and have never received a transfusion usually can be transfused without a crossmatch, but the patient should be monitored closely for any immune-mediated reactions including delayed reactions that may not show up for several weeks.

Answer 207

Since cats have naturally occurring alloantibodies, they must be typed or ideally crossmatched prior to transfusing since even a few drops of type A blood given to a type B cat can cause death.

Answer 208

If a large volume of anticoagulated blood was infused, calcium levels should be closely monitored. The citrate will bind the serum calcium causing a clinically significant hypocalcemia.

Answer 209

Patients with acute hypoalbuminemia (less than 2.0 g/dL) should receive a source of albumin to maintain the albumin as close to 2.0 g/dL as possible. It takes approximately 15 to 20 mL/kg of plasma to raise the albumin 0.5 g/dL assuming no ongoing losses.

Answer 210

Known coagulopathic patients should receive coagulation factors (fresh blood or fresh frozen plasma depending on the situation) as soon as possible. Patients with SIRS or sepsis are often at risk for becoming coagulopathic, and transfusion should be considered as soon as signs of coagulation abnormalities are noted. Plasma also provides a source of α-macroglobulin, which binds the activated and liberated proteases in patients with pancreatitis and therefore has some as yet clinically unproven benefits in these patients.

Answer 211

Blood and blood products are typically infused over 2 to 6 hours; however, they can be infused as fast as necessary to restore perfusion parameters in patients who need rapid volume resuscitation.

Answer 212

The intraosseous route typically can be used safely to administer any fluid that would be administered via a central catheter. The exception to this is hypertonic saline, which should not be infused intraosseously until further data are available since it has been shown experimentally to cause myonecrosis.

Answer 213

Based on Poiseuille's law, flow is directly proportional to the radius to the fourth power and indirectly proportional to length; therefore, a large-gauge, short catheter will allow the most rapid administration rates.

Answer 214

Ideally, significantly hyperosmolar fluids (greater than approximately 550 mOsm/L) should be infused via a central catheter. If this is not possible, the smallest gauge catheter possible should be inserted. The small gauge of the catheter encourages blood flow around the catheter, which helps dilute the hyperosmolar fluid and prevent phlebitis. Subcutaneous fluids should be given with caution in cats with occult cardiomyopathy since the sudden absorption of a large volume of fluid can precipitate congestive heart failure.

Answer 215

Moderate to large volumes of subcutaneous fluids should also be given with caution in patients with polyuric renal failure and hypokalemia since the ensuing diuresis can lead to a hypokalemia severe enough to cause severe muscle weakness. Irritating or hypertonic fluids should not be given subcutaneously.

Answer 216

Fluids are chosen based more on an understanding of the pathophysiology behind a disease process than on a diagnosis. Significant volumes of whole blood loss ideally should be replaced with whole blood.

Answer 217

Patients with protein-losing enteritis should ideally receive a combination of electrolyte-containing fluids and albumin-containing fluids. Patients with pure water and electrolyte loss should receive a fluid that replaces the water and electrolytes. Evaluation of recent laboratory tests such as hematocrit, albumin, glucose, electrolytes, urea, creatinine, and blood gases also can help guide the choice of fluid.

Answer 218

Figure 129-1 Algorithm to formulate a fluid therapy plan. PCV, Packed cell volume.

Answer 219

FLUID ADDITIVES Fluid additives are often required as a part of patient therapy. The most common are potassium (Table 129-4) and dextrose. The amount of potassium to be added to the fluid should be adjusted based on the fluid being administered, the patient's underlying disease, the patient's pH and serum potassium concentration, and the rate of fluid administration. A rate of 0.5 mEq/kg/hr ideally should not be exceeded without close cardiac monitoring. Potassium along with other electrolytes should be checked daily—more frequently if the potassium supplementation rate is high or there are concerns for severe, ongoing losses.

Answer 220

RECOMMENDED CONCENTRATION IN FLUID 3.5-5.5 mEq/L: 20 mEq/L 3.0-3.5 mEq/L: 30 mEq/L 2.5-3.0 mEq/L: 40 mEq/L 2.0-2.5 mEq/L: 60 mEq/L <2.0 mEq/L: 80 mEq/L

Answer 221

The addition of medications increases the osmolality of the fluids. This is rarely a problem but should be evaluated on a patient-by-patient basis. Additives should always be checked for compatibility with the fluid being used as a diluent to ensure the pH or the constituents of the fluid will not inactivate the medication or cause it to precipitate. Compatibility with other medications or fluids that are being infused through the same intravenous line also should be checked. For instance, calcium-containing fluids should not be administered concurrently through the same line as blood products anticoagulated with ............. since the resultant ..................... may be detrimental to the patient. Additives should be checked carefully for light stability.

Answer 222

Fluid should be infused until signs of perfusion have normalized. In an ideal situation this would mean that the heart rate is normalized, blood pressure (systolic pressure of 100 to 120 mm Hg, diastolic pressure of 60 to 80 mm Hg) and CVP (6 to 9 cm H2O) are normalized, mucous membrane color and capillary refill time are normalized, temperature (toe web and central) is normalized, and urine output is normalized.

Answer 223

If blood pressure measurement is not available, the strength of peripheral pulses (dorsal metatarsal) should be assessed rather than femoral pulses. Ideally, blood gas values and/or lactate concentrations should also be used to help determine the effectiveness of resuscitation

Answer 224

If blood volume has been maximized based on estimation of jugular venous distention, measurement of CVP, or evidence of fluid overload, but the patient is still hypotensive, positive inotropes or vasopressors may be required.

Answer 225

More specific goals recently defined for septic human patients in order to reduce morbidity include achieving a mean arterial pressure of greater than 65 mm Hg, a CVP of 6 to 9 cm H2O, a urine output greater than 0.5 mL/kg/hr, and a central venous oxygen saturation of 70%. These goals remain untested in dogs and cats; however, they may prove to be of value

Answer 226

The maximum fluid volume to be infused is chosen to some extent based on the blood volume of the patient, which in the dog is approximately 80 mL/kg and in the cat is 60 mL/kg. Fluids should be given as fast as necessary to resuscitate the patient. Because of the rapid redistribution rate of crystalloid fluids, very rapid boluses are required in order to determine if the patient is responding to volume infusion.

Answer 227

Resuscitation is usually started with a bolus of 20 to 30 mL/kg of a buffered, balanced electrolyte solution. This volume is reduced by approximately 30% in cats. Doses of 4 mL/kg of a 7.5% saline solution are given to dogs and 2 to 4 mL/kg to cats for patients in extremis.

Answer 228

If the patient is suspected—based on clinical presentation, lack of response to an initial bolus of crystalloids, or initial lab work—of having a low colloid osmotic pressure, synthetic colloids are used during initial resuscitation with sequential boluses of 5 mL/kg to a maximum of 20 ml/kg in the dog and 15 mL/kg in the cat to improve the blood volume and blood pressure to the desired end point. Doses of Oxyglobin of 3 to 5 mL/kg can be given in lieu of other synthetic colloids.

Answer 229

Ongoing hemorrhage, ongoing losses through vomiting, diarrhea, polyuria, or third-space losses, as well as movement of crystalloids out of the vascular space.

Answer 230

Hypotensive resuscitation refers to a controversial form of resuscitation provided to trauma patients that may still be actively hemorrhaging internally.[16] It involves the use of limited fluid resuscitation until the hemorrhage is controlled. The systolic blood pressure is maintained between approximately 80 and 100 mm Hg with the goal being to avoid increased hemorrhage from normotension or hypertension that might cause fragile clots to be disrupted. This not only helps prevent loss of hemoglobin but also other plasma proteins including albumin and clotting factors. Dilution of clotting factors from excessive administration of crystalloids or synthetic colloids also is avoided. There is danger of maintaining inadequate perfusion to various organs, especially the gastrointestinal tract, kidneys, muscles, and skin, since the patient is not being adequately resuscitated. The advantage is that severe hemorrhage may ultimately be controlled without requiring administration of multiple units of blood products and the patient's life may be saved. Hypotensive resuscitation can be particularly helpful in patients with significant intraabdominal hemorrhage.

Answer 231

Mild dehydration rarely causes severe problems other than making the patient feel unwell; however, if the patient has other underlying diseases such as renal insufficiency, even mild dehydration can lead to serious problems. If severe enough, dehydration can lead to perfusion problems. In dehydrated patients perfusion deficits should be dealt with using intravenous fluids according to the guidelines above (see Table 129-1).

Answer 232

The body weight in kilograms is multiplied by the estimated percent dehydration (as a decimal). This will indicate fluid deficit in liters of fluid. For instance a 5-kg patient estimated at 8% dehydrated has a fluid deficit of 0.4 L, or 400 mL.

Answer 233

Fluid deficits should always be calculated since estimating fluid rates by placing an animal on two or three times maintenance rates will almost always significantly underestimate fluid requirements, which can lead to significant patient morbidity. Along with assessment of physical examination parameters, monitoring urine specific gravity (assuming renal function is normal) can help determine if adequate volumes of fluid are being administered.

Answer 234

Fluids should be given more slowly to restore dehydration since the fluids need to have time to redistribute. Patients with no underlying disease that could lead to volume overload (advanced heart disease, liver or oliguric renal failure) should be rehydrated over 4 to 12 hours. Shorter time frames are used in patients who became dehydrated very acutely or if there are concerns for severe, ongoing losses. Older patients or patients with concurrent disease process may need to be rehydrated over 24 hours.

Answer 235

CALCULATING DAILY REQUIREMENTS Daily fluid requirements will vary based on maintenance requirements and ongoing losses. Recommendations for daily maintenance requirements vary considerably from 40 to 60 mL/kg/day or 2 mL/kg/hr. These formulas may underestimate for smaller patients and overestimate for much larger patients.

Answer 236

Some advocate using a volume based on the daily energy requirement formula of (30 × body weight [kg]) + 70 in dogs and 50 × body weight (kg) in cats.

Answer 237

Puppies and kittens will generally have much higher fluid requirements than adult animals, and recommendations are to double the adult fluid requirement in these patients.

Answer 238

Polyuric patients, especially those with renal dysfunction (e.g., renal failure, postobstructive diuresis), can have extremely high fluid requirements. Some cats will need as much as 100 mL/hr. Fluid rates should be adjusted to match measured urine production and to ensure elevated serum urea nitrogen and creatinine concentrations are continuing to decrease.

Answer 239

An increase in renal blood tests may be in indication of pending oliguric and anuric renal failure but more commonly is associated with inadequate fluid therapy, especially if the potassium concentrations are not rising. In renal failure patients it is almost impossible to maximize fluid diuresis without measuring CVP without causing fluid overload. Regardless of the formula chosen, the patient must be monitored clinically every 4 to 8 hours for signs of dehydration, normal hydration, and overhydration, and based on findings the fluid plan should be adjusted accordingly.

Answer 240

FLUID OVERLOAD Normal patients are quite tolerant of excessive volume administration; it is removed by the kidneys in the form of increased urine production. The sick patient may not be so tolerant. If the intravascular space is expanded too rapidly, the patient may develop signs of pulmonary edema. This is a late sign and indicates the earlier signs were overlooked or the patient had unrecognized cardiac disease. Central venous pressure or jugular filling will increase followed by an increase in respiratory rate and effort (often more easily monitored in the cat than the dog) before auscultable or radiographic signs of pulmonary edema develops.

Answer 241

If excessive crystalloids are administered, patients will typically develop signs of overhydration before they develop signs of hypervolemia. If the kidneys are functioning normally again, increased urination will usually be noted.

Answer 242

Signs of pathologic overload include chemosis and serous nasal discharge. Weight gain also will be noted although accurate weights in animals often can be complicated by variations based on how the animal sits on the scales. If the patient is hypooncotic the first sign may be peripheral edema. In recumbent dogs this most commonly occurs in the distal pelvic limbs, usually the downside limb. If “fat face” occurs the patient has significant fluid overload; this is often a poor prognostic finding.

Answer 243

As a rule of thumb a patient without underlying renal dysfunction should be producing 1 mL/kg/hr or urinating every 4 to 6 hours when receiving intravenous fluid therapy.

Answer 244

Infusions of excessive volumes of crystalloids should be avoided since patients who are given large volumes of crystalloids during resuscitation will develop interstitial edema, which will worsen oxygen delivery at the cellular level.

Answer 245

Synthetic colloids, not plasma, should be used for volume resuscitation if the patient has an albumin less than 2 g/dL. Synthetic colloids are not a replacement for albumin or clotting factors, and patients who need synthetic colloids frequently need plasma. Ideally, serum albumin levels should be maintained as close to 2 g/dL as possible using species-specific albumin sources.

Answer 246

The patient's hematocrit should be maintained at or above 27% to 30% in the case of acute hemorrhage and below 48% in hemorrhagic gastroenteritis patients to maintain good rheology and oxygen delivery.

Answer 247

Infusion of whole blood or HBOC to anemic patients that are euvolemic can rapidly cause fluid overload and should be avoided or given very slowly.

Answer 248

Colloids should be avoided in patients with chronic hypoalbuminemia because they are not always hypovolemic and it is easy to fluid overload them.

Answer 249

When rehydrating patients, the degree of dehydration should always be estimated and a fluid deficit calculated and replaced over 6 to 12 hours unless the patient is at risk for fluid overload. This deficit needs to be added to the maintenance requirements as well as estimated ongoing losses.

Answer 250

Fluids should be given based on the needs of the patient. Polyuric patients may produce far more urine than anticipated and providing “three times maintenance” may severely underestimate their requirements.

Answer 251

It is difficult to maximize fluid administration without assessing central venous pressure. Fluids should be infused to achieve a desired end point.

Answer 252

Dogs and cats afflicted with either diabetic ketoacidosis (DKA) or hyperglycemic hyperosmolar syndrome (HHS) can become acutely ill and benefit from prompt diagnosis and treatment. These disorders usually occur in middle-aged to old pets, often after a variable period of time characterized by polydipsia, polyuria, and weight loss. Alternatively, they can occur as acute metabolic complications of other conditions, such as acute pancreatitis or sepsis.

Answer 253

Hyperglycemia and accelerated ketogenesis occur when there is an absolute or relative deficiency of insulin and a relative excess of glucagon and other “counter-regulatory hormones” such as cortisol, growth hormone, and epinephrine. Consequently, glucose and ketoacids are both overproduced and underutilized.

Answer 254

Ketoacidosis can occur as a result of insulin deficiency, but coexisting glucagon excess will accelerate the process.

Answer 255

The nitroprusside reaction is used to detect and semiquantitate plasma, serum, and urinary ketones. The test detects acetone and acetoacetate but does not react with beta hydroxybutyrate. This characteristic has clinical importance in situations in which shocklike states promote the production of beta hydroxybutyrate, thereby disabling clinical detection of ketoacidosis with the nitroprusside test.

Answer 256

After institution of insulin treatment, the beta hydroxybutyrate–to-acetoacetate (B:A) ratio decreases as a result of the metabolism of beta hydroxybutyrate to acetoacetate.

Answer 257

Although acetoacetate concentrations eventually decrease, the shifting B : A ratio explains the clinical paradox occasionally encountered in which test results may initially be negative for ketones, but the same test performed on the second and third days of treatment may, occasionally, be positive despite clinical improvement.

Answer 258

A lingering ketonuria can also occur as a dog or cat improves because of the delayed clearance of acetone. Therefore, it is not uncommon for ketones to persist well into the third or fourth hospital day while the pet shows signs of improvement. It is for this reason that the calculation of insulin dosages should depend solely on the blood glucose concentration

Answer 259

anorexia, depression, weakness, and vomiting may have been seen for only 1 to 3 days.

Answer 260

Oliguria or anuria should be suspected if the owner reports polyuria for days or weeks and then no urine for 1 to 2 days prior to the examination. It has been suggested that both conditions are invariably associated with concurrent disorders.

Answer 261

The term diabetic coma is frequently used to describe the mental effects of the ketoacidotic and hyperosmolar conditions, but only a small percentage of dogs or cats actually have profound decreases in consciousness.

Answer 262

DIAGNOSTIC EVALUATION Because hepatic production of glucose is increased in diabetic dogs or cats, the degree of hyperglycemia is determined by the severity of plasma volume depletion.

Answer 263

Therefore, extreme levels of hyperglycemia tend to occur only when extracellular fluid volume and blood pressure have decreased so much that urine flow is impaired. This is most obvious in dogs or cats that have extreme increases in blood glucose concentrations with minimal glucosuria, which will usually signify oliguria.

Answer 264

Metabolic acidosis is mainly attributed to ketoacid buildup, but acidosis can be enhanced by coexisting disease, such as renal failure and lactic acid production. The metabolic acidosis often is accompanied by a large anion gap (AG) (greater than 30 mEq/L)

Answer 265

AG= (Na+ + K+)-(HCO3- + Cl-=

Answer 266

Hyponatremia in both syndromes can be factitious (attributable to hypertriglyceridemia) or real (due to urinary or gastrointestinal loss of sodium ions).

Answer 267

When any rapid increases in the plasma glucose concentration draw water into the extracellular space, there by diluting plasma constituents and allowing for cellular dehydration.

Answer 268

The serum potassium concentration in DKA and HHS can range from less than the reference range to normal to greater than the reference range. Hyperkalemia can result from a shift of potassium from the intracellular to the extracellular space as a consequence of acidemia, insulin deficiency, and increased plasma hyperosmolarity. It may also be associated with oliguric or anuric acute renal failure.

Answer 269

Pseudohyperkalemia can accompany any patient that has a thrombocytosis as can be found with coexisting hypercortisolism.

Answer 270

Hypokalemia is the most common and most serious electrolyte disturbance. This is usually a reflection of a substantial reduction in total body potassium stores. Even dogs and cats with normokalemia can have life-threatening deficits of total body potassium; because 98% of total body potassium is intracellular, these concentrations are not easily assessed.

Answer 271

Vomiting and osmotic diuresis and can be further complicated by therapy. A coexisting ketoalkalosis can also cause hypokalemia, usually caused by losses through excessive vomiting.

Answer 272

Serum dilution from rehydration, continued urinary losses, correction of acidosis, and increased cellular uptake can “unmask” hypokalemia.

Answer 273

Phosphorus is an integral component of lean body mass. The enhanced catabolism of muscle and fat that invariably occurs in diabetes mellitus results in increased urinary phosphorus excretion and phosphorus wasting.

Answer 274

Increased serum liver transaminase (ALT) and alkaline phosphatase (SAP) activity is commonly attributable to the hepatic lipidosis that occurs in patients with DKA. Hypovolemia-induced central lobular necrosis can also increase liver enzyme values as can cholangiostasis due to coexisting acute pancreatitis. These hepatic changes are completely reversible, and serum liver enzyme activity moves toward normal after successful treatment. Because diabetic dogs and cats almost always have abnormal liver enzyme values, it is common for these test results to completely “normalize” within a week or two so long as the hepatic lipidosis does not progress.

Answer 275

Azotemia can be either prerenal or renal in origin. Extensive primary renal dysfunction is characterized by isosthenuria (fixed urine specific gravity of 1.008 to 1.012) in a dehydrated patient and an accompanying azotemia that does not readily resolve with rehydration. It should be remembered, however, that both glycosuria and hyperosmolarity can raise a urine specific gravity that remains “isosthenuric” (a specific gravity of 1.020 when the serum osmolality is 400 does not indicate good renal function).

Answer 276

Urine sediment should be screened for any signs of infection such as pyuria and bacteriuria. Urine output should be monitored to detect oliguria or anuria. A leukocytosis with a mature neutrophilia in the 20 × 103 range can be due to the stress associated with both disorders. Detection of bands and toxic cell changes should prompt a search for an inflammatory focus, which may or may not be accompanied by an infection.

Answer 277

Figure 130-1 Algorithm for the management of the critically ill dog and cat with diabetic ketoacidosis and hyperglycemic hyperosmolar syndrome. 

Answer 278

Dehydration volume deficit (mL) = Dehydration% x BW (kg) x 1000

Answer 279

The 24-hour maintenance volume is roughly estimated (assuming adequate urine output) at 66 mL/kg (30 mL/lb). Therefore, the first 24-hour total fluid volume is the sum of the dehydration and the maintenance volumes plus any ongoing losses from vomiting or diarrhea.

Answer 280

If the animal is 8% to 12% dehydrated, half of the estimated dehydration deficit should be administered intravenously over the first 2 to 4 hours of hospitalization; the remaining replacement and maintenance volumes, given over the following 20 to 22 hours, should be accompanied by any adjustments necessitated by changes in urine volume.

Answer 281

Oliguria and anuria call for major parenteral fluid reductions to where the amount infused will include measured urine output, insensible fluid losses, and any ongoing losses.

Answer 282

Hydration alone can substantially decrease the blood glucose level and hyperosmolarity. Hypovolemia in DKA and HHS is corrected with isotonic solutions, such as lactated Ringer's solution or 0.9% saline. Recommended maintenance solutions include 0.45% saline or half-strength lactated Ringer's solution so long as hyponatremia does not occur. Dextrose solutions (2.5% to 5%) are used when the patient's blood glucose declines to 250 mg/dL or less in the setting of continued insulin administration.

Answer 283

Hyponatremia for both disorders is corrected with intravenous 0.9% saline solution to avoid any plasma hypoosmolality that might occur when the hyperglycemia is reduced with insulin treatment.

Answer 284

Plasma hypoosmolality can cause a reversal of osmotic gradients and overexpansion of the intracellular compartment with resultant potentially fatal cerebral edema.

Answer 285

Potassium supplementation is best provided by adding potassium chloride solution to the parenteral fluids. If concurrent hypophosphatemia is present, one third of the potassium supplement can be in the form of potassium phosphate. Potassium supplementation is best begun after the first 2-hour period of fluid replacement, when hydration, blood pressure, and urine output are improved. If the patient is initially hypokalemic, potassium chloride (KCl) can be added to the hydrating solution; however, the infusion should be slowed so that half the dehydration replacement volume is delivered over an additional 1 to 3 hours.

Answer 286

Although most texts list the maximum rate of potassium ion administration as 0.5 mEq per kilogram of body weight (BW) per hour, the author's experience has shown that this rate can be safely doubled when the patient is severely hypokalemic (serum potassium level less than 2.5 mEq/L) as long as electrocardiographic and urine output monitoring is done. The recommended amount of potassium that can be added to the parenteral fluids over a 24-hour period is shown, using two different but equally effective methods.

Answer 287

Administer 2 to 3 mEq/kg or add 30 to 40 mEq KCl per liter of replacement fluid.

Answer 288

Administer 3 to 5 mEq KCl/kg or add 40 to 60 mEq KCl per liter of replacement fluid.

Answer 289

Administer 5 to 10 mEq KCl/kg or add 60 to 80 mEq KCl per liter of replacement fluid

Answer 290

Any needed phosphate replacement can be given as potassium phosphate solution at the recommended dose of 0.01 to 0.03 mmol/kg BW/hr, with repeat serum phosphorus determinations every 6 hours. Attention should be given to avoiding iatrogenic hyperphosphatemia and hypocalcemia. These complications can be avoided if the phosphate replacement is discontinued when the serum level is restored to 2.5 mg/dL.

Answer 291

Hypomagnesemia has been shown to cause specific problems, especially cardiac arrhythmias, in diabetic humans; however, its association with any particular dysfunction in diabetic dogs and cats has not yet been demonstrated.

Answer 292

Sodium bicarbonate treatment for DKA is controversial. Advocates of this treatment cite concern that severe acidosis (blood pH less than 7.0) can adversely affect cardiovascular function; opponents base their concern on the treatment's causal relationship with paradoxical cerebrospinal fluid acidosis, hypokalemia, and worsened intracellular acidosis with overshoot alkalosis and delayed ketoanion metabolism.

Answer 293

The use of sodium bicarbonate should be restricted to dogs or cats with a blood pH below 7.1 or those with a serum total carbon dioxide (CO2) concentration less than 10 to 12 mEq/L.

Answer 294

1. The cessation of ketogenesis, 2. The metabolic conversion of ketones to bicarbonate after initiation of insulin treatment, 3. Improved renal function, 4. Conversion of the lactate in lactated Ringer's solution to bicarbonate.

Answer 295

NaHCO3 (mEq) = Base deficit (mEq) x 0,3 x BW (kg)

Answer 296

Subsequent alkali treatment depends on the results of repeat plasma pH measurements; it should be discontinued when the blood pH has been restored to 7.2 or higher or until the serum total CO2 concentration is greater than 10 to 12 mEq/L.

Answer 297

Mixed acid-base disorders can also occur. Ketoalkalosis can occur from excessive vomiting of gastric secretions. Combined metabolic acidosis and respiratory acidosis can occur when severe hypokalemia impairs respiratory muscle function.

Answer 298

Regular crystalline insulin is used when the pet has signs of depression, dehydration, anorexia, and vomiting. Regular insulin has several advantages, including its various routes of administration (intravenous, intramuscular, and subcutaneous), rapid onset of action, and short duration of action. These properties allow adequate insulin titration throughout the day according to the animal's needs. The clinician must remember that the blood glucose concentration declines much earlier than ketones, allowing for the persistence of ketonuria for the first 48 to 96 hours. Regular insulin given intravenously by slow constant rate infusion (CRI) is the preferred method of treatment for the critically ill hypotensive pet. The patient's hypovolemia should be partially corrected with isotonic fluids over the first 2 hours, before the insulin is administered.

Answer 299

To avoid any complicating osmotic disequilibrium effects on the brain, the rate of decline in the blood glucose level should not exceed 75 to 100 mg/dL/hr. When the blood glucose level has declined to 250 mg/dL after several hours of the CRI insulin infusion, the rate should be decreased to half the initial amount (i.e., 0.05 U/kg/hr), and dextrose should be added to the intravenous fluid to achieve a 2.5% to 5% dextrose concentration. The blood glucose level subsequently should be determined every 2 hours, using glucose oxidase reagent strips or a reflectance meter. Thereafter, the rate of insulin infusion should be adjusted to maintain a blood glucose range of 150 to 250 mg/dL to avert hypoglycemia.

Answer 300

If the patient initially is hypokalemic, the clinician can begin treatment with isotonic fluids containing added potassium chloride and delay insulin treatment for the first 4 to 8 hours.

Answer 301

Low doses of regular insulin also can be given intramuscularly. Initially, 2 U are injected into the thigh muscles of cats and dogs weighing less than 10 kg. For dogs weighing more than 10 kg, the initial dose is 0.25 U/kg BW. Subsequent hourly injections of 1 U for cats and small dogs and 0.1 U/kg BW for larger dogs are given until the blood glucose level is less than 250 mg/dL, at which time the subcutaneous route can be used to administer the insulin every 6 hours or as needed. The low doses used in this technique can be accurately measured with a special low-dose calibrated syringe. Subcutaneous administration of regular insulin is a suitable alternative to the intravenous and intramuscular methods when intensive care monitoring is unavailable and when the patient is alert and normotensive. The initial dose is 0.5 U/kg BW, with subsequent doses given every 6 to 10 hours, depending on the need

Answer 302

Normal hydration has been restored, blood glucose levels are below 250 mg/dL, serum and urine ketones are minimal to absent, and eating resumes. Subsequent insulin treatment can be changed to the intermediate-acting or the ultra–long-acting type.

Answer 303

Hypoglycemia, hypokalemia, cerebral edema, metabolic alkalosis, and paradoxical cerebrospinal fluid acidosis. Most of these problems are avoidable with meticulous medical management geared toward avoiding overtreatment of the patient.

Answer 304

Extreme dehydration, renal dysfunction, abnormal brain function, marked hyperglycemia, and the lack of significant ketoacidosis. The incidence of this disorder in the dog and cat has not been reported; however, isolated case reports can be found in the veterinary literature spanning the past 25 to 30 years. Underlying renal disease and a precipitating condition, such as an infection or pancreatitis, can often be found.

Answer 305

(1) decreased insulin utilization and glucose transport, (2) increased hepatic gluconeogenesis and glycogenolysis, (3) impaired renal excretion of glucose.

Answer 306

Two concepts have been advanced to reasonably explain the pathophysiology of HHS. The first suggests that an insulinized liver (reflecting residual beta cell secretory activity) coexists with a diabetic periphery, resulting in inactivation of intrahepatic oxidation of incoming free fatty acids, which are directed largely along nonketogenic metabolic pathways, such as triglyceride synthesis. This could account for the absence of hyperketonemia. The absence of hyperketonemia can also occur when the primary ketone body is beta hydroxybutyrate, which will not be detected with the nitroprusside reagent that is used for body fluid ketone detection. The second proposal suggests that enhanced gluconeogenesis occurs in the liver due to the prevailing elevated portal vein ratio of glucagon to insulin. This effect plus those due to severe dehydration (greater than 8%) and reduced urine production are responsible for the development of marked hyperglycemia.

Answer 307

The decrease in consciousness and the onset of the associated neurologic abnormalities that characterize HHS result from the direct effects of the serum sodium concentration and hyperosmolarity-induced dehydration on the brain parenchyma. A direct pathogenetic role, independent of osmotic diuresis, for hyperglycemia in causing coma is difficult to establish.

Answer 308

Although acute, massive intravenous administration of glucose can cause a transient reduction in brain water in animals, over longer periods hyperglycemia does not appear to dehydrate the brain. The reasons for this include that the brain is relatively permeable to glucose, even in the absence of insulin, and that brain tissues restore their intracellular water content in response to hyperglycemia by accumulating electrolytes and “idiogenic osmols” over several hours or days when the hyperglycemia occurs gradually.

Answer 309

One hypothesis that explains why some extremely hyperglycemic animals show neurologic deterioration rests on the serum sodium concentration. A normal or elevated serum sodium implies that substantial cellular dehydration has taken place and that the risk of neurologic abnormalities is high, whereas hyponatremia suggests that cellular dehydration has not occurred or has occurred to only a limited extent.

Answer 310

1. The blood glucose levels are often elevated above 800 mg/dL. 2. Serum osmolality is elevated (normal serum osmolality is 290 to 310 mOsm/kg body water) 3. Most dogs and cats with HHS are azotemic, a condition that may be renal or prerenal in origin. 4. It should be noted that an elevated serum sodium level during severe hyperglycemia can be explained only by significant plasma volume contraction caused by large water losses associated with hypotonic urine excretion.

Answer 311

Parenteral fluid therapy in this situation can be harmful if the solution is hypotonic or free of sodium because this would favor a rapid influx of water into the brain cells, which would be harmful if the brain cells were dehydrated. The adverse effect caused by this cerebral edema can be prevented by administering a sodium-containing solution and by administering insulin in such a way as to avoid lowering the blood glucose any faster than 75 to 100 mg/dL per hour.

Answer 312

1. Reestablishment of normal hydration and adequate urine output, 2. judicious use of insulin to avoid a precipitous decline in blood glucose levels, 3. ample potassium supplementation to make up the total body potassium deficit. Treatment techniques were described in the previous section. The regular insulin dosage requirements for the hyperglycemic hyperosmolar diabetic are often less than those needed to treat diabetic ketoacidosis, but the technique for delivery is the same. The diabetic ketoacidotic and hyperglycemic hyperosmolar syndromes pose noteworthy challenges to the practicing clinician. A sound understanding of the underlying pathophysiology, along with logical and timely therapeutic intervention, can usually lead to a remarkably optimistic outcome.

Answer 313

Severe inflammation results in loss of blood, fluids, electrolytes, and proteins from the capillaries into the GI tract (third body fluid spacing).

Answer 314

Distension or inflammation of the GI tract can cause peripheral receptor stimulation of the vomiting center in the brainstem (Figure 131-1). Alterations in GI motility, secretory function, or permeability can result in diarrhea. In addition, vomiting and diarrhea can have life-threatening consequences such as increased vagal tone, aspiration pneumonia, bacterial translocation, and malnutrition.

Answer 315

Stimulation of receptors associated with the vomiting center and chemoreceptor trigger zone, as well as stimulation of peripheral GI receptors, can be caused by organ inflammation or distention, drugs or toxins in the circulation, and central nervous system pathology (see Figure 131-1). Alterations in nerve conduction and smooth muscle action of the GI tract can occur as a result of toxins, electrolyte disturbances, or acid-base imbalances, any of which could alter GI function.

Answer 316

Figure 131-1 Vomiting reflex and antiemetics. Receptors located in the vomiting center and chemoreceptor-trigger zone (CRTZ) in the brainstem can be triggered by sensory and chemical input from multiple sources. Targeting the different neurotransmitters is the basis of antiemetic therapy. Specific antiemetic therapy should be selected based on the most likely mechanism initiating the stimulus to vomit. 5-HT, 5-Hydroxytryptamine; ENK, enkephalin; NK, neurokinin.

Answer 317

Poor perfusion is seen as pale mucous membranes, a prolonged capillary refill time, poor pulse quality, and tachycardia (in the dog) on physical examination. Dehydration is detected by dry mucous membranes, increased skin tenting, and, when severe, dry corneas. An altered level of consciousness or the presence of a dysrhythmia can suggest electrolyte and/or acid-base imbalances, hypoglycemia, circulating toxins, or hypoxia. Bradycardia may be a primary problem or the result of excessive vagal stimulation, severe hyperkalemia, or late-stage decompensatory shock. Abdominal pain or distension or a fluid wave alerts the clinician to shock, dehydration, and serious primary GI pathology.

Answer 318

Balanced isotonic crystalloids (dogs: 20 to 50 mL/kg; cats: 5 to 10 mL/kg) should be infused IV and repeated as necessary to reach desired end points. Synthetic colloids such as hetastarch (15 mL/kg dogs; 5 mL/kg cats) are infused simultaneously with initial crystalloid therapy, with the colloid dosage (5 mL/kg) repeated as necessary to improve flow to the tissues and reach desired end points of resuscitation.

Answer 319

Hypoglycemia is treated with IV dextrose (0.5 g/kg). Life-threatening bradycardia is treated with atropine (0.02 mg/kg) IV and a rapid assessment of the serum potassium level is made.

Answer 320

Vomiting (active abdominal contractions preceeding expulsion of gastric contents) must be differentiated from regurgitation (passive expulsion of food contents). Nonproductive vomiting or retching may indicate the presence of a gastric dilatation-volvulus. Vomiting and/or diarrhea should be characterized by color, consistency, and frequency

Answer 321

gastric outflow obstruction: hypochloremia with a metabolic alkalosis.

Answer 322

Hyperphosphatemia may reflect intestinal ischemia or severe intestinal inflammation.

Answer 323

When esophageal or gastric ulceration is suspected, H2-blockers (famotidine 0.5 mg/kg IV every 12 hours in the dog or SC in the cat every 24 hours) or H-pump inhibitors (omeprazole, 1 mg/kg up to 20 mg given orally every 24 hours, or pantoprazole 1 mg/kg IV every 24 hours) are administered to reduce acid secretion and reflux and promote mucosal healing. Liquid sucralfate (1 g/10 kg given orally every 4 to 8 hours) is administered to protect the area of ulceration once vomiting has been controlled.

Answer 324

Oxygen delivery depends on the blood oxygen content and tissue perfusion Figure 132-1 Determinants of tissue oxygen delivery. Hb, Hemoglobin

Answer 325

More objective assessments of the oxygenation of blood include pulse oximetry and arterial blood gas analysis. Supplemental oxygen should be provided to any critically ill traumatized animal until it is proved that oxygen supplementation is not necessary

Answer 326

A variety of conditions associated with trauma can result in respiratory distress and decreased oxygenation of hemoglobin (Figure 132-2; also see Chapter 141), but the most common are pneumothorax and pulmonary contusions.

Answer 327

Figure 132-2 Causes of respiratory distress in a trauma patient.

Answer 328

Increased bronchovesicular sounds in a traumatized animal are commonly a result of pulmonary contusions. Pulmonary contusions often worsen before they improve. Intravenous fluid therapy for other conditions should be given with caution in these dogs and cats. There is no specific therapy for pulmonary contusions. Supportive care with oxygen supplementation and pain relief are the mainstays of treatment. Most dogs and cats with pulmonary contusions begin to improve 24 to 36 hours after the initial insult

Answer 329

Neurogenic pulmonary edema occurs rarely but is most often associated with severe head trauma. This form of pulmonary edema can range from mild to severe enough to require mechanical ventilation. Generally, respiratory problems in animals with neurogenic pulmonary edema caused by head trauma improve substantially within 48 hours, or death ensues due to the severe respiratory compromise.

Answer 330

An adequate amount of hemoglobin in the vascular space is essential to maintenance of tissue oxygen delivery. Decreased hemoglobin content severely limits the oxygen-carrying capacity of the blood and can contribute to decreased tissue oxygen delivery. The packed cell volume (PCV) provides the most rapid estimate of the hemoglobin concentration in a traumatized dog or cat, but it should be interpreted in conjunction with assessment of the vascular volume status (see Tissue Perfusion, below) to get a complete assessment of the total hemoglobin content of the vascular space.

Answer 331

Typically, acute blood loss is not reflected by the initial PCV measurement because of splenic contraction in the dog and the length of time it takes for interstitial fluid to shift into the vascular space to dilute the PCV. Initial total solids (TS) and serial measurements of both PCV and TS as intravenous fluids are administered can be more sensitive indicators of acute blood loss. There is no specific PCV at or below which transfusion is required.

Answer 332

Transfusion therapy should be based on whether the animal is affected by the decreased hemoglobin content, which is indicated by clinical signs such as pale mucous membranes, tachycardia, tachypnea, bounding or weak pulses, depressed mentation, or cardiac arrhythmias. As with any animal in critical condition, it is best to anticipate and treat problems before they cause physiologic compromise. For example, if the PCV is dropping rapidly, it is best to start a blood transfusion or administer hemoglobin solutions before the hemoglobin content drops to a life-threatening level.

Answer 333

Figure 132-3 Assessment of tissue perfusion Pale or gray mucous membranes, a prolonged capillary refill time, a rapid heart rate, and weak pulses. The most common cause of poor tissue perfusion after a traumatic event is hypovolemia secondary to hemorrhage

Answer 334

Administration of a balanced electrolyte solution at a rate of 90 mL/kg body weight/hr in the dog (40 to 60 mL/kg body weight/hr in the cat) is indicated with physical evidence of poor tissue perfusion.

Answer 335

Ongoing intravascular volume loss (most commonly due to ongoing hemorrhage) or, less commonly, cardiogenic causes, such as arrhythmias, pericardial effusion, myocardial depression or failure, electrolyte abnormalities, decreased venous return (e.g., tension pneumothorax), or ischemic organs. The peritoneal space represents the most common location of substantial hemorrhage that can lead to hypovolemia. Less common locations are the pleural space and retroperitoneal space, external hemorrhage, and hemorrhage into the muscles surrounding the femur.

Answer 336

Hypertonic solutions can be considered after head trauma if a dog or cat is hypovolemic (see Chapter 128) or if an animal appears to be in severe hypovolemic shock and may die before an adequate amount of balanced electrolyte solution can be administered (see Chapter 139).

Answer 337

poor oxygen delivery, direct tissue damage, intracranial hemorrhage, cerebral edema, ischemia, and/or increased intracranial pressure.

Answer 338

Therapeutic considerations with head trauma and brain dysfunction include optimization of tissue perfusion, administration of mannitol (0.5 to 1.5 g/kg given intravenously), mild elevation of the head (avoiding flexion of the neck and occlusion of the jugular veins), and maintenance of oxygenation (see Chapter 128). Spinal cord assessment should include palpation of the spine and assessment of spinal function, including voluntary motor movement, conscious proprioception, ambulation, spinal reflexes, and pain sensation.

Answer 339

. Potential renal system abnormalities include direct kidney damage (e.g., contusions, hematomas, avulsion), ureteral rupture, bladder rupture, and urethral trauma. Any animal that has been traumatized may have experienced renal system trauma. Serial assessment of the blood urea nitrogen, creatinine, and serum potassium concentrations, as well as of urine output, should be considered. It should be remembered that animals with a ruptured urinary bladder might still urinate.

Answer 340

If free abdominal fluid is present, it should be analyzed for the creatinine and potassium concentrations, which should be compared to the concentrations in peripheral blood. If the abdominal fluid is urine, its creatinine and potassium concentrations are higher than that of blood.

Answer 341

Hyperthermia is defined as a severe elevation body temperature from 104.9° to 109.4° F after an animal has been exposed to elevated ambient temperatures or has performed strenuous activity.

Answer 342

Pyrogenic hyperthermia is associated with the body increasing the hypothalamic thermoregulatory center set point in response to a variety of endogenous or exogenous pyrogens and in most cases is a normal physiologic process.

Answer 343

Nonpyrogenic hyperthermia, however, is abnormal: an inability to dissipate heat.

Answer 344

Exertion or exercise in animals in locations with high environmental temperature and elevated ambient humidity can cause hyperthermia in as little as 30 minutes, particularly in animals without access to shade or opportunity to cool down and rest.[2,4,5] This can result in exertional heat stroke or exertional hyperthermia when animals cannot dissipate heat

Answer 345

PATHOPHYSIOLOGY Body temperature is maintained by the thermoregulatory center in the hypothalamus. Thermoregulation allows the core body temperature to remain constant despite exposure to a wide range of environmental and physiologic conditions.

Answer 346

oxidative metabolism of foodstuffs, exercise or increased metabolic activity, and elevated environmental temperature

Answer 347

Behavioral changes such as seeking a cooler location, changes in circulation that include peripheral vasodilation, evaporative cooling primarily in the form of respiratory heat exchange, radiation, and convection.

Answer 348

When environmental temperature increases and approaches body temperature, evaporative heat loss becomes important to maintain normothermia.[2,3] Animals, who lack sweat glands, depend primarily on the dissipation of heat from evaporative cooling from the respiratory system in the form of panting.[2,6] When body temperature increases, the thermoregulatory center in the hypothalamus is activated and sends a relay of signals to the panting center. This is a basic reflex mechanism by which an animal responds to heat excess and dissipates heat to prevent hyperthermia. As air comes in contact with the mucous membranes of the upper airways, evaporative cooling occurs.

Answer 349

If high ambient humidity is present, however, evaporative cooling mechanisms are not as effective and body temperature can continue to rise despite the body's efforts to cool itself. As core body temperature rises, metabolic rate also increases and results in further heat accumulation. A second method of cooling can occur by convection, in which an overheated animal lies on a cooler surface and the body heat is passively transferred to the cooler surface.

Answer 350

high ambient humidity, upper airway obstruction, laryngeal paralysis, brachiocephalic airway syndrome, collapsing trachea, obesity, and a previous history of hyperthermia or heat-induced illness.

Answer 351

The differential diagnosis of heat stroke or hyperthermia must be considered in any animal with a rectal temperature greater than 104.9° F and no other signs of infection. Pyrogenic hyperthermia results from the hypothalamic thermoregulatory center increasing its set point in response to any number of endogenous or exogenous pyrogens. Nonpyrogenic hyperthermia, however, results from the body's inability to adequately dissipate heat. Therefore, antipyretic agents are often ineffective in reducing body temperature in animals with heat-induced illness and are actually contraindicated due to potentially adverse side effects.

Answer 352

1. Inflammatory diseases of the central nervous system such as meningitis and encephalitis and 2. hypothalamic mass lesions that affect the thermoregulatory center. 3. Malignant hyperthermia in affected animals, particularly Labrador Retrievers, and unwitnessed seizure activity. 4. Toxins such as metaldehyde, strychnine, and neurogenic mycotoxins can also cause seizures and muscle fasciculations to such an extent that core temperature rises

Answer 353

panting, increasing dead space ventilation and increasing evaporative cooling mechanisms in an attempt to dissipate heat.

Answer 354

Metabolic alkalosis.

Answer 355

The effects of prolonged hyperthermia override the body's normal adaptive mechanisms, and cerebrospinal fluid hypocapnia and alkalosis, factors that normally decrease panting, are no longer effective, and panting continues.

Answer 356

Additionally, as core body temperature increases, the body compensates by peripheral vasodilation. Increased blood flow to the skin and periphery can help to decrease heat by convective mechanisms. To help maintain adequate blood pressure, splanchnic vessels constrict to maintain adequate circulating volume.[6] Further, circulating catecholamines increase heart rate and cardiac output in an attempt to increase peripheral circulation.[3] Early in hyperthermia, there is an increase in cardiac output and decrease in peripheral vascular resistance.[6] As hyperthermia progresses, however, blood pressure and cardiac output decrease.[6] There is also a decrease in circulating plasma volume that can result in hypovolemia. As perfusion to vital organs is decreased, widespread organ damage can result.

Answer 357

As body temperature rises, widespread thermal injury occurs to neuronal tissue, cardiac myocytes, hepatocytes, renal parenchymal and tubular cells, and gastrointestinal barrier function.[3] Additionally, oxidative phosphorylation and enzyme activities are reduced, causing a decrease in energy production.

Answer 358

The combined effects of decreased organ perfusion, enzyme dysfunction, and uncoupling of oxidative phosphorylation are a decrease in aerobic glycolysis and an increase in tissue oxygen debt, both of which contribute to increased lactate production and lactic acidosis.[3] Lactic acidosis can occur within 3 to 4 hours of initial heat-induced injury.

Answer 359

The kidneys are affected by direct thermal injury to tubular and parenchymal cells. Additionally, decreased renal blood flow and hypotension cause hypoxic damage to the tubular epithelium and cell death. With disease progression, thrombosis of renal vessels can occur with disseminated intravascular coagulation (DIC). Consistent findings in severely hyperthermic pets are renal tubular casts and glycosuria. Both factors indicate severe renal injury. Rhabdomyolysis can also be associated with severe myoglobinuria and pigment-associated damage to the renal tubular epithelium

Answer 360

The gastrointestinal tract is a key player in multiorgan failure associated with hyperthermia. Decreased perfusion to the mesentery and thermal injury to enterocytes often results in a disruption of the gastrointestinal mucosal barrier and subsequent bacterial translocation.

Answer 361

Bacteremia and elevation of circulating bacterial endotoxin can lead to sepsis, systemic inflammatory response (SIRS), and multiorgan failure. Patients with severe hyperthermia often present with hematemesis and severe hematochezia, and often slough the lining of their intestinal tract.

Answer 362

Thermal injury to hepatocytes results in decreased hepatic function, with elevations of hepatocellular enzyme activities, increased ALT, AST, and total bilirubin. Persistent hypoglycemia in affected patients may be associated with hepatocellular dysfunction and glycogen depletion. Decreased hepatic macrophage function and portal hypotension can also predispose the patient to sepsis with associated bacteremia and SIRS.

Answer 363

Hyperthermia also induces widespread endothelial damage, one of the key players in the development of DIC.[8] All elements of Virchow's triad, which consists of vascular endothelial injury, venous stasis, and a hypercoagulable state, occur during hyperthermia. Sluggish blood flow during periods of hypotension and decreased production of clotting factors due to hepatic injury both contribute to DIC. Exposure of subendothelial collagen and tissue factor cause widespread platelet activation, consumption of clotting factors, activation of the fibrinolytic pathway, and subsequent DIC. Massive global thrombosis associated with DIC can result in multiorgan failure and death. Although one study demonstrated no significant outcome associated with treatment for DIC, many authors advocate empiric therapy to prevent DIC in all patients with hyperthermia. Thrombocytopenia, prolonged prothrombin time and activated partial thromboplastin time and elevated fibrin degradation products may be observed if DIC is present. Destruction or consumption of clotting factors can occur. In some dogs and cats, thrombocytopenia may not become apparent for several days after the initial insult. Thrombocytopenia is one of the most common clinicopathologic abnormalities observed in animals with heat-induced illness.

Answer 364

Finally, hyperthermia can cause direct damage to neurons, neuronal death, and cerebral edema. Thrombosis or intracranial hemorrhage can also occur with DIC. Damage to the hypothalamic thermoregulatory center, localized intraparenchymal bleeding, infarction, and cellular necrosis can all lead to seizures. Altered levels of consciousness are among the most common clinical signs of heat-induced illness. As hyperthermia progresses, severe central nervous system depression, seizures, coma, and death may occur.

Answer 365

Arterial blood gas analyses can be variable, as respiratory effort may be increased in heat stroke, producing a respiratory alkalosis. However, increased circulating lactate, can produce a metabolic acidosis, thus a mixed acid-base disturbance can occur. The need for administration of sodium bicarbonate is a negative prognostic indicator.

Answer 366

It is important to cool the patient to 103° F within 30 to 60 minutes of initial presentation but to avoid overcooling. As the thermoregulatory center becomes deranged in animals with heat-induced illness, overcooling past 103° F will cause a rapid drop in core temperature.

Answer 367

Overcooling can also be injurious, as patients who presented with hypothermia were more likely to die.[4] As cooling progresses to less than 103° F, shivering can occur, which will increase metabolic rate and further increase core body temperature. Immersion in ice baths or cold water is absolutely contraindicated, as cold water immersion causes peripheral vasoconstriction and prevents vasodilation, one of the animal's primary methods of cooling. Vasoconstriction results in further elevation of core body temperature and thus should be avoided at all costs.

Answer 368

Massaging the skin can increase peripheral circulation, improve peripheral blood flow, and improve heat loss. Other methods of cooling that have been described but offer no real advantage or improvement of clinical outcome include administration of cool intravenous fluids, gastric lavage, cold-water enemas, and cool peritoneal lavage. Placing alcohol on the footpads has been described, but can further complicate overcooling and thus should not be performed.

Answer 369

Intravenous fluid administration should be tailored to each patient's individual needs, and can be administered based on central venous pressure, acid-base and electrolyte status, blood pressure, thoracic auscultation, and colloid oncotic pressure.

Answer 370

Obesity, renal failure, and DIC all increase the risk of death associated with hyperthermia. Permanent damage to kidneys, liver, and brain can occur, including permanent changes in the hypothalamic thermoregulatory center that can predispose the patient to further hyperthermic episodes

Answer 371

Figure 133-1 General algorithm for approach to the patient with heatstroke. Approach can be tailored to the individual patient, with more aggressive monitoring in the most critically ill animals.

Answer 372

Traumatic injury to the liver or spleen, or rupture of splenic or hepatic masses can cause life-threatening intraperitoneal hemorrhage. Trauma to these organs is often associated with motor vehicle accidents, falls, and accidental or malicious blunt abdominal injuries. The most common nontraumatic cause of hemoperitoneum in dogs is rupture of splenic hemangiosarcoma.[1] Less commonly, hemorrhage can occur from other vascular intraabdominal masses, including splenic hematomas and hepatic tumors. Hemorrhage from hepatic and splenic neoplasms accounts for approximately 50% of feline nontraumatic hemoperitoneum.[2]

Answer 373

Rupture of the Biliary System Rupture of the biliary system is more commonly seen in dogs than cats and is usually caused by abdominal trauma or associated with severe cholecystitis and rupture of the gall bladder. Rupture has also been reported in dogs secondary to gall bladder infarction. Once substantial bile leakage occurs, clinical signs of peritonitis develop, thus prompting owners to seek veterinary attention.Blood work often shows a leukocytosis, elevated serum bilirubin concentration, and elevations of serum ALP and ALT. A diagnosis of bile leakage is made from an analysis of peritoneal fluid samples. The finding of free bile crystals on cytology or a peritoneal fluid bilirubin level higher than that of the serum should prompt exploratory surgery. It should be noted that these changes may not be seen in patients with bile peritonitis secondary to a ruptured gallbladder mucocele because the gelatinous bile often fails to disperse throughout the abdomen

Answer 374

Hepatic encephalopathy is a complex syndrome of neurologic alterations seen in association with moderate to severe liver disease. The cause of the neurologic signs seen in HE is multifactorial; elevations in serum and central nervous system (CNS) ammonia levels alter the glutamate, gamma-aminobutyric acid, and serotonin neurotransmitter systems. Changes in the central and peripheral benzodiazepine receptor systems also occur.

Answer 375

Physical examination findings are rarely specific; signs of spontaneous hemorrhage including ecchymosis, icterus, and cranial organomegaly increase suspicion for liver disease but do not differentiate between an acute hemolytic crisis and extrahepatic biliary obstruction. Owners should be questioned carefully about possible drug or toxin exposures.

Answer 376

A diagnosis is suspected based on the history and physical examination findings and the results of serum biochemical and liver function tests, including a coagulation profile (see Chapter 192). Abdominal ultrasound is helpful to visualize the liver and obtain either aspirates or biopsy specimens for cytology, culture, and histopathology. Treatment is largely supportive and involves cardiovascular support with crystalloid and colloid fluids, correction of electrolyte and acid-base imbalances, lowering serum ammonia levels, and treating any seizure activity. The clinician should pay particular attention to hypokalemia and alkalosis as both of these conditions increase ammonia uptake to the CNS.

Answer 377

Serum ammonia is lowered by administering lactulose, a nondigestible disaccharide that acidifies the colon, decreasing ammonia production and converting ammonia into nonabsorbable ammonium ions. In comatose animals, lactulose is administered as an enema (10 to 80 mL). In some instances, administration of flumazenil, a benzodiazepine receptor antagonist (0.01 to 0.02 mg/kg IV or SQ) may ameliorate clinical signs. In animals with HE and seizurelike activity, propofol is administered as a bolus (0.5 to 1 mg/kg IV), then as an infusion (0.05 to 0.1 mg/kg/min IV). Although surgical or minimally invasive radiologic intervention for identified single intrahepatic and extrahepatic shunts may be indicated, it is important that these animals be medically managed and stabilized for signs of hepatic dysfunction prior to addressing the underlying etiology.

Answer 378

Oxygen therapy increases the concentration of inspired oxygen in an attempt to increase the content of oxygen in the arterial blood. The concentration of oxygen delivered to patients is quantified as the fraction of inspired oxygen (FIO2) and may be recorded as a percentage (21% to 100%) or a decimal (0.21 to 1.0). The concentration of oxygen in room air is always 21%. Supplemental oxygen can provide an FIO2 of 30% to 100% depending on the technique and equipment utilized.

Answer 379

Oxygen therapy aims to increase the delivery of oxygen to the tissues. The determinants of oxygen delivery are hemoglobin concentration, arterial blood oxygenation, and cardiac output

Answer 380

1. significant anemia, 2. hemodynamic compromise, 3. decreased blood oxygen concentrations (hypoxemia).

Answer 381

The patient's clinical signs or it may be documented directly with pulse oximetry and/or arterial blood gas measurement. Clinical signs suggestive of hypoxemia include respiratory distress, apnea, and cyanosis. Unfortunately, clinical assessment of hypoxemia is insensitive.

Answer 382

An uncommon but important indication for oxygen therapy is carbon monoxide poisoning. Oxygen therapy will both attenuate tissue hypoxia and accelerate the elimination of carbon monoxide binding to hemoglobin.

Answer 383

GOALS OF OXYGEN THERAPY The goal of oxygen therapy will depend upon the reason for its administration. In patients with anemia, hemodynamic compromise, or carbon monoxide poisoning, the goal is to maximally increase arterial oxygen content in an attempt to increase oxygen delivery to the tissues until more definitive therapy can be instituted. To this aim, the highest possible FIO2 should be provided. In most pets that require oxygen therapy beyond the initial stabilization period, the goal is to correct hypoxemia.

Answer 384

Hypoxemia is defined as a partial pressure of arterial oxygen (PaO2) less than 80 mm Hg or an arterial oxygen saturation of less than 95%. Severe hypoxemia is present when the PaO2 is less than 60 mm Hg or the arterial oxygen saturation is less than 90%. Ideally, oxygen therapy is adjusted as needed for the patient to maintain a PaO2 of 80 to 120 mm Hg. This will maintain hemoglobin saturation between 95% and 100%. A higher PaO2 is of little clinical benefit assuming the patient has an adequate hematocrit and stable cardiovascular status.

Answer 385

%. A higher PaO2 is of little clinical benefit assuming the patient has an adequate hematocrit and stable cardiovascular status. Animals with a normal hematocrit and normal cardiovascular function will often tolerate mild to moderate hypoxemia (PaO2 of 60 to 80 mm Hg). In animals with severe disease, acceptance of mild to moderate hypoxemia may be preferable to the use of higher FIO2 levels for prolonged periods of time, in an attempt to avoid oxygen toxicity.

Answer 386

An oxygen flow rate of 2 to 3 L/min will provide an FIO2 of approximately 25% to 40%.[3]

Answer 387

Mask Oxygen A face mask will allow administration of a higher FIO2 than can be achieved with simple flow-by oxygen, but close-fitting masks may not be well tolerated by many pets with respiratory distress. It is possible to deliver 60% or higher FIO2, and the exact FIO2 can be measured by placing an oxygen sensor in the mask alongside the animal's nose (Web Figure 135-2).[3] Disadvantages include the possibility for heat and carbon dioxide to accumulate in tight-fitting face masks.

Answer 388

Elizabethan Collar An Elizabethan collar with an oxygen source secured inside and the front covered with clear plastic wrap is a cheap, readily available method by which reasonably high levels of oxygen can be administered (Web Figure 135-3). It is important to make a window in the top of the plastic wrap to prevent accumulation of heat and carbon dioxide. Flow rates of 0.5 to 1 L/min can provide an FIO2 of 30% to 40%.

Answer 389

Nasal Prongs A simple method of oxygen administration is placement of human nasal prongs (Figure 135-1). These are only practical in medium-sized dogs or larger. The advantages of the nasal prongs are their ease of placement and ready availability.

Answer 390

Nasal Oxygen Catheter A nasal oxygen catheter is generally well accepted by most pets and can supply an FIO2 of 37% to 58% with oxygen flow rates of 50 to 200 mL/kg/min. Bilateral nasal oxygen catheters can provide an FIO2 of up to 77% (see Table 135-1).

Answer 391

Transtracheal Oxygen Transtracheal oxygen delivery requires the placement of a catheter into the trachea. An oxygen source is then connected directly to the catheter and flow rates of 50 to 200 mL/kg/min used

Answer 392

Oxygen Cage An oxygen cage allows administration of a known FIO2 to patients in a low-stress, noninvasive manner. It is particularly effective for cats in respiratory distress as they may quickly decompensate when handled. The advantages include patient comfort, the ability to control FIO2 accurately, and the ability to provide very high FIO2 levels when required.

Answer 393

Positive Pressure Ventilation When hypoxemia cannot be corrected with oxygen therapy or if a patient requires FIO2 levels of greater than 60% for long periods of time (24 to 48 hours), positive pressure ventilation is indicated. Positive pressure ventilation will often allow correction of hypoxemia at a lower FIO2.

Answer 394

Humidification Inspired gases are normally humidified by the upper airways. The delivery of dry gas to the nose, trachea, or lower airways can cause irritation, inflammation, and thickening of airway secretions. For this reason any oxygen administration method that delivers high gas flows intranasally or intratracheally should use humidified gas.[7] This is especially important if oxygen therapy is provided for more than a few hours. Humidification is most simply achieved by use of a bubble humidifier attached to the oxygen source (Web Figure 135-4). The reservoir should be kept filled with sterile water. The entire unit can be sterilized between patients

Answer 395

MONITORING Arterial blood gas measures the PaO2 and is the gold standard for evaluation of arterial oxygenation. Assessment of arterial blood gases requires an arterial blood sample and a blood gas analyzer. The normal or “expected” PaO2 is dependent on the FIO2 and the barometric pressure.

Answer 396

A useful rule of thumb is that the normal PaO2 in a patient at sea level is approximately 5 times the FIO2 measured in percent. For example, for 21% room air at sea level, the normal PaO2 is approximately 100 mm Hg while the normal PaO2 on an FIO2 of 100% at sea level is approximately 500 mm Hg. The expected PaO2 for a given FIO2 when at a high altitude is lower due to the decrease in barometric pressure.

Answer 397

As previously mentioned, the goal of oxygen therapy is to maintain a PaO2 of 80 to 120 mm Hg. If the PaO2 is less than 80 mm Hg, the FIO2 should be increased; if the PaO2 is greater than 120 mm Hg, the FIO2 should be decreased. Reevaluation of oxygenation status following any change in FIO2 is always important.

Answer 398

In the absence of arterial blood gas analysis, pulse oximetry can be utilized. Pulse oximetry evaluates the arterial saturation of hemoglobin with oxygen (SpO2). Hemoglobin saturation is determined by the PaO2, and this relationship is defined by the oxygen-hemoglobin dissociation curve.

Answer 399

A PaO2 of 80 mm Hg correlates to a SpO2 of approximately 95%, while a PaO2 of 60 mm Hg correlates to an SpO2 of approximately 90%. Consequently the aim of oxygen therapy is to maintain a SpO2 of greater than 95%.

Answer 400

When the SpO2 is 99% to 100% consistently, the FIO2 should be gradually decreased until the FIO2 at which the SpO2 decreases is identified. The FIO2 should then be set at or just above this point in an attempt to avoid the use of unnecessarily high FIO2 levels.

Answer 401

The lung is the organ most vulnerable to oxygen toxicity, and the associated damage is often severe and irreversible.

Answer 402

Guidelines for Oxygen Administration Oxygen toxicity is not just a function of the level of oxygen administered, it is also related to the duration of oxygen exposure. The general recommendation for dogs and cats is to avoid the administration of 100% oxygen for longer than 12 to 24 hours and in situations of long-term oxygen therapy the fraction of inspired oxygen should be maintained at less than 60%.

Answer 403

Critical illness is commonly associated with depletion of endogenous antioxidant levels; for this reason it is possible that inspired oxygen levels of less than 60% could be potentially toxic. In addition, there is no way to predict an individual animal's susceptibility to toxicity. This leads to the recommendation that the FIO2 should always be titrated to the lowest level a patient can tolerate.

Answer 404

Acute kidney injury (AKI) can vary from mild damage that does not elevate commonly measured renal parameters (such as creatinine) to complete anuria. AKI can result from prerenal, intrinsic renal, or postrenal causes, and AKI can be superimposed on chronic kidney disease. When faced with a patient who is not excreting an adequate amount of urine (1 to 2 mL/kg/hr), immediate action is necessary.

Answer 405

A wide variety of factors can cause acute intrinsic renal failure, which may exist as oligoanuria (2 mL/kg/hr).

Answer 406

Patients with chronic kidney disease presenting in a decompensated uremic crisis are initially managed as nonoliguric acute renal failure (ARF). Owners may present the pet with a known history of potential renal insult (e.g., ingestion of nephrotoxic drug or antifreeze, recent ischemic event) or with signs suggestive of ARF (recent onset of polyuria and polydipsia, vomiting, anorexia). Physical examination may reveal renomegaly or pain, uremic ulcers or halitosis.

Answer 407

Central nervous system (CNS) depression, incoordination, ataxia, somnolence, seizures, or coma. Hypothermia and vomiting are also common. Marked polydipsia occurs in dogs, and both dogs and cats initially become polyuric. These signs may resolve, followed by signs of ARF after 24 to 72 hours in dogs and as early as 12 hours after ingestion in cats.

Answer 408

Fever, musculoskeletal pain, severe and persistent vomiting and diarrhea, oculonasal discharge, hemorrhagic diathesis, peripheral lymphadenopathy, or dyspnea icterus The presence of icterus in a patient with ARF is suggestive of leptospirosis, although not all serovars are associated with hepatic involvement. Leptospirosis is a zoonotic disease, and appropriate precautions should be utilized when handling any dog that is suspected to have leptospirosis.

Answer 409

Obstructing ureterolithiasis in cats is increasing in frequency. Hydronephrosis can usually be identified with ultrasonography; intravenous or antegrade pyelography may be required to determine the location and extent of obstruction.

Answer 410

Cage-side tests that suggest ARF include presence of a high–anion gap metabolic acidosis, hypocalcemia, or hyperkalemia. Ethylene glycol toxicity may cause hyperglycemia. In addition to isothenuria, urinalysis may reveal proteinuria, glucosuria, hematuria, pyuria, or cylindruria. Oxalate crystals may be present with ethylene glycol toxicity. With ethylene glycol toxicity, the kidneys may appear more radiopaque than surrounding soft tissue structures. Ethylene glycol toxicity will frequently cause hyperechoic cortices compared to liver.

Answer 411

Thoracic radiographs may show an interstitial pattern with leptospirosis, or an interstitial to alveolar pattern if volume overload has led to pulmonary edema. Serum chemistry panel will document azotemia and hyperphosphatemia. Liver enzymes may be elevated with leptospirosis, with peak liver involvement occurring about 6 to 8 days after the onset of renal involvement. Changes in the complete blood count are usually nonspecific. Dogs with leptospirosis may have a mild nonregenerative anemia, leukocytosis, or thrombocytopenia. Urine culture may reveal bacterial growth in cases of bacterial pyelonephritis. Leptospirosis serology is not available on an emergency basis.

Answer 412

Specific tests available for ARF include an ethylene glycol test to confirm exposure. However, due to limits of detection of the test, cats can have nephrotoxic ethylene glycol levels with a negative test, and the test may be negative in both dogs and cats 12 hours after ingestion, due to metabolism of ethylene glycol.

Answer 413

Fluid therapy is one of the first considerations for treatment of renal emergencies. Rehydration should occur over 4 to 24 hours, depending on the cardiovascular status. Most ARF patients should be rehydrated over a short time (4 to 6 hours). If the patient appears hydrated, a fluid volume equal to 3% to 5% of body weight should be administered to account for clinically undetectable dehydration. Urine output should be assessed after rehydration and fluid therapy should be tailored to fluid output (ins-and-outs). Administered fluid should be at a base rate equaling insensible loss (22 mL/kg/day) plus the volume of sensible loss (urine production) over the previous time period. If vomiting is profuse, an estimate of this volume is added to measurements of urine output. This method is appropriate for both oliguric/anuric patients, to avoid overhydration, and for polyuric patients, who frequently have volumes of urine exceeding the clinician's estimate. Plasma or colloids (e.g., hetastarch, dextran) may be indicated.

Answer 414

If urine output remains low (80 mm Hg MAP), diuretics are indicated. Mannitol (0.5 g/kg administered IV over 20 minutes) is an osmotic diuretic, but is contraindicated in dehydrated or overhydrated patients.

Answer 415

Furosemide, a loop diuretic, may induce urine flow in 20 to 30 minutes after an initial IV bolus of 2.2 mg/kg. If not, the dose can be doubled, up to 10 mg/kg. Higher doses may lead to ototoxicity. Furosemide does not improve the renal outcome. Furosemide and mannitol can be given together. Dopamine is no longer recommended for treating oliguric acute renal failure.

Answer 416

Treatment of metabolic acidosis is recommended when the blood pH is below 7.2 or the serum bicarbonate concentration is less then 16 mEq/L.

Answer 417

Body weight (kg) × 0.3 × (20 − patient bicarbonate concentration). One quarter to ⅓ of the calculated dose can be administered as an IV bolus, and an additional ¼ to ⅓ of the dose administered over the next 4 to 8 hours. Rapid administration, excessive dosing, or administration to a patient with impaired respiratory function can lead to paradoxical CNS acidosis.

Answer 418

Bradycardia, wide, flattened or absent P waves, peaked T waves, wide QRS complex, atrial standstill, idioventricular rhythm, ventricular fibrillation, or asystole.

Answer 419

Regular insulin (0.1 to 0.25 U/kg IV) with dextrose to prevent hypoglycemia (1 to 2 g/unit of insulin as an IV bolus, followed by 1 to 2 g/unit over the next 4 to 8 hours) or bicarbonate (0.5 to 2 mEq/kg IV) temporarily shifts potassium intracellularly, with an effect occurring within about 20 to 30 minutes. If more immediate effect is needed, 10% calcium gluconate (0.5 to 1.0 mL/kg IV) can be administered as a slow IV bolus for its cardioprotective effect, although it does not decrease plasma potassium concentration. These emergency treatments need to be followed by procedures that remove potassium from the body (e.g., inducing urine flow or dialysis).

Answer 420

Uremia may induce gastritis or gastric ulceration. Histamine (H2 receptor) blockers are commonly used to treat gastritis and include famotidine (0.5 to 1 mg/kg IV q24h), ranitidine (2.2 mg/kg IV q24h), or cimetidine (2.5 to 5 mg/kg IV q12h). Because of significant renal excretion of ranitidine and cimetidine, this is a reduced dosage.

Answer 421

Sucralfate (0.25 to 1 g PO q6-8h) aids in healing of uremic ulcers. It should be given at least 30 to 60 minutes prior to oral antacids. Uremic toxins can induce nausea by stimulation of the chemoreceptor trigger zone. Metoclopramide is a centrally acting antiemetic. Metoclopramide is a dopamine receptor antagonist and should not be administered concurrently with dopamine. Cerenia can be used to treat vomiting in dogs. Anecdotally, 5-HT3 serotonic receptor antagonists, like ondansetron or dolasetron, seem more effective than metoclopramide.

Answer 422

Hyperphosphatemia is common in both acute and chronic renal failure as a result of decreased renal excretion. An acute increase in phosphate concentration will cause a compensatory decrease in calcium concentration.

Answer 423

The ionized calcium concentration is usually maintained within normal limits, so signs of hypocalcemia tetany are infrequently observed. Oral phosphate binders (e.g., aluminum hydroxide) should be used once vomiting is controlled and the patient is being fed enterally.

Answer 424

Respiratory compromise from pleural effusion caused by volume overload may require thoracocentesis. No effective method of addressing pulmonary edema exists in the anuric patient other than ultrafiltration via dialysis. Careful attention to fluid therapy and urine output is crucial to avoiding this complication.

Answer 425

Hypertension may accompany either acute or chronic renal failure, and excessive volume expansion (particularly in the face of oliguria or anuria) can exacerbate the condition. Therapy may not be necessary if the hypertension is mild and the renal failure is resolving rapidly. However, emergency therapy may be necessary to prevent catastrophic effects in more severe cases.

Answer 426

Anorexia is common with acute renal failure. Because of the highly catabolic state associated with ARF, nutritional support should be started early in the course of the illness. If vomiting can be adequately controlled pharmacologically, enteral feeding with a feeding tube should be started. If enteral feeding is not possible, partial or total parenteral nutrition should be instituted. Although feeding a restricted quantity of high-quality protein is established therapy for chronic kidney disease, the need for protein restriction in ARF is less clear.

Answer 427

Uremia induces a thrombocytopathy, and the risk of bleeding should be considered when planning invasive procedures (e.g., renal biopsy, feeding tube placement). Because coagulation parameters and platelet numbers may be normal, a buccal mucosal bleeding time is the preferred method of assessment.

Answer 428

For ethylene glycol toxicity, specific antidotes are indicated. Four-methylpyrazole (4-MP, fomepizole, Antizol-Vet, Orphan Medical, Minnetonka, Minn.) is effective in dogs if given within 8 hours of ingestion. Standard doses are not effective in cats. Dosing for dogs is 20 mg/kg IV initially, then 15 mg/kg at 12 and 24 hours, followed by 5 mg/kg at 36 hours. If 4-MP is not available, 20% ethanol can be used to competitively inhibit alcohol dehydrogenase. A dose of 5.5 mL/kg every 4 hours for five treatments, then every 6 hours for four treatments can be given as an intermittent IV bolus, but is better as a constant rate infusion. In cats, 20% ethanol can be dosed at 5 mL/kg every 6 hours for five treatments, then every 8 hours for four treatments. Drinking alcohol (50% ethanol [100 proof]) can be diluted with saline. Respiratory depression can be profound with alcohol. Neither 4-MP nor alcohol is effective if started more than 8 hours after ingestion.

Answer 429

Antibiotics should be administered if leptospirosis or pyelonephritis is suspected or documented. High doses of penicillin are effective at clearing leptospiremia. Doxycycline (2.5 mg/kg q12h) is effective at clearing leptospiremia and possibly leptospiruria. The most common cause of bacterial pyelonephritis is Escherichia coli. Empiric antibiotic choice should have a good gram-negative spectrum and not be nephrotoxic.

Answer 430

The systemic inflammatory response syndrome (SIRS) refers to the complex clinical response to a nonspecific insult of either infectious or noninfectious origin. Heart rate, respiratory rate, body temperature, and white blood cell count are the clinical criteria used to categorize patients with SIRS in veterinary medicine (Table 138-1).

Answer 431

Sepsis is a Greek work meaning “decomposition of animal or vegetable organic matter in the presence of bacteria.”In the clinic, sepsis has come to mean infection with concurrent clinical evidence of the systemic inflammatory response (i.e., SIRS because of infection). At one time, sepsis and bacteremia were considered synonymous terms. However, as our knowledge of sepsis has grown we have realized that the clinical manifestations of sepsis relate to widespread inflammation and not necessarily widespread infection.

Answer 432

In dogs and cats, bacterial infections are the most common cause of sepsis with Escherichia coli being the most common isolate. However, any microbial organism (e.g., fungus, parasite, virus) may cause sepsis. Sepsis most commonly originates from the abdomen followed by the respiratory tract in dogs. In cats, sepsis is commonly associated with septic peritonitis, pyothorax, and hepatic abscessation

Answer 433

PATHOGENESIS The sequence of events leading to sepsis is complex and incompletely understood. In the initial phases of infection, microbial products (e.g., endotoxin from gram-negative bacteria; exotoxins, peptidoglycans, and superantigens from gram-positive bacteria; and fungal cell wall material) induce systemic inflammation through activation of immune cells. The induction of systemic inflammation may start at a local site like an abscess on the limb. For sepsis to develop from a local infection, inflammatory mediators and/or microbial products must enter into the systemic circulation and activate inflammatory cells throughout the body. Since E. coli bacterial infection is the most common cause of sepsis, the focus of this chapter is on the interaction of gram-negative bacteria and the immune system.

Answer 434

During gram-negative sepsis, lipopolysaccharide (LPS), the glycolipid component of the cell wall of gram-negative bacteria, is released.

Answer 435

Upon release, the lipid A portion of LPS binds to LPS-binding protein. The LPS–LPS-binding protein complex is recognized via macrophage cell surface receptors like CD14. The main function of CD14, which lacks a transmembrane domain, is to transfer LPS to toll-like receptor-4 (TLR4) and MD-2 for subsequent cellular activation. Once LPS binds to these cell surface receptors, the macrophage becomes activated and intracellular signaling through activation of nuclear factor kappa-B (NF-κB) is initiated.

Answer 436

Activation and nuclear translocation of NF-κB results in the transcription of multiple inflammatory mediators that have been implicated in the induction and maintenance of sepsis. Interestingly, many physical and chemical stimuli are capable of activating NF-κB. This may be one explanation for why, although there is a plethora of inciting causes for SIRS, the inflammatory outcome is similar in many cases.

Answer 437

There are many inflammatory mediators involved with sepsis and SIRS. Tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), nitric oxide, and leukotrienes are examples of important mediators contributing to the pathology of sepsis in dogs and cats.

Answer 438

Sepsis is not simply the induction of inflammation, but rather it is induction of proinflammatory components of the immune system to the extent that they overwhelm normal antiinflammatory counter-regulatory mechanisms allowing inflammation to go unchecked. Ultimately, the unchecked proinflammatory cascade leads to inflammatory cell infiltration, altered thermoregulation, vasodilation, vascular leakage, coagulation, hemodynamic instability, and multiple organ failure.

Answer 439

Web Figure 138-1 Pathophysiology of gram-negative sepsis. LPS, Lipopolysaccharide; TLR4, toll-like receptor 4. (Figure art by Donald Connor.)

Answer 440

Multiple organ dysfunction syndrome (MODS) is a devastating consequence of sepsis. Pathogenesis of organ failure (e.g., renal failure) during sepsis is multifactorial but centers around the development of mitochondrial dysfunction.

Answer 441

Circulatory collapse, microcirculatory changes, hypoxemia, and inflammation lead to tissue ischemia, reduced mitochondrial and then cellular function. The resultant organ damage may be permanent, or may resolve when sepsis is resolved.

Answer 442

Some forms of organ dysfunction, like acute respiratory distress syndrome (ARDS), are the result of inflammation, not circulatory collapse and mitochondrial damage. During the initiation of ARDS, inflammatory mediators and microbial products activate pulmonary macrophages resulting in vasodilation, vascular leak, pulmonary edema, and neutrophilic inflammation.

Answer 443

CLINICAL ASPECTS Clinically, dogs can have either a hyperdynamic or hypodynamic response during sepsis. The hyperdynamic response is characterized by fever, brick-red mucous membranes, tachycardia, and bounding pulses. As the disease process progresses, a hypodynamic response characterized by hypotension, pale mucous membranes, and hypothermia may be observed.

Answer 444

Often dogs will have gastrointestinal (GI) or respiratory signs associated with endotoxemia. Hyperglycemia or hypoglycemia, hypoalbuminemia, azotemia, hyperbilirubinemia, increased alanine aminotransferase and/or alkaline phosphatase, leukocytosis, neutrophilia with a left shift or a leukopenia, anemia, and thrombocytopenia are clinicopathologic abnormalities that have been recognized during sepsis.

Answer 445

Decreased protein C and antithrombin concentrations, prolonged prothrombin time, partial thromboplastin time, and increased D-dimer concentrations

Answer 446

Many dogs with sepsis will have myocardial dysfunction and vasodilation leading to hypotension. Poor perfusion, tissue hypoxia, and cellular metabolic derangement can lead to metabolic acidosis.

Answer 447

Bradycardia, hypothermia, and abdominal pain are frequent, unique findings in cats with sepsis. Cats also appear to develop septic shock more readily than dogs, and typically the hyperdynamic phase is not recognized during feline sepsis. The mechanisms by which these unique manifestations develop are unknown.

Answer 448

The incidence of sepsis-induced MODS is not known in dogs or cats with sepsis although cardiovascular, GI, hepatic, renal, endocrine, and respiratory dysfunction/failure have been recognised

Answer 449

For patients with suspected bacterial peritonitis, glucose concentration of the blood can be compared to the peritoneal fluid to achieve a rapid diagnosis. A difference of >20 mg/dL between blood and peritoneal fluid glucose concentrations is diagnostic for septic peritoneal effusion. In some cases, identification of infection is difficult and/or delayed and a presumptive diagnosis of infection based on the clinical picture will be necessary. However, it is important to remember that there are many causes of the SIRS that are noninfectious in origin (e.g., acute pancreatitis, autoimmune disease, envenomation). Care should be taken to consider noninfectious differentials for SIRS when appropriate

Answer 450

Broad spectrum, bactericidal antimicrobial agents (e.g., fluoroquinolone + beta-lactam antibiotic) administered IV should be instituted as quickly as possible in patients with suspected sepsis.

Answer 451

Figure 138-2 Algorithm for the diagnosis and treatment of sepsis in dogs. CRI, Constant rate infusion; GI, gastrointestinal; HR, heart rate; NMDA, N-methyl-D-aspartic acid; NSAIDs, nonsteroidal antiinflammatory drugs; PPN, partial parenteral nutrition; RR, respiratory rate; SIRS, systemic inflammatory response syndrome; T, temperature; TPN, total parenteral nutrition; WBC, white blood

Answer 452

Most pets with sepsis will have a relative or absolute hypovolemia, hypotension, and/or poor tissue perfusion. Isotonic crystalloids can be used for rapid initial volume resuscitation and administered based on evaluation of end points (e.g., heart rate, blood pressure, central venous pressure). Then, fluid therapy should be tailored to the needs of the patient. Patients with sepsis will have a propensity to develop interstitial edema because of increased vascular permeability and decreased blood colloid osmotic pressure. Colloids (e.g., hetastarch) may help prevent interstitial edema and should be considered for volume resuscitation and during maintenance of sepsis patients.

Answer 453

Since the goal of treating septic shock is to maintain tissue perfusion, medications that cause vasoconstriction should be used only if absolutely necessary. Positive inotropic drugs (e.g., dobutamine) may be a good initial management choice for septic shock since they help combat decreased cardiac output caused by myocardial dysfunction without inducing peripheral vasoconstriction.

Answer 454

If volume resuscitation and positive inotropic support has failed to restore blood pressure, a vasopressor agent (e.g., dopamine, norepinephrine, epinephrine, or vasopressin) could be added. Although there are no clinical trials evaluating these drugs, epinephrine was found to adversely affect organ function, systemic perfusion, and survival compared to the use of norepinephrine or vasopressin and had detrimental effects on gastric mucosal pH and plasma lactate concentrations compared to dobutamine and norepinephrine in experimental canine sepsis. Relative adrenal insufficiency has been documented in dogs with sepsis and refractory hypotension and should be considered in any dog requiring vasopressor therapy during sepsis.

Answer 455

Hyperglycemia can be a complication of nutritional therapy, especially parenteral nutrition. Hyperglycemia has been associated with increased inflammation and a poorer prognosis in people with sepsis and SIRS. Although the importance of glucose homeostasis in dogs and cats with sepsis is unknown, iatrogenic hyperglycemia should be avoided.

Answer 456

For the majority of patients, acid-base abnormalities are related to lactic acidosis secondary to poor tissue perfusion. Typically these abnormalities will resolve once perfusion is restored. Therefore, bicarbonate administration is rarely needed. When organ dysfunction is recognized, specific therapy aimed at maintaining homeostasis should be considered.

Answer 457

Although many analgesics like ketamine[32] and buprenorphine[33] may offer specific antiinflammatory advantages during endotoxemia, some may be detrimental. Morphine, for instance, augments the inflammatory response to endotoxin, has a detrimental effect on mean arterial pressure, and increases mortality in endotoxemic rats. It is not known if morphine is detrimental during canine or feline sepsis.

Answer 458

For example, despite their strong antiinflammatory properties, the use of corticosteroids for the treatment of sepsis has fallen out of favor due to their lack of efficacy combined with their immunosuppressive, ulcerogenic, and prothrombotic nature.[35,36] One exception may be the use of low or physiologic doses of corticosteroids for management of relative adrenal insufficiency during sepsis.

Answer 459

Activated protein C and administration of regular insulin to maintain tight glycemic control are two antiinflammatory treatments that have been shown to be beneficial in human clinical trials. Hyperglycemia has been linked to increased inflammatory cytokine production and an increased risk of mortality in people. This management strategy has not been evaluated in dogs or cats. Regardless, good glycemic control should be a consideration in septic patients.

Answer 460

The only antiinflammatory therapy with some positive benefit that has been tested in canine clinical trials is polymyxin B. Polymyxin B binds to endotoxin from gram-negative bacteria, preventing the interaction between endotoxin and the immune system.

Answer 461

Historically, shock was described as the effect of generalized circulatory abnormalities that led to inadequate tissue perfusion. Although this classic description still holds important clinical relevance, it has been recognized that the complexity of shock states result not from the initial insult per se, but the host's systemic response to that insult. Furthermore, the ultimate result of shock is decreased cellular energy metabolism and adenosine triphosphate (ATP) production. It is recognized that these abnormalities may occur despite normal tissue perfusion. Utilizing this definition of shock, one may consider a functional classification system whereby shock is defined as decreased cellular energy production and shock categories are expanded to include types other than the classic hypovolemic, distributive, and cardiogenic types

Answer 462

Etiologies of shock with this system include syndromes that are clinically apparent causes of shock but that do not fit into the traditional classification scheme; for example, severe anemia, methemoglobinemia, and bromethalin exposure are often associated with clinical shock states, yet the patient has normal blood volume, cardiac function, and systemic vascular resistance.

Answer 463

Figure 139-1 Algorithm for assessment and treatment of shock. *, When administering fluids for shock, ¼ to ⅓ a shock volume is administered over 5 to 15 minutes, with repeated evaluations of cardiovascular response.

Answer 464

TYPES Hypovolemic shock is defined as a life-threatening decrease in circulating blood volume and is the most common form. It leads to inadequate delivery of oxygen and nutrients to tissues and an accumulation of byproducts of cellular metabolism due to insufficient circulating blood volume. Intravascular volume depletion can result from: 1. hemorrhage (internal or external), 2. nonhemorrhagic fluid losses (e.g., gastrointestinal, urinary, third spacing), or 3.decreased intake of fluid.

Answer 465

Cardiogenic shock results predominantly from failure of adequate forward blood flow. The dysfunction can occur in either the diastolic or systolic phase or can result from an obstruction of flow.

Answer 466

Systolic or forward flow failure results from an overt failure of contractility (e.g., intrinsic heart disease, drug overdose) or severe tachyarrhythmias. Diastolic failure can result from primary cardiac disease such as hypertrophic or restrictive cardiomyopathy.

Answer 467

Obstructive shock is the result of occlusion of either forward flow or venous return, as seen in pericardial tamponade, tension pneumothorax, thromboembolic disease, tumors, or distended organs (e.g., gastric dilatation and volvulus). Obstructive disease and systolic and diastolic dysfunction all lead to decreased cardiac output, hypotension, and reduced coronary blood flow.

Answer 468

Neurohormonal compensatory mechanisms such as catecholamine release and salt and water retention worsen the situation by increasing myocardial oxygen demand and afterload, thus creating a downward spiral of cardiac function and systemic perfusion.

Answer 469

Distributive shock is a condition in which the systemic vascular resistance (SVR) is abnormal causing a maldistribution of blood flow. Distributive shock is most commonly associated with decreased SVR; however, there may also be regional vasoconstriction and endothelial dysfunction that cause sluggish capillary blood flow and arteriovenous shunting, both of which are forms of maldistribution of blood flow.

Answer 470

The classic example of distributive shock (commonly referred to as vasodilatory shock) is septic shock. Other vasodilatory states, however, can also lead to distributive shock, such as systemic inflammatory response syndrome (SIRS), adverse drug reactions or overdose, anaphylaxis, heat stroke, and neurogenic shock. Sepsis and heat stroke are both complicated by a vigorous systemic inflammatory response and further compromise of tissue oxygenation due to maldistribution of blood flow (i.e., arteriovenous shunting) and microcirculatory and mitochondrial dysfunction.

Answer 471

Hypoxemic shock is caused by decreased blood oxygen content. Examples of diseases associated hypoxemic shock include anemia, methemoglobinemia, carbon monoxide poisoning, hypoventilation, and pulmonary parenchymal disease. Despite normal blood volume and blood pressure, an animal can display cardinal signs of shock secondary to severely decreased blood oxygen content.

Answer 472

Metabolic shock is caused by deranged cellular metabolism that, as in all shock states, leads to decreased cellular energy production. Examples of altered cellular metabolism might include cyanide and bromethalin toxicity (both cause direct interference with mitochondrial function and ATP production), severe hypoglycemia, relative adrenal insufficiency, and severe pH derangements. In addition to the vasomotor abnormalities of septic shock, there is a component of metabolic shock, and it is thought that there is an acquired defect in oxidative phosphorylation that causes decreased cellular energy production (called cytopathic hypoxia)

Answer 473

The categories of shock are not mutually exclusive, and many animals with distributive shock will also have some degree of hypovolemia, particularly as SIRS leads to increased vascular permeability and fluid loss. Mediators of SIRS and ischemia reperfusion injury include substances that contribute to cardiac dysfunction. Thus progression of both distributive and hypovolemic shock can lead to cardiogenic shock. Cardiogenic shock can cause hypoxemic shock when complicated by pulmonary edema. Any animal with inadequate intestinal perfusion may develop bacterial translocation and sepsis.

Answer 474

There may be genetic and immune factors that play a role in how the host responds to the insult. This is most clearly demonstrated in septic shock, where the cascade of events that leads to irreversible cardiovascular collapse is the systemic inflammatory response initiated by products of infectious agents. It has been recognized that SIRS can also be triggered by noninfectious insults including tissue hypoxia, tissue acidosis, pancreatitis, trauma, and major surgery. Similarly, although hypovolemia can be reversed, reperfusion of ischemic tissues leads to inflammation and production and release of inflammatory mediators. These complex cascades confound the treatment of shock, since reversing the perfusion abnormalities may not stop the progression once the inflammatory cascade has been initiated.

Answer 475

The normal physiologic response to shock is to increase sympathetic tone, which causes vasoconstriction and increases in both heart and respiratory rates. In the early (sometimes called compensated) stages of shock, tachycardia may be the only clinical sign.

Answer 476

Early stages of shock may not be clinically obvious, as compensatory mechanisms are recruited to maintain cardiac output and tissue perfusion. With time and progression to the intermediate stages (also referred to as early decompensated shock), profound vasoconstriction results from the attempt to increase venous return and maintain stroke volume. In the intermediate stages, additional compensatory mechanisms trigger an increase in salt and water retention (i.e., the renin-angiotensin-aldosterone system and antidiuretic hormone) and release of vasoconstrictors (e.g., vasopressin) in an effort to increase cardiac output and redistribute blood flow to vital organs. Organ dysfunction appears, and most patients in this progressive stage of shock will die without intervention Patients in the intermediate stages of shock will show pale mucous membranes and prolonged capillary refill time (CRT); tachycardia, poor pulse quality, and hypotension; decreased mentation and weakness; tachypnea; cool extremities; and decreased rectal temperature.

Answer 477

In late stages of shock (also referred to as late decompensated or irreversible shock), compensatory mechanisms fail and systemic inflammation leads to multiple organ failure and death. Successful clinical intervention is uncommon. Patients in the late stages of shock will show stupor or coma; pale mucous membranes with prolonged or absent CRT; bradycardia; hypothermia; and poor to absent pulse quality. This chapter will focus on the clinical presentations associated with the major types of shock in the early and intermediate stages.

Answer 478

A hallmark clinical sign of all types of shock is mental dullness, especially as shock progresses beyond the early compensated state. In contrast, the hallmark of distributive shock is the failure of effective vasoconstriction, secondary to circulating mediators that interfere with vascular tone. This failure leads to relative hypovolemia; this is most commonly seen with distributive shock secondary to sepsis.

Answer 479

Red mucous membranes, rapid CRT (<1 second), normal or increased rectal temperature, tachycardia, tachypnea, bounding pulses, hypotension, and depressed mentation.

Answer 480

Distributive shock that is complicated by concurrent fluid loss (due to changes in vascular permeability and fluid compartment shifts or the underlying etiology) may initially be associated with clinical signs more typical of hypovolemic shock, but upon resuscitation, clinical signs of distributive shock may develop. One other unique feature of septic shock is that cats frequently become bradycardic rather than tachycardic.

Answer 481

In order to differentiate cardiogenic shock from all other forms of shock that would require fluid therapy, careful heart auscultation, an electrocardiogram, and a thorough physical examination are required. Chest radiographs and cardiac ultrasound are beneficial; however, animals in shock are frequently not stable enough to obtain extensive diagnostic tests. Emergency treatment can (and should) be initiated based on physical examination and historical findings.

Answer 482

The goal of treatment in early shock is to restore effective tissue perfusion and oxygenation. In later stages of shock, restoration of perfusion alone is usually insufficient to halt the progression of the inflammatory cascade. Aggressive support of organ function and prevention of additional proinflammatory stimuli (including hypotension, hypoxia, and infection) are critical. At all stages, correction of the inciting cause is necessary.

Answer 483

Oxygen is universally administered regardless of the type of shock. Additional therapy depends on the etiology of the shock.

Answer 484

For most forms of shock, except systolic and diastolic forms of cardiogenic shock, fluid therapy is essential and the goal is to increase the effective circulating volume. The choice of fluids depends on the cause of shock; however, crystalloids (isotonic-balanced electrolyte solutions) or colloids are typically used for initial treatment. The fluid rate and the actual volume given should be tailored to each individual animal. A shock volume of isotonic crystalloid fluid is considered to be equivalent to a blood volume of approximately 90 mL/kg in the dog and 60 mL/kg in the cat. Typically, ¼ to ⅓ of a shock volume is provided within the first 5 to 15 minutes, with repeated evaluation of the cardiovascular response (e.g., heart rate, mucous membrane color, pulse quality, blood pressure, and CRT). Colloids should be used for shock resuscitation of hypoproteinemic animals; they may also be used to hasten resuscitation of large animals where the time taken to administer the required large volume of crystalloid fluids may be too long and, therefore, life-threatening

Answer 485

The same general principles apply to resuscitation using colloids (i.e., giving fractions of shock doses at a time) but the volumes are smaller (5 to 20 mL/kg bolus in dogs, and 3 to15 mL/kg bolus in cats). Synthetic colloids have been associated with prolongations in clotting times at doses of greater than 20 mL/kg in 24 hours but this effect is unpredictable. Hypertonic solutions (e.g., 7.2% to 7.5% saline) are quite effective at rapidly expanding the intravascular space; however, this crystalloid fluid rapidly redistributes to the extravascular space and should be combined with a colloid to lengthen the effect on the intravascular space.

Answer 486

Never administer undiluted 23% saline to a patient because it will cause hemolysis and phlebitis

Answer 487

The resuscitative fluid of choice for hemorrhagic hypovolemic shock is blood. Administration of 1 mL/kg of packed red blood cells or 2 mL/kg of whole blood will raise the hematocrit by approximately 1%. Massive transfusions (greater than one blood volume in 24 hours or greater than ½ blood volume in 3 hours) may be required in some cases (see Chapter 142). Expected side effects of massive transfusions include thrombocytopenia, ionized hypocalcemia, and coagulopathy.

Answer 488

In systolic and diastolic forms of cardiogenic shock and in hypoxemic shock due to lung injury, aggressive fluid therapy may be fatal. Treatment of cardiogenic shock relies on correction of the underlying cause. Treatment with antiarrhythmics, diuretics, vasodilators, or inotropes may be required.

Answer 489

In obstructive shock, fluid therapy is often required. Resolution of obstruction to flow may require physical intervention (e.g., surgery for tumors and gastric dilation and volvulus) or medical management (e.g., thrombolytics for thromboembolic disease). Prior to intervention, adequate circulatory volume and optimal perfusion must be established.

Answer 490

Specific therapy should be directed at the cause of shock. For example, in hemorrhagic hypovolemia, bleeding must be controlled, and in septic shock the source of infection must be eliminated. Vasopressors may be required when hypotension persists despite adequate volume repletion.

Answer 491

Venous oxygen saturation: SvO2 is pathologically decreased (below 65% to 70%) when oxygen delivery is decreased (e.g., decreased cardiac output, anemia, hypoxemia) or when oxygen consumption is increased. Mixed venous oxygen saturation can be pathologically increased in states of decreased tissue oxygen consumption (e.g., cytopathic hypoxia, microvascular shunting) or increased oxygen delivery (e.g., increased cardiac output in the hyperdynamic phase of septic shock).

Answer 492

Systemic anaphylaxis is an acute, life-threatening allergic reaction resulting from massive, generalized release of mast cell mediators, including histamine. Anaphylaxis can be triggered by venoms from insects and reptiles; medications such as hormones, antibiotics, nonsteroidal antiinflammatory drugs, anesthetics, and sedatives; parasiticides; and other miscellaneous drugs and foods (Box 140-1). Immediate recognition and treatment of anaphylaxis in a dog or cat is essential for a successful outcome.

Answer 493

Type I, immediate (immunoglobulin E [IgE] dependent); Type II, cytotoxic (IgG, IgM dependent); Type III, immune complex (IgG or IgM complex dependent); Type IV, delayed (T lymphocyte dependent).

Answer 494

Anaphylaxis can be caused by either an anaphylactic or anaphylactoid reaction. Anaphylactoid and anaphylactic reactions have exactly the same clinical appearance and are treated identically.

Answer 495

Anaphylaxis is defined as a type I, IgE-mediated hypersensitivity reaction with an interaction of antigen and IgE antibody on the surface of sensitized mast cells. This interaction causes the release of histamine and other inflammatory mediators.

Answer 496

Sensitization requires previous exposure to an antigen or hapten, which can range in size from a protein to a small, low–molecular weight drug. Proteins act directly as an antigen, while the smaller drugs will bind to cells and act as haptens.

Answer 497

IgE is produced by and bound on the surface of mast cells and basophils by high-affinity receptors (FcϵRI) for the Fc portion of the immunoglobulin. When an antigen causes cross-linkage of two surface IgE molecules, the mast cell is activated and primary and secondary mediators are released (Table 140-1).

Answer 498

The cross-linking of the FcϵRI receptors activates tyrosine kinases, which cause activation of phospholipase C, leading to production of diacylglycerol and inositol triphosphate. These mediators increase intracellular calcium concentrations and activate multiple protein kinases. Phosphorylation of myosin, found in intracellular filaments, causes granules to move to the cell surface, fuse, and release the primary mediators of anaphylaxis: histamine, heparin, tryptase, kallikreins, proteases, proteoglycans, eosinophilic chemotactic factor of anaphylaxis (ECF-A), and neutrophil chemotactic factor of anaphylaxis (NCF-A). Cross-linking of the FcϵRI receptors also activates phospholipase A2, which produces arachidonic acid from membrane phospholipids, resulting in release of the secondary mediators: leukotrienes, prostaglandins, thromboxanes, and platelet-activating factor. The protein kinases also alter gene expression, causing synthesis and secretion of other cytokines (interleukin-4 [IL-4], IL-5, IL-6, IL-13, tumor necrosis factor-α, macrophage inflammatory protein-1α), responsible for the late-phase inflammatory response.

Answer 499

Release of the inflammatory mediators is rapid: granule exocytosis occurs within seconds to minutes, activation of the arachidonic acid cascade in minutes, and cytokine synthesis and secretion within 2 to 24 hours.

Answer 500

Anaphylactoid reactions cause anaphylaxis without IgE, either through directly activating mast cells to release histamine or, more commonly, by activating the complement pathway. They do not require previous exposure and sensitization.

Answer 501

Activation of complement results in production of C3a and C5a, the anaphylatoxins, which causes degranulation of mast cells and release of histamine and other primary mediators, activation of the arachidonic acid cascade, and gene expression and synthesis of the inflammatory mediators.

Answer 502

Both anaphylactoid and anaphylactic types of reactions result in hypovolemia and vasodilation, potentially leading to severe hypovolemic shock. Histamine and the leukotrienes are potent vasodilators and increase vascular permeability, allowing leakage of protein and fluid into the interstitial space.

Answer 503

Activation of H1 receptors results in pruritus and bronchoconstriction and stimulates endothelial cells to produce nitric oxide, a potent vasodilator that significantly contributes to hypotension. H1 receptors also mediate coronary artery vasoconstriction and cardiac depression. H2 receptors stimulate gastric acid production, as well as cause coronary artery and systemic vasodilation and increase heart rate and contractility. H3 receptors are located on presynaptic terminals of sympathetic effector nerves that innervate the heart and systemic vasculature and inhibit endogenous norepinephrine release from sympathetic nerves.[1] Activation of the H3 receptors results in worsened signs of anaphylactic shock because it inhibits normal compensatory sympathetic responses.

Answer 504

hypotension, bronchospasm, urticaria, erythema, pruritus, pharyngeal and laryngeal edema, arrhythmias, vomiting, and hyperperistalsis. Clinical signs are dependent on species and method of exposure.

Answer 505

In dogs, the liver is considered the shock organ, and clinical signs result from hepatic vein congestion and portal hypertension. Initial signs may include excitement, vomiting, defecation (often diarrhea), then progress to respiratory distress, collapse secondary to hypovolemic shock, and death within 1 hour if not treated. A dog with anaphylaxis may have generalized wheals, angioedema (particularly of the face), pruritus (Web Figure 140-1), pale mucous membranes, poor capillary refill time, tachycardia, poor pulse quality, and appear depressed or even collapsed. Severe cases may result in respiratory distress secondary to upper airway obstruction from laryngeal and pharyngeal edema.

Answer 506

In cats, the lungs are considered the shock organ, and respiratory distress is the first sign in cats with systemic anaphylaxis.

Answer 507

Respiratory distress results from airway obstruction secondary to laryngeal edema, bronchoconstriction, and increased mucus production. Other signs in cats include severe pruritus, vomiting, diarrhea, depression, and death. On physical examination, a cat in anaphylactic shock usually will be in severe respiratory distress, have wheezes on auscultation, and have pale mucous membranes, poor capillary refill time, and poor pulse quality.

Answer 508

The most severe anaphylactic reactions are generally seen if the antigen is given by parental injection. Oral ingestion often causes vomiting, diarrhea, urticaria, and angioedema. Inhalation can result in rhinitis and bronchospasm. Topical administrations can cause conjunctivitis and urticaria with or without systemic signs. In general, patients that have the most rapid onset of clinical signs after exposure to an antigen develop the most severe signs of anaphylactic shock.

Answer 509

Epinephrine is useful because of its inotropic and chronotropic effects on the heart. Epinephrine also causes bronchodilation and increased intracellular concentrations of cyclic adenosine monophosphate, which decreases synthesis and release of inflammatory mediators of anaphylaxis.

Answer 510

Pressors, glucocorticoids, antihistamines, aminophylline, atropine. Dopamine at a dose of 4 to 10 µg/kg/min or other pressors may be used if refractory hypotension is present. Aminophylline may be used if bronchoconstriction is refractory to epinephrine. It will cause bronchodilation, increase respiratory drive, and increase contractility of the muscles of respiration. Glucocorticoids are useful in blocking the arachidonic acid cascade and reducing the severity of the late-phase anaphylactic reactions.. Antihistamines competitively bind at the histamine receptors and block its effects. Diphenhydramine, an H1 blocker, should be administered at 0.5 to 1.0 mg/kg slow IV or IM to reduce pruritus and angioedema. The H2 blockers such as ranitidine at 1 mg/kg IV or famotidine at 0.5 mg/kg IV can be used to decrease gastric acid secretion stimulated by histamine. These antihistamines are not very useful in the acute, life-threatening stage of anaphylaxis, but may be helpful after a dog or cat has been stabilized. In one study, pretreatment of dogs with the experimental H3 blocker thioperamide maleate resulted in increased heart rate and improved left ventricular stroke work, but its clinical usefulness in naturally occurring anaphylaxis after the onset of signs remains to be determined.[1]

Answer 511

Trauma to the thorax can be classified as blunt or penetrating.

Answer 512

Pneumothorax, hemothorax, and diaphragmatic hernia. As a group, these injuries are most likely to manifest with varying degrees of dyspnea accompanied by muffled lung and heart sounds on auscultation of the thorax

Answer 513

Pneumothorax is the accumulation of air in the pleural space between the parietal and visceral pleurae and is one of the two most commonly recognized results of traumatic injury to the thorax. Traumatic pneumothorax is classified as “closed” or “open.”

Answer 514

Tension pneumothorax occurs due to a one-way–valve effect, in which air enters the pleural space during inspiration and cannot be evacuated during expiration. The resultant increase in intrapleural pressure results in hypoventilation and decreased venous return, manifesting with signs of severe respiratory and cardiovascular compromise.

Answer 515

Disruption of pulmonary, thoracic wall, or mediastinal blood vessels. Hemothorax can also be seen in dogs and cats with diaphragmatic hernia and concurrent hemoabdomen. Clinically significant hemothorax (although uncommon) is a physical examination diagnosis. Hemothorax results in decreased lung and heart sounds ventrally to diffusely and concurrent signs of hypovolemic shock (pale mucous membranes, slow capillary refill time [CRT], high pulse rate, weak pulses) and dyspnea

Answer 516

Diaphragmatic hernia is most often recognized after blunt thoracic trauma and is thought to result from rapid compression of the abdomen with the majority of the force directed cranially. Penetrating thoracic and abdominal injuries can also cause diaphragmatic hernia. The dog or cat with diaphragmatic hernia may not show clinical signs or may have dyspnea, decreased lungs sounds ventrally to diffusely, borborygmi on auscultation of the thorax, an “empty” abdominal palpation, or a combination thereof. Diaphragmatic hernia is commonly associated with pleural effusion. Some dogs and cats may develop clinical signs of diaphragmatic hernia months to years after the initial trauma

Answer 517

TRAUMA-ASSOCIATED PULMONARY INJURIES Pulmonary contusion (PC) refers to lung lesions that occur after a compression-decompression injury. Subsequent hemorrhage and edema lead to alveolar collapse and lung consolidation.[2-4] Hypoxemia results from ventilation: perfusion mismatch, shunt, diffusion impairment, and in severe cases, hypoventilation. Much like pneumothorax, pulmonary contusion is common after trauma. All dogs that have sustained trauma have PC until proven otherwise. The presence of clinically significant PC (severe enough to cause clinical signs) is a physical examination diagnosis. Treatment of PC is largely supportive. The cornerstones of therapy include oxygen delivery by cage, hood, or nasal cannulae to maintain SpO2 greater than 92% on FiO2 less than 0.60 without severe increases in respiratory effort. Despite numerous opinions, there is no clear answer to the question of whether crystalloid or colloid therapy is most appropriate for dogs with PC.

Answer 518

Se i Ettinger

Answer 519

Pneumomediastinum Pneumomediastinum is defined as an accumulation of air within the mediastinal space and, like rib fractures, should serve as a “flag” for concurrent injuries. Pneumomediastinum may result from injury to the large airways (see below), esophagus, alveoli (with subsequent tracking of air back into the mediastinum), and the skin in the cervical region. In the cervical region, air can track along the trachea and vascular structures of the neck into the mediastinum. Pneumomediastinum is rarely of clinical consequence. Pneumomediastinum can be definitively diagnosed on thoracic radiographs. An effort should be made to identify and definitively treat concurrent and causative injuries.

Answer 520

Tracheal Avulsion Tracheal avulsion is thought to occur due to a rapid and extreme hyperextension injury to the head or neck and is more common in cats than in dogs. Tracheal avulsion may affect the intrathoracic or extrathoracic trachea. Both intrathoracic and extrathoracic tracheal avulsion can be associated with subcutaneous emphysema, signs of respiratory distress, and airway obstruction on initial physical examination.

Answer 521

Blood transfusions can play an essential role in the management of diseases of nearly every body system. Transfusion's critical role in replenishing red blood cells, coagulation factors, platelets, and albumin can provide lifesaving supportive treatment until a primary disorder can be controlled or resolved. A wide variety of clinical conditions require blood transfusions and multiple factors must be considered in determining a transfusion protocol. The decision to transfuse an anemic dog or cat is usually based on the “transfusion trigger,” commonly defined as the packed cell volume (PCV, or hemoglobin [Hb] or hematocrit [Hct]) below which a transfusion is considered needed to sustain life. Although the PCV (or Hb concentration or Hct) provides information about the oxygen-carrying capacity of the blood and serves as a general guideline for the initiation of transfusion in patients, it is inadequate as the sole criterion for instituting red blood cell transfusion (Table 142-1). Additional factors considered in the decision to administer a red blood cell transfusion to a dog or cat include the perfusion status, the ability of the lungs to oxygenate the blood, the chronicity of the anemia, and the regenerative capacity of the bone marrow

Answer 522

Pneumonia, pulmonary edema, myocardial failure, or sepsis may require more liberal transfusion strategies while more restrictive transfusion criteria may be applied in chronic anemia due to retroviral infection, bone marrow failure, or chronic renal failure. When the PCV reaches approximately 10%, the myocardium exhausts its ability to compensate for anemia and becomes hypoxic, and providing increased oxygen-carrying capacity becomes imperative.[3]

Answer 523

TRANSFUSION IN ANEMIC DOGS AND CATS Red blood cells can be provided via whole blood transfusion or by transfusion of packed red blood cells.

Answer 524

1. Hemolysis, 2. blood loss, 3. erythropoietic failure.

Answer 525

Blood loss anemia is the most common anemia category for which red blood cells are transfused in both dogs and cats (Table 142-2). Dogs and cats with coagulation disorders often require treatment of anemia in addition to coagulopathy treatment. Because each of these categories of anemia is different with regard to transfusion needs, the following sections of this chapter will discuss the transfusion needs for each category. Regardless of the category of anemia being treated, the goals of a red blood cell transfusion are to reduce morbidity, mortality, and functional impairment caused by inadequate delivery of oxygen.

Answer 526

PRETRANSFUSION TESTING IN ANEMIC DOGS AND CATS Prior to transfusion of red blood cells, data should be collected to ensure compatibility, safety, and efficacy. Pretransfusion compatibility testing prior to transfusion of a red blood cell–containing component should include a blood type if a cat has not previously been transfused to ensure the recipient and donor are the same blood type.

Answer 527

Feline blood types A, B, and AB can be determined by card typing, gel tube typing, or slide typing. If these methods are not available, crossmatching can be performed prior to the first transfusion to determine red blood cell compatibility. Blood typing or crossmatching prior to the first transfusion is not necessary in dogs.

Answer 528

Blood-typing cards or gel tube typing can determine the dog erythrocyte antigen (DEA) 1.1 status of a dog. Blood typing is useful in dogs even if the recipient has not previously been transfused if the donor blood is DEA 1.1–positive.

Answer 529

DEA 1.1–positive blood administered to a DEA 1.1–negative dog causes production of antibodies against DEA 1.1 and may cause an acute hemolytic transfusion reaction if DEA 1.1–positive blood is administered in subsequent transfusions.[7] DEA 4 alloantibodies can also cause an acute hemolytic transfusion reaction if a DEA 4− dog is transfused with DEA 4+ blood and an anti–DEA 4 antibodies are produced. Subsequent transfusions of DEA 4+ blood are likely to cause an acute hemolytic transfusion reaction.

Answer 530

Recently, two new blood groups have been identified, one in dogs (Dal) and one in cats (Mik).

Answer 531

Dal appears to be common in dogs and transfusion of Dal− dogs with Dal+ blood results in antibody production that may lead to an acute hemolytic transfusion reaction. The Dal antigen appears to be lacking in some Dalmatians.

Answer 532

Mik− cats appear to have a naturally occurring anti-Mik alloantibody that may cause transfusion incompatibility without prior transfusion. The prevalence of these antigens in the general pet population is unknown, and their significance in transfusions is not known. When a second transfusion is administered more than 4 days after the first transfusion, a crossmatch should be performed in both dogs and cats to determine compatibility of the red blood cells to be transfused.

Answer 533

If Oxyglobin is the product being used to treat anemia, blood typing and crossmatching are not necessary.

Answer 534

In order to assess the effect of a red blood cell transfusion on the dog or cat, a Hct, PCV, or Hb should be measured prior to and following administration of red blood cells. The choice can be based on test availability, except in the case of Oxyglobin administration.

Answer 535

Oxyglobin is a hemoglobin-based oxygen carrier (HBOC), and although it is used to treat anemia, it does not contain red blood cells. Measurement plasma Hb and total Hb should be used to determine the response to administration of Oxyglobin.

Answer 536

A transfusion should be discontinued if vomiting, diarrhea, collapse, or urticaria are noted.

Answer 537

TRANSFUSION FOR BLOOD LOSS ANEMIA The transfusion trigger is variable in cases of blood loss anemia. Acute blood loss resulting in hemodynamic instability despite volume replacement requires red blood cell transfusions at a higher PCV than does chronic blood loss. If blood loss is internal, approximately 50% of the hemorrhaged red blood cells will reenter the circulation over 24 hours. In those cases, red blood cell dosage can be more conservative than in cases of external hemorrhage.

Answer 538

If blood loss has been slow, allowing for physiologic compensation, a PCV of greater than 15% may be adequate for routine diagnostic testing, but if anesthesia is required, if a pet has cardiac or respiratory disease, or if blood loss from an invasive procedure may occur, red blood cell transfusion is indicated. Chronic blood loss may result in erythropoietic failure.

Answer 539

Several products are available to increase oxygen-carrying capacity in blood loss anemia (Table 142-3). Whole blood is the least appropriate since it contains plasma, which is unnecessary for the treatment of anemia.

Answer 540

Although Oxyglobin does not contain red blood cells, it is recommended for treating reduced oxygen-carrying capacity when appropriate blood products are not available. Oxyglobin should be used cautiously in dogs and cats with cardiovascular disease and circulatory overload states.

Answer 541

Massive transfusion is defined as transfusion dose greater than 1 blood volume in a 24-hour period. In the dog, this had been defined as 90 mL/kg in 24 hours or 45 mL/kg in 3 hours.[12] The large volume of citrate-based anticoagulant administered with the red blood cells results in hypocalcemia and hypomagnesemia. Dilutional coagulopathy results if the blood administered has been stored and does not contain active coagulation factors. Acid-base abnormalities may also occur after a massive transfusion. Therefore, after any dog or cat is given a massive transfusion, electrolytes, coagulation parameters, and acid-base status should be monitored.

Answer 542

TRANSFUSION FOR IMMUNE-MEDIATED HEMOLYTIC ANEMIA Red blood cell transfusion is a common treatment for dogs and cats with immune-mediated hemolytic anemia (IMHA). Historically, red blood cell transfusion was discouraged because of the fear it would promote hemolysis and worsen the patient's condition. This has largely been refuted in recent years. Determining the patient's requirement for increased oxygen-carrying capacity has become the major factor influencing the transfusion trigger in IMHA, as it should be for animals with other conditions. If clinical signs indicate need for increased oxygen-carrying capacity, withholding transfusion risks progressive hypoxic damage to the heart, liver, and kidneys.

Answer 543

A reasonable recommendation is to transfuse DEA 1.1–negative red blood cells in the smallest volume necessary to improve a dog or cat's clinical status.[18] Any of the packed red blood cell products are appropriate selections in IMHA (see Table 142-3). Daily transfusions may be required until immunosuppressive therapy arrests the hemolytic process and the pet is able to maintain its own oxygen-carrying capacity. Concerns of inducing accelerated hemolysis have led to the recommendation to use a HBOC (Oxyglobin) for increasing oxygen-carrying capacity in IMHA because the antigenic red blood cell membranes have been removed during manufacturing. This theoretical recommendation not been confirmed in clinical trials, but individual cases of IMHA respond well to transfusion of HBOC

Answer 544

IMHA may represent a unique situation where blood typing and crossmatching are not possible due to autoagglutination of the patient's sample; however, blood from most dogs and cats with this disorder can successfully be crossmatched to a donor

Answer 545

TRANSFUSION FOR ANEMIA OF ERYTHROPOIETIC FAILURE Because anemia caused by erythropoietic failure typically takes weeks to resolve, red blood cell–containing products are optimal. The half-life of red blood cell–containing products depends on the storage medium but ranges from 21 to 35 days.[20-26] The half-life of Oxyglobin is 18 to 43 hours when it is administered at a dose of 10 to 30 mL/kg. Packed red blood cell products have an advantage over both whole blood and Oxyglobin in the treatment of anemia caused by erythropoietic failure. Animals with this type of anemia are usually normovolemic or hypervolemic, and packed red blood cells have the same amount of oxygen-carrying capacity in a smaller volume than either whole blood or Oxyglobin.

Answer 546

The initial dosage of red blood cell–containing blood products varies based on the product selected and the type of anemia being treated (Table 142-4). Chronic and nonregenerative anemia may require a smaller increase in oxygen-carrying support, and thus a lower dosage to alleviate clinical signs, than acute and regenerative anemia since the body will have responded to chronic anemia through compensatory mechanisms. The rate of administration of oxygen-carrying products will be influenced by the volume status of the pet, which depends on the concurrently administered intravenous solutions as well as the type of anemia.

Answer 547

Initially, 1 to 3 mL of red blood cells can be administered over a period of about 5 minutes while the pet is observed for adverse reactions. Following the initial transfusion, normovolemic patients and those with chronic anemia can be transfused at a rate of 10 to 20 mL/kg/hr.[28] Hypovolemic patients with acute anemia may be given as much as 60 mL/kg/hr. Slow transfusion rates are indicated in dogs or cats with cardiac disease.

Answer 548

POSTTRANSFUSION MONITORING IN DOGS AND CATS TRANSFUSED FOR ANEMIA In order to assess the effect of the red blood cell transfusion on the patient and determine if additional transfusion is required, Hct, PCV, or Hb should be measured following administration of red blood cells. Measurement of Hb is the appropriate test to determine the response to administration of Oxyglobin. Body temperature, respiratory rate, heart rate, and blood pressure should be monitored after any transfusion. Changes in any of these parameters during or immediately following transfusion are an indication of a transfusion-associated adverse event. Extra emphasis should be placed on monitoring respiratory rate, heart rate, and thoracic auscultation when Oxyglobin is administered because this product increases the risk of circulatory overload.

Answer 549

ADVERSE EVENTS ASSOCIATED WITH RED BLOOD CELL ADMINISTRATION The most serious adverse effect of administration of any red blood cell–containing component is acute hemolytic transfusion reaction due to recipient antibodies against the donor red blood cells. Transfusions also carry risk of circulatory overload, Type I hypersensitivity reactions, vomiting, and fever.

Answer 550

The most common reaction, fever, is believed to be due to cytokines contained in the transfused blood or from antibodies against red blood cells, white blood cells, or platelets. Fever also occurs with bacterial contamination of blood. An increase in body temperature of 1° C should be considered a transfusion-associated fever.

Answer 551

Adverse events associated with Oxyglobin are different than those related to transfusion of red blood cell–containing products and are due to the unique properties of Oxyglobin. Oxyglobin does not contain antigenic red blood cell membranes and will not cause an acute hemolytic transfusion reaction. The most common adverse event associated with Oxyglobin administration is circulatory overload, manifested as pulmonary edema or pleural effusion.[39] Posttransfusion monitoring should focus on assessment of parameters, such as blood pressure or central venous pressure, either of which could aid in identifying development of circulatory overload. Oxyglobin has strong colloid effect because its colloid osmotic pressure (COP) is 43 mm Hg and it also causes transient discoloration of mucus membranes (muddy pink, icteric orange, or brown), skin, and urine (pigmenturia). Vomiting and diarrhea are less commonly seen adverse effects.

Answer 552

POTENTIAL LONG-TERM PROBLEMS AFTER TRANSFUSIONS FOR ANEMIC DOGS AND CATS Diseases where multiple transfusions are given over a prolonged period of time are uncommon in veterinary transfusion medicine; consequently, long-term problems caused by transfusion are rarely described. One such adverse event is posttransfusion purpura.[40] In this transfusion complication, thrombocytopenia occurs 1 to 2 weeks following transfusion. The recipient, sensitized by transfusions containing platelet antigens, can produce antibodies against platelets which, in turn, can cause thrombocytopenia. The syndrome usually naturally resolves in 1 to 4 weeks. A second long-term problem caused by transfusions in dogs is hemochromatosis.[41] Iron from senescent transfused red blood cells accumulates in the liver, ultimately resulting in liver failure from transfusional hemochromatosis. All transfusions carry the risk of infectious disease transmission. Of greatest concern in veterinary patients are canine and feline vector-borne diseases and feline retroviral diseases.[42] Blood donor screening recommendations have been made to minimize the risk of disease transmission, but transmission of infectious disease via transfusion does cause morbidity and mortality.

Answer 553

TRANSFUSION IN COAGULOPATHIC DOGS AND CATS Deficiencies of coagulation factors and platelets can be treated with fresh frozen plasma and its related products, cryoprecipitate and cryosupernate plasma, platelet-rich plasma, or platelet concentrates. These products are not appropriate for the treatment of nutritional deficiencies, hypoalbuminemia, or as colloid supplementation.

Answer 554

Treatment of decreased colloid osmotic pressure will be discussed in a following section. Cats frequently have abnormal coagulation tests despite the absence of spontaneous hemorrhage. Coagulation test results are commonly abnormal in cats with liver disease, neoplasia, and infectious diseases. In dogs the most common inherited coagulation disorder is von Willebrand disease (vWD) and the most common acquired coagulation disorder is immune-mediated thrombocytopenia.

Answer 555

PRETRANSFUSION TESTING IN COAGULOPATHIC DOGS AND CATS Prior to transfusion of plasma products for the treatment of coagulopathy, safety and efficacy testing should be performed. Compatibility testing, which is critical in red blood cell transfusions, is not routinely performed in the dog, but blood type–compatible plasma must be given to cats since Type A cat plasma contains anti-B antibodies and Type B cat plasma contains anti-A antibodies.

Answer 556

Compatibility can be determined by crossmatching or blood typing using card, gel tube, or slide-typing methods. Both anti-A and anti-B antibodies can cause a hemolytic transfusion reaction if plasma is given to a cat with a different blood type.

Answer 557

he availability of point of care coagulation testing has made possible pretransfusion testing to assess efficacy of plasma transfusions for coagulation disorders. A dog or cat with hemorrhage should be evaluated for coagulopathy using a prothrombin time (PT) and either an activated partial thromboplastin time (aPTT) or activated clotting time. Platelet count should be determined by reviewing a blood smear or by automated methods. Once an abnormality in one or more of these parameters has been identified as the cause of hemorrhage, a diagnosis can be made and the appropriate transfusion initiated.

Answer 558

Correcting abnormal coagulation tests or thrombocytopenia is not necessary in the absence of hemorrhage unless an invasive procedure is planned. Major bleeding complications are more common when platelet counts are lower than 80,000/µL. Kidney biopsies are associated with more bleeding complications than liver biopsies.

Answer 559

ADMINISTRATION AND MONITORING OF PLASMA PRODUCT TRANSFUSIONS Body temperature, respiratory rate, heart rate, and blood pressure should be monitored prior to plasma transfusion to establish baseline monitoring criteria. Frozen plasma products must be thawed prior to administration, but warming is not usually required. Warming may be advantageous if large volumes of cold products are being administered, if the recipient is hypothermic, or if the animal is small.

Answer 560

TRANSFUSION FOR SPECIFIC COAGULOPATHY Anticoagulant rodenticide intoxication is a significant cause of morbidity and mortality in dogs and cats. Although dogs appear to be more commonly affected, anticoagulation rodenticide intoxication in cats does occur, resembling the disorder in dogs both in clinical signs and laboratory abnormalities. Vitamin K is the antidote for the rodenticide-induced depletion of coagulation factors. In pets with life-threatening hemorrhage, central nervous system hemorrhage, pulmonary or pleural hemorrhage, or hemorrhage resulting in severe anemia, replacement of coagulation factors by transfusion should be initiated in addition to administration of vitamin K. Cryosupernatant plasma is the ideal product for treatment of anticoagulant rodenticide intoxication because it contains factors II, VII, IX, and X (Table 142-6).

Answer 561

OPTIMAL COMPONENT Anticoagulant rodenticide intoxication: Cryosupernatant plasma Disseminated intravascular coagulation: Fresh frozen plasma von Willebrand disease: Cryoprecipitate Hemophilia A: Cryoprecipitate Factor VIII deficiency: Cryoprecipitate Fibrinogen (factor I) deficiency: Cryoprecipitate Hemophilia B: Cryosupernatant plasma Factor IX deficiency: Cryosupernatant plasma Factor II, VII, X, IX deficiency: Cryosupernatant plasma Liver disease coagulopathy (hepatic synthetic failure):Fresh frozen plasma Thrombocytopenia/thrombocytopathy: Platelet-rich plasma

Answer 562

Although fresh whole blood can be used to treat anticoagulant rodenticide toxicity, if the pet is not anemic from hemorrhage, the red blood cells contained in the whole blood transfusion are not necessary. Administration of one plasma dose often stops hemorrhage and improves coagulation test results.

Answer 563

Deficiency of von Willebrand factor (vWF, FVIIIR:a) results in vWD, which is a common inherited bleeding disorder in dogs.[54-56] It is rarely reported in cats.[57] Spontaneous hemorrhage occurs in severe conditions; however, dogs with 30% or less of the normal level of vWF are usually at risk for surgical hemorrhage

Answer 564

Control of spontaneous hemorrhage or prevention of interoperative hemorrhage is often required in dogs with vWD. Treatment has predominantly been empiric with either fresh frozen plasma or cryoprecipitate.

Answer 565

Cryoprecipitate is rich in the hemostatically active high–molecular weight multimers of vWF. Evidence suggests using cryoprecipitate prepared by treating donors with arginine vasopressin (1 µg/kg SQ) prior to blood donation for the treatment of vWD results in higher plasma levels of vWF and improved buccal mucosal bleeding times when compared with treatment using fresh frozen plasma[56,59] (see Table 142-6). The recommended dosage of cryoprecipitate does not always result in control of hemorrhage, and additional cryoprecipitate may be required. Plasma levels of vWF remain elevated for approximately 2 hours following infusion. Additional infusions of cryoprecipitate may be required 4 hours after initial infusion. Because vWD is rare in the cat, little is known about treatment, and canine treatment recommendations should be adapted for cats with vWD.

Answer 566

Disseminated intravascular coagulation (DIC) is a secondary syndrome provoked by a primary disease and resulting in excessive consumption of coagulation factors and platelets. In veterinary patients, most pets with DIC are recognized when consumption of platelets and coagulation factors exceed their production and hemorrhage occurs. Coagulation testing in these patients typically shows thrombocytopenia, prolonged coagulation times, and evidence of increased fibrinolysis (increased fibrin degradation products, or D-dimer). Treatment of DIC with blood products is empiric and symptomatic. Fresh frozen plasma is used concurrently with treatment of the primary disease to replace coagulation factors and to control hemorrhage. A dosage of 12-15 mL/kg BID resulted in improvement of prolonged aPTT and PT in critically ill dogs.[61] Additional units of plasma should be administered based on daily reevaluation of the clinical status, platelet count, and coagulation times.

Answer 567

Liver disease is a common cause of coagulation abnormalities. Liver disease–associated coagulation disorders include hepatic synthetic failure, vitamin K deficiency, and DIC.

Answer 568

Treatment of DIC is described above. Pets with hepatic failure can be treated with fresh frozen plasma if spontaneous hemorrhage is recognized or if a liver biopsy is required (see Table 142-6). Plasma can be administered as often as TID until coagulation times normalize.

Answer 569

Congenital factor deficiencies other than canine vWD are rare in veterinary patients.[64-66] Clinical signs of hemophilia appear in puppies and kittens associated with normal activity, during teething, or following neutering. Deficiencies of fibrinogen (factor I) and hemophilia A (factor VIII) necessitate transfusion of cryoprecipitate or fresh frozen plasma.

Answer 570

Fresh whole blood can be administered if the patient is also anemic. Deficiencies of other factors, such as factor IX (hemophilia B), factor II, VII, X, or XI are treated with cryosupernatant or stored plasma. Stored whole blood can be administered to these patients if they are also anemic.

Answer 571

Thrombocytopenia is the most common acquired coagulation disorder in the dog. Immune-mediated thrombocytopenia (ITP) is relatively common in dogs but rarely occurs in cats. Red blood cell transfusion is common in cases of ITP; if the patient requires an increase in oxygen-carrying capacity guidelines can be found in the previous section on blood loss anemia. In cases of ITP with life-threatening hemorrhage, central nervous system hemorrhage, pulmonary or pleural hemorrhage, or hemorrhage resulting in severe anemia, transfusion of platelet-containing products should be considered; however, the efficacy of platelet transfusions in this disease (where platelets are destroyed) remains unproven. Some evidence indicates transfusion of platelets is of little benefit in increasing the platelet count in ITP. Fresh platelets, either as platelet concentrate or platelet-rich plasma have a shelf life of 48 hours. Frozen platelets have a 6-month shelf life, but lose function as a result of cryopreservation.

Answer 572

ADVERSE EVENTS ASSOCIATED WITH TRANSFUSION FOR COAGULOPATHY Physical examination parameters should be monitored intermittently during and for several hours after the transfusion to promote early identification of a transfusion-related adverse event. The occurrence of vomiting, diarrhea, collapse, or urticaria during a transfusion should result in the discontinuation of the transfusion and investigation of its cause. The most common adverse event associated with administration of plasma-containing transfusions is urticaria.[65] Slowing the rate of transfusion and administering antihistamines and glucocorticoids are adequate in most cases. Circulatory overload is another potential complication of plasma transfusion and is especially common in patients receiving large volumes of crystalloids and colloid solutions in addition to blood products. The use of cryoprecipitate, when appropriate, as opposed to fresh frozen plasma, lessens the risk of this complication because cryoprecipitate is contained in a smaller volume of plasma (30 to 40 mL) compared to fresh frozen plasma, which has a volume of approximately 250 mL.

Answer 573

The serum albumin concentration contributes 60% to 70% of the vascular COP component of Starling's forces and is critical in maintaining fluid homeostasis.

Answer 574

Repair of hypoalbuminemia with 25% human albumin has been described in critically ill dogs and cats with hemorrhage, protein-losing enteropathy and nephropathy, liver failure, malnutrition, and septic peritonitis.[72-74] Administration of 25% human albumin results in an increase in total solids, albumin concentration, and blood pressure, but should be reserved for those patients with hypoalbuminemia where standard therapy has failed to improve the clinical condition. The PCV, total protein concentration, serum albumin concentration, or the COP should not be the sole criterion for administration of colloid supplementation. Patients with hypoalbuminemia but lacking clinical signs of hypoalbuminemia should not automatically be administered colloid support.

Answer 575

For patients requiring surgery, the recommendation has been made to keep the total protein above 3.5 g/dL and in those not requiring surgery to keep the albumin between 2.0 and 2.5 g/dL and the COP between 13 and 20 mg Hg.[75] The choice of synthetic colloid, species-specific plasma, or heterologous albumin depends on the underlying disease, cost, and product availability. Species-specific plasma requires administration of a large volume to increase the albumin. One calculation suggests 45 mL of plasma per kilogram of body weight is required to increase the albumin 1 g/dL. The limited availability of plasma and the large volume required to increase albumin concentration restricts its utility for treatment of hypoalbuminemia.

Answer 576

In protein-losing nephropathy and enteropathy, administration of albumin-containing colloid solutions is likely to only transiently increase the albumin concentration and hydroxyethyl starch may be more appropriate since the large molecules in this product are less likely to be lost through the kidney or intestine. Prior to administration of species-specific plasma or heterologous albumin, testing should include COP, total protein concentration, and serum albumin concentration as well a measurement of vital signs to establish a baseline for the recipient. Monitoring blood pressure is critical with administration of albumin since it has been shown to increase blood pressure.[72] A suggested dosage for administering 25% human albumin solutions is 2 mL/kg. Albumin can be administered as a slow bolus (recommended maximum dosage of 4 mL/kg) or as a continuous rate infusion (0.1 to 1.7mL/kg/hr).[72]

Answer 577

ADVERSE EVENTS ASSOCIATED WITH TRANSFUSION FOR DECREASED COLLOID OSMOTIC PRESSURE Clinical investigations of administration of both human to normal dogs unexpectedly resulted in anaphylactoid and Type III (delayed) hypersensitivity reactions. In a few dogs these reactions were fatal; however, the adverse reactions to administration of albumin to hypoalbuminemic dogs and cats have been minor. Dogs without a history of prior human albumin administration appear to have IgG antibodies against human albumin and may have a hypersensitivity reaction in response to an initial albumin infusion. Dogs administered human albumin develop a pronounced IgG response following exposure; consequently, repeated administration appears to result in adverse reactions.

Answer 578

During albumin administration, dogs and cats should be carefully monitored for signs of an anaphylactoid reaction. When the pet is discharged, the owners should be advised to monitor for signs of delayed hypersensitivity reactions, which have been described to occur as late as 14 days after human albumin administration. Facial edema and urticaria with vomiting, inappetence, and lethargy appear to be the common clinical signs.

Answer 579

TRANSFUSIONS IN PATIENTS WITH MISCELLANEOUS DISORDERS Failure of Passive Transfer Neonatal puppies and kittens that have failed to receive adequate colostrum may benefit for replacement of immunoglobulin through transfusion. Fresh plasma, fresh frozen plasma, frozen plasma, or serum may all be used as the source of immunoglobulin; the choice depends on the most readily available product. Pretransfusion testing is not recommended.

Answer 580

Immune-Mediated Disorders Using the traditional definition of blood transfusion, transfusions replace a missing component of blood—for example, red blood cells in an anemic patient. Purified human immunoglobulin is transfused not to replace immunoglobulin deficiency but as an immunomodulatory agent in disorders of the immune system such as IMHA, ITP, and some immune-mediated dermatologic disorders.

Answer 581

Laboratory investigation demonstrates the mechanism of action of human intravenous immunoglobulin occurs via binding to the Fc receptor of canine lymphocytes and monocytes and through inhibition of Fc-mediated phagocytosis of antibody-coated red blood cells.

Answer 582

The use of intravenous immunoglobulin has been recommended in the treatment of immune-mediated diseases because of its apparent rapid onset of immunosuppression. When the drug is effective in IMHA, hemolysis abates within 7 days and sometimes as soon as 2 days following infusion. A similar rapid response has been seen in cases of ITP and cutaneous manifestations of adverse drug reactions. It is not used frequently for long-term management of these diseases because of the risk of anaphylaxis due to antibody formation following repeated administrations, its cost, and the concern that a single administration of the drug does not result in long-term immunosuppressive effects. Blood typing and crossmatching are not necessary prior to administration. Multiple different doses of intravenous immunoglobulin have recommended (Table 142-7). The patient's volume status should be monitored closely during and following administration since these dogs typically have received multiple transfusions and large volumes of crystalloids or colloids and are at risk for circulatory overload. Reported adverse events following administration of intravenous immunoglobulin for the treatment of IMHA include thrombosis and thrombocytopenia; however, these adverse events are common complications of IMHA and may not be associated with administration of intravenous immunoglobulin.

Answer 583

(1) upper airway obstruction, (2) lower airway obstruction, (3) flail chest, (4) abdominal enlargement, (5) pulmonary parenchymal disease, (6) pleural cavity disorders, (7) pulmonary thromboembolism (PTE), and (8) “look-alike” syndromes. This classification system is useful because the first four causes can be usually be recognized quickly at the time of initial assessment. Each of these four conditions can be distinguished by the physical appearance of the dog or cat, the cycle of respiration predominantly affected, and audible sounds that might be heard resulting from certain disorders (to be discussed later). The remaining four causes will require additional diagnostic testing to establish a definitive diagnosis

Answer 584

eight major categories OF RESPIRATORY DISTRESS Upper airway obstruction is due to mechanical or functional obstruction of the large airways (pharynx, larynx, or trachea cranial to the thoracic inlet) and includes intraluminal or extraluminal masses (neoplasia, granuloma, abscess, blood clots, polyps), foreign bodies, laryngeal paralysis, laryngeal collapse, elongated soft palate, everted laryngeal saccules, tracheal collapse, tracheal stenosis, or tracheal stricture.

Answer 585

Obstruction of the trachea within the thoracic cavity is included in the category of lower airway obstruction. Lower airway obstruction also arises from narrowing of the bronchial lumen due to bronchospasm, accumulation of mucus or other exudate, bronchial wall edema, or diffuse bronchomalacia. The classic example of a disease associated with the first three of these changes is feline asthma. Asthma in dogs is an exceedingly rare diagnosis, but lower airway obstruction in dogs can be seen with severe chronic bronchitis due to bronchomalacia, which allows for passive collapse of the airways on exhalation.

Answer 586

Flail chest results from trauma to the thoracic cavity, where there is destabilization of a portion of the rib cage (i.e., multiple ribs are fractured at two different locations, leaving a segment that is detached from the rest of the rib cage). Paradoxical respiration is seen so that, as an animal inhales, the chest wall segment is sucked inward, and as it exhales, the segment is blown outwards.

Answer 587

Severe abdominal enlargement can put pressure on the diaphragm and make it more difficult for the thoracic cavity to expand on inhalation. Examples of conditions associated with abdominal enlargement include ascites, gastric dilatation, hepatosplenomegaly, neoplastic abdominal masses, pregnancy, or pyometra.

Answer 588

Pulmonary parenchymal diseases are disorders affecting the terminal and respiratory bronchioles, interstitium, alveoli, or vasculature. They may be associated with infiltration by infectious microorganisms, inflammatory cells, or neoplastic cells; the airspaces may be filled with edema fluid or foreign material; or lung tissue may be replaced with fibrotic tissue.

Answer 589

Examples of conditions affecting the pulmonary parenchyma include infectious pneumonia (bacterial, fungal, viral, protozoal, and parasitic), aspiration pneumonitis, aspiration pneumonia, interstitial lung diseases, pulmonary edema (cardiogenic or noncardiogenic), hemorrhage, neoplasia, and acute lung injury (ALI) or acute respiratory distress syndrome (ARDS).

Answer 590

Pleural cavity disorders arise when the space between the parietal and visceral pleura, which normally contains just a small amount of fluid for lubrication, fills with fluid (pleural effusion), air (pneumothorax), a mass, or abdominal organs (e.g., diaphragmatic hernia).

Answer 591

Pulmonary thromboembolism refers to obstruction of blood flow in the pulmonary vasculature by a thrombus or embolus formed in the systemic venous system or right side of the heart. Any condition causing an abnormality in blood flow, endothelial damage, or hypercoagulability can predispose to thromboembolism.

Answer 592

Finally, look-alike syndromes are conditions that result in apparent difficulty in breathing due to nonrespiratory causes, such as pain, severe anemia, hyperthermia, acidosis, drugs (e.g., opioids), and hypotension.

Answer 593

Figure 143-1 Flow chart to localize the cause of respiratory distress based on the pattern of breathing.

Answer 594

CONCLUSION Having a scheme to classify the causes of respiratory distress can help in the approach to patients presenting in an emergency situation. Identification of breathing patterns (inspiratory distress, expiratory distress, paradoxical breathing, and mixed inspiratory and expiratory distress) assists in localizing the site of respiratory disease. After stabilizing the patient, appropriate diagnostics and therapeutics can be targeted to focus on the location of the respiratory disease.

Critical care- Ettinger Flashcards

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