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Emergency Medicine/Critical Care Kenneth J. Drobatz, DVM, MSCE, DACVIM, DACVECC Philadelphia, PA Approach to the Emergency Patient INTRODUCTION Critically ill patients often have multiple life-threatening problems and present a confusing challenge to even the most experienced clinician. Prioritization of treatment of the most immediate life-threatening problems is key to the successful outcome of these patients. This lecture will present an overview of the medical management of the critically ill patient. The principles discussed here are applicable to medical as well as surgical patients. OVERVIEW Treatment and monitoring of the four major organ systems - respiratory, cardiovascular, central nervous system (CNS), and renal system are important in the successful management of the critically ill patient. The initial goal of the critical care clinician is to maintain adequate oxygen delivery to the tissues through treatment of the respiratory and cardiovascular systems. Failure of this goal results in the demise of the patient despite successful management of other major problems. Management of central nervous and renal systems follows. OXYGENATION OF BLOOD Adequate oxygenation of blood must be assured. Oxygen supplementation should be provided to any critically ill patient until proven that it is not necessary. Complications of oxygen toxicity do not develop until 12 hours or more of inspired oxygen concentrations of greater than 40 - 50%. Modes of oxygen supplementation include mask oxygen, flow-by, nasal insufflation, trans-tracheal catheter, oxygen cage, and positive pressure ventilation. Mask or flow-by oxygen supplementation is inexpensive, effective, and convenient because it allows simultaneous examination and treatment of the patient. Nasal oxygen insufflation is also effective and has similar advantages although some patients do not tolerate the nasal catheter well and continually dislodge it. We have not had much requirement or experience with the trans-tracheal catheter. The major advantages of the oxygen cage are that humidity, temperature, and inspired oxygen concentration may be controlled, as well as there is minimal stress to the patient. The major disadvantages are expense, oxygen wastage, and most importantly-inability to monitor the patient. If used judiciously, the oxygen cage it is quite efficacious. Intubation and positive pressure ventilation allows for absolute control of a patient's respiration. Disadvantages include the need for sedation, intubation and bypassing of upper airway defense mechanisms, intensive monitoring, and barotrauma. The decision to ventilate a patient should not be taken lightly, but should not be avoided when it is necessary. Indications for positive pressure ventilation include respiratory distress resistant to high inspired oxygen concentration, inadequate ventilation (increased PaC02), required high inspired oxygen concentrations for a prolonged period of time, and respiratory muscle fatigue. Assessment of oxygenation of hemoglobin includes evaluation of mucus membrane color, pulse oximetry, and arterial blood gas measurement. Pale mucous membranes may indicate anemia, poor tissue perfusion, or peripheral vasoconstriction secondary to pain, catecholamines, or hypothermia. Cyanosis isn't detected in tissue until there is greater than 5 grams/deciliter of unoxygenated hemoglobin. Therefore, anemic patients may be severely hypoxemic yet have no detectable cyanosis and cyanosis is an insensitive and late indicator of respiratory disfunction. The hemoglobin/oxygen dissociation curve illustrates an important point. Many of our patients with respiratory difficulty have a Pa02 of 60mmHg to 80 mmHg or lower. These patients may be maintaining enough oxygenation and delivery to appear stable. Looking at the sigmoidal shape of the curve, the Pa02 of these patients rests at the junction of the steep portion of the curve. Any minor change in Pa02 from simple procedures such as venipuncture, restraint, radiographic positioning, or change in posture may cause a profound decrease in hemoglobin saturation and demise of the patient. Patients with respiratory distress are fragile and may decompensate at anytime. All efforts to improve oxygenation should be attempted before stressful procedures are employed. Oxygen saturation of hemoglobin may be noninvasively evaluated with the pulse oximeter. It gives moment by moment changes in hemoglobin saturation and can detect serious desaturation of hemoglobin that is not detectable from physical examination. We often use this instrument as a constant monitor in our critically ill patients as well as in routine anesthetic procedures. It's major disadvantages are that the probe is most consistently effective when placed on the tongue or lip (therefore precluding its continuous use in fully alert or fractious patients) and it is difficult to obtain accurate readings in patients with poor tissue perfusion. Arterial blood gas measurements are considered the gold standard in assessment of respiratory function in the clinical patient. Arterial blood gas measures the partial pressure of oxygen within the plasma, which is a minor component of total oxygen content of the blood (see below). TISSUE OXYGEN DELIVERY Adequate tissue oxygen delivery requires oxygenation of the blood and delivery of that blood to the tissues. The latter requires adequate cardiovascular function. The major parameters that contribute to whole blood oxygen content include blood hemoglobin concentration, oxygen saturation of hemoglobin, the plasma concentration of hemoglobin, and the vascular volume. The contribution of hemoglobin and the oxygen it carries far outweigh the amount of oxygen carried in plasma. Therefore maintenance of adequate hemoglobin concentration and its saturation are extremely important in maintaining oxygen delivery. The three major causes of inadequate tissue perfusion are hypovolemia, sepsis, and inadequate cardiac function. The most common cause of hypoperfusion in veterinary critically ill patients is hypovolemia. Physical examination parameters such as pale mucus membranes, prolonged capillary refill time, and rapid, weak pulses suggest inadequate tissue perfusion. Septic patients often have hyperemic mucus membranes, rapid capillary refill time, and bounding pulses. Immediate auscultation of the heart and lungs is indicated to determine cardiovascular dysfunction as the cause of the poor perfusion. A heart murmur, gallop rhythm, and/or persistent arrhythmia is usually present in most dogs and cats with cardiac disease. Cardiac disease in dogs is unlikely if cardiovascular abnormalities are not present on auscultation. Some cats may not have easily auscultable cardiac abnormalities and still have significant heart disease. The initial therapy for patients with hypovolemia or sepsis is intravenous fluids, colloids, and/or blood products as indicated. The initial choice is a balanced electrolyte fluid challenge. Initial fluid volumes and rates of administration are 90 ml/kg/hr in the dog and 40 - 60 ml/kg/hr in the cat. Most cases of uncomplicated hypovolemia respond to half this amount of fluid. A positive response is indicated by improvement in mucus membrane color, normalization of capillary refill time, decreased heart rate, and improved pulse quality. Frequent auscultation of the lungs is indicated to detect vascular volume overload and pulmonary edema. Arterial blood pressure measurement may be used to guide fluid therapy and perfusion status in the critically ill patient. The draw back is that patients may have poor tissue perfusion despite normal or even high blood pressure measurements. Blood pressure may be indirectly measured by doppler ultrasound and oscillometric methods. Doppler ultrasound gives a measurement of systolic blood pressure. In clinical human studies, a systolic blood pressure of 90 mmHg or less is used as a indicator of shock in trauma patients. Oscillometric measurements utilize blood vessel wall vibrations and give systolic, diastolic, and mean arterial blood pressures as well as heart rate. The machine is easy to use but somewhat expensive. The other major disadvantage is that is sometimes difficult to get accurate measurements in patients with poor perfusion, the very patients we prefer to use it on. One criteria for belief in the measurement obtained is if the actual heart rate and the machine measured heart rate are similar. Direct measurement of arterial blood pressure is the gold standard. We place a catheter percutaneously in the dorsal metatarsal artery as our first choice. If it is too difficult to palpate the artery, then we cutdown to the artery to place the catheter or catheterize the femoral artery percutaneously. Direct arterial measurements require a transducer and oscilloscope that has arterial measurement capabilities. Direct arterial pressure measurement allows visualization of the arterial waveform and accurate measurement of systolic, diastolic, and mean arterial pressures. Central venous pressure may be used to guide fluid therapy. Central venous pressure measures the pressure within the jugular vein and gives an indirect assessment of the heart's ability to pump the blood it is receiving. It is inexpensive and relatively easily performed. Measurements from 0 - 5 cm H20 are considered normal though it is the trend that is more important. Rapid increases of 3 to 5 cm of H20 during fluid therapy suggests possible fluid overload and decreased fluid administration is indicated. Using central venous pressure as a guide for fluid administration may prevent fluid overload and pulmonary edema. A relatively new technique in veterinary critical care is the use of the pulmonary artery catheter. This inflatable balloon tipped catheter is placed via a percutaneous introducer into the jugular vein. The balloon is then inflated and the blood flow guides the catheter into the right atrium, right ventricle and finally into the pulmonary artery. The catheter is connected via a pressure transducer to an oscilloscope so that pressure waveforms transmitted from the end of the catheter may be visualized. The location of the catheter can be determined by characteristic pressure waveforms that are produced by the various blood vessels as well as the right atrium and ventricle. The location may also be confirmed by fluoroscopy or radiography. Valuable information may be obtained from the catheter including thermodilution cardiac output measurements, pulmonary capillary wedge pressure, pulmonary artery pressures, central venous pressure, right atrial and ventricular pressures, pulmonary vascular resistance, peripheral vascular resistance, oxygen delivery, oxygen consumption, and central venous oxygen concentration and saturation. The pulmonary artery catheter allows a more accurate assessment of tissue oxygen delivery and cardiovascular dynamics. CENTRAL NERVOUS SYSTEM We are limited in our ability to assess and monitor the central nervous system. Serial neurologic examination is the mainstay of monitoring of this organ system. Although computed tomography scans, magnetic resonance imaging, and direct measurement of intracranial pressure are routine modalities in human medicine, expense and limited access make these techniques impractical in veterinary critical care. Every critical patient should have a baseline complete neurologic examination performed. This should include assessment of mentation, cranial nerve function, spinal reflexes and peripheral nerve function. The frequency of monitoring should reflect the degree of central nervous system function and the potential for CNS insult. Critically ill patients with CNS dysfunction should be monitored as constantly as possible, at least every one to two hours. Maintenance of adequate oxygen delivery and ventilation optimize CNS function. In patients with increased intracranial pressure administration of mannitol, mild elevation of the head (avoiding jugular vein obstruction), and mild hyperventilation (PaC02 = 25 - 30 mmHg) will help decrease intracranial pressure. In patients with CNS dysfunction, good nursing care such as turning the patient every four hours, corneal lubrication in patients without a blink reflex, maintenance of oral mucus membrane hydration, urinary bladder expression, and keeping the patient clean, dry, and well padded go a long way in decreasing morbidity in these critically ill patients. RENAL SYSTEM Inadequate urine production and renal dysfunction is a common problem in emergency and critically ill patients. Prompt recognition and aggressive treatment of the oliguric patient may prevent serious complications related to inadequate urine production. Oliguria may result from poor renal perfusion, renal parenchymal disease or obstruction to urine flow. Successful diagnosis and therapy requires the clinician to be aware of factors which predispose to oliguria and to monitor the renal function and urine production in those patients at risk. In the canine, oliguria has been defined as urine production less than 6.5 ml/kg/day (0.27ml/kg/hr). Inadequate urine production may be related to diminished glomerular filtration or obstruction of urine flow as it travels through the tubules, collecting ducts, renal pelvis, ureters, bladder and urethra. Changes in renal blood flow, glomerular capillary hydrostatic pressure, hydrostatic pressure within the tubular lumen, concentration of plasma proteins, and the glomerular ultrafiltration coefficient all affect GFR. The most common cause of oliguria in critically ill patients is diminished hydrostatic pressure gradient across the glomerular capillary membrane secondary to hypovolemia, sepsis and/or poor cardiac function. The glomerular hydrostatic pressure is determined by systemic blood pressure and the balance between the pre and post glomerular capillary sphincters. GFR and renal blood flow remain constant through a range of mean arterial blood pressures from 80 -100 mmHg. This occurs as result of renal autoregulation through a balance of pre and post glomerular capillary vasoconstriction. When mean systemic arterial blood pressure decreases to less than 80 mmHg this autoregulation is lost and glomerular hydrostatic pressure diminishes in parallel with systemic blood pressure. In critically ill patients, an indwelling, closed urine collection system allows for precise measurement of urine output. Urine output should be measured every 2 - 4 hours. Normal urine output in the dog is 1 -2 ml/kg/hr but should be evaluated in light of the amount of fluid that is being given and other areas of loss such as the gastrointestinal tract. In addition to urine output measurement, monitoring of patients at risk for renal dysfunction or oliguria should involve daily assessment of renal function by measurement of serum creatinine, serum urea nitrogen, and serum electrolytes as well as serial urinalyses. The goal in the management of the oliguric patient is to minimize detrimental changes in water, solute, and electrolyte balance while optimizing renal perfusion and urine output until renal function and urine production returns. In many instances, the underlying cause may not be known and therapy to improve urine output should be directed at correcting perfusion abnormalities, renal parenchymal, and obstructive causes of oliguria. Obstructive causes of oliguria are reversible and should be treated as soon as possible. Urinary obstruction may result in the death of the patient within 65 to 72 hours of onset. In our critically ill patients, one of the most common causes of oliguria in a patient with an indwelling urinary catheter is catheter obstruction secondary to kinking. In any patient, catheter patency should be assured. Therapy for inadequate perfusion and renal parenchymal causes of oliguria are similar. Both involve optimization of renal perfusion and judicious use of diuretics and vasopressor agents. Hypovolemia is the most common cause of hypoperfusion in our critically ill patients. In a patient with oliguria, measurement of arterial blood pressure is indicated as an indirect assessment of renal perfusion (see above). Judicious use of intravenous fluids, colloids, and vasopressor agents may be necessary to treat the oliguria and provide adequate renal perfusion when poor perfusion is the suspected cause of the oliguria and primary cardiac disease has been ruled out. Frequently, aggressive fluid therapy is all that is necessary. An intravenous fluid challenge of 90 ml/kg/hr may be required in the hypovolemic, hypotensive canine patient (40-60ml/kg/hr in the feline patient). Mean arterial pressure should minimally be at least 60 - 80 mmHg. Fluid therapy should be used with great care in the oliguric patient because of the potential for vascular fluid overload. Measurement of central venous pressure in these patients is a useful guide. Auscultation of the heart and lungs and measurement of packed cell volume and total solids will also help guide fluid volume and rate of administration. If fluid therapy alone is not adequate to improve or maintain sufficient arterial blood pressure then a positive inotrope such as dobutamine (5 - 10 ug/kg/min) or a vasopressor such as dopamine (5 - 10 ug/kg/min) should be utilized. If oliguria persists despite improvement in arterial blood pressure, other pharmacologic agents will be required. Mannitol (0.1 g/kg - 0.5 g/kg), an osmotic diuretic may be given intravenously. Mannitol improves GFR, renal blood flow, osmolar clearance, and preserves renal tubular blood flow and prevents tubular obstruction resulting in increased urine output. Mannitol is most effective in the early stages of oliguric renal failure. Diuresis should be expected within one hour of mannitol infusion. If diuresis does not occur then mannitol will probably not be effective. Mannitol should not be used in the patient that has a high CVP, is near vascular volume overload or is anuric. Loop diuretics should be used to promote diuresis only when proper fluid therapy has been applied and blood pressure is adequate. We combine furosemide (1 mg/kg/hr) and dopamine (2 - 5 ug/kg/min) to promote diuresis. Diuresis should occur within 30 minutes of therapy. If urine output is still inadequate, any further medical therapy to induce diuresis is pointless. Elimination of uremic toxins can only be achieved by hemo or peritoneal dialysis. If diuresis is achieved, monitoring of urine output, serum electrolytes, blood gases, and serum creatinine should be continued. Key Words: Tissue oxygen delivery, oliguria, pulse oximetry, hemoglobin saturation, central nervous system, blood pressure Emergency Management of Respiratory Distress INTRODUCTION Respiratory distress is a common presenting complaint in veterinary emergency medicine. Animals with respiratory distress represent a diagnostic and therapeutic challenge. The initial approach to these patients can often make the difference between life and death in this acute phase of their disease. SIGNS OF RESPIRATORY DISTRESS When an animal develops difficulty in oxygenation it makes attempts to improve oxygenation. This may be manifested simply as an increase in respiratory rate or more severely as extended head and neck posture with abduction of the elbows, flaring of the nares, and open-mouth breathing. With severe resistance to movement of air, there may be paradoxical motion of the chest and abdomen. Normally, the chest and abdomen move together during respiration. On inspiration the abdominal wall and chest wall move out and during expiration they both move in. Paradoxical motion occurs when they move in opposite directions e.g. the chest moves in and the abdomen moves out. This suggests extreme resistance to air movement. Dogs are more demonstrative in manifesting clinical signs of respiratory distress. Some cats may have severe respiratory dysfunction and only manifest tachypnea at rest. In either species, postural changes suggest extreme respiratory distress and warrant immediate attention. INITIAL APPROACH TO THE PATIENT Oxygen Supplementation At presentation, a patent airway should be assured. If the airway is not patent, then attempts should be made to clear the airway and intubate the patient. If an obstruction prevents intubation, then an emergency tracheostomy should be performed if it will by-pass the obstruction and assure a patent airway. To provide perspective, it is extremely rare that an emergency tracheostomy is required. Most patients can be intubated and the tracheostomy then performed in a more controlled way. Immediate oxygen supplementation should be provided while assessing for a patent airway. Our first choice is via mask or flow-by. This is convenient, inexpensive, and provides an opportunity to examine the patient as well as do procedures if necessary. Other modes of oxygen supplementation include an enriched oxygen environment (oxygen cage or tent), transtracheal catheter, nasal oxygen, and intubation with positive pressure ventilation. Each has its advantages and disadvantages. The oxygen cage is an excellent method for oxygen supplementation, but has some major disadvantages including isolation of patient for caregivers, expense, large volumes of oxygen are necessary, large size of the cage itself, and large dogs can overheat the cage. Advantages of this method include minimal stress to the patient and control of Fi02, carbon dioxide concentration, temperature, and humidity. If used judiciously with recognition of its limitations, an oxygen cage can be advantageous. Nasal oxygen supplementation is an inexpensive method of oxygen supplementation and can be done using commonly available equipment. Its major medical advantage is that oxygen supplementation can be continuously given while procedures and physical assessments are performed. Inspired oxygen concentration may be as high as 40-60%. Disadvantages include that it can be stressful to place and some animals will not tolerate the nasal catheter. This mode of oxygen supplementation is most commonly utilized on hospitalized animals that need ongoing oxygen supplementation. An oxygen tent, plastic bag, or an E. collar with plastic wrap over the top with oxygen supplied into this "microenvironment" can be an effective means of oxygen supplementation. Fi02 of nearly 100% can be achieved with high oxygen flow. Disadvantages include that some animals will not tolerate this method, condensation can develop inside the plastic cover, the animal can overheat and carbon dioxide can build up. Leaving an opening at the top for heat, carbon dioxide and condensation to escape can minimize some of these complications. Transtracheal oxygen supplementation is rarely used in our practice. It can be used to provide oxygen support with upper airway obstruction if the catheter is placed between the lungs and the obstruction. Intubation and positive pressure ventilation is the ultimate in control of ventilation but is more invasive than other methods and requires sedation/anesthesia. One can control nearly all aspects of ventilation with this method. Indications for positive pressure ventilation include hypoventilation, persistent hypoxemia despite high-inspired oxygen concentration, and respiratory fatigue. Once oxygen supplementation has been provided, further evaluation can be performed if the patient's condition will allow it. Animals that are in respiratory distress can be difficult work with. One must provide oxygen and assess the patient while minimizing stress to the patient. Excessive stress or struggling can be catastrophic in an animal with respiratory distress. Even dorsal recumbency positioning for ventral dorsal radiographs can be devastating. Any stress that causes the patient to consume more oxygen or decrease inspired oxygen concentration from breath holding while struggling can severely compromise some patients and result in death.At presentation we also place an intravenous catheter and collect blood for an emergency database (packed cell volume, total solids, dipstick BUN, blood glucose and a blood smear). This minimal amount of bloodwork can provide valuable additional information about the patient and sometimes provides a diagnosis of the cause of the respiratory distress. In addition, intravenous access allows for the immediate administration of fluids or drugs. GENERAL DIAGNOSTIC THOUGHTS During or after assuring a patent airway, providing oxygen supplementation, and acquiring intravenous access, examination of the patient should be done. The most important clues may be obtained from auscultation of the thorax and neck, as well as observation of the respiratory pattern. Respiratory patterns may be helpful in localizing the problem. Irregular respiratory rhythms are almost invariably associated with central nervous system abnormalities. Poor airway compliance due to pulmonary parenchymal disease or restricted lung expansion often results in rapid and shallow respirations. Airway narrowing or fixed obstruction may be manifested as very slow and prolonged respirations. Respiratory difficulty is mainly on inspiration with extrathoracic dynamic obstruction and on expiration with intrathoracic dynamic obstruction (intrathoracic collapsing trachea, feline asthma). It is convenient from a diagnostic point of view to approach respiratory distress in an algorithmic fashion. SPECIFIC CONDITIONS Heart Disease If there are auscultable heart abnormalities, then empirical therapy for heart failure should be considered if the patient's condition will not allow further diagnostic tests (e.g. thoracic radiographs). Intravenous or intramuscular furosemide (2mg/kg) should be given (we often exceed these doses in severely affected patients). In severely affected dogs we also use nitroprusside (arterial and venous vasodilator) and begin a constant rate of infusion at 1ug/kg/min and slowly increase every 15 minutes. In most dogs, the effective dose is usually between 5 - 10 ug/kg/min. This is a very potent vasodilator and may cause severe hypotension. Therefore, blood pressure monitoring is warranted when using this drug. If used judiciously, this drug is very effective in relieving respiratory distress in patients with severe pulmonary edema secondary to heart failure. It is rare that we use this drug in cats. Most commonly, if vasodilatation is necessary in cats with heart failure, 2% nitroglycerine paste is our first drug of choice. An area on the flank, axilla or groin is clipped and the ¼ inch of paste is applied (wear gloves). In the acute emergency situation, furosemide and these vasodilators are our first line treatments. In mild to moderate heart failure patients, oxygen supplementation and furosemide is often all that is needed for initial stabilization. Endomyocarditis is an inflammatory condition of the endocardium and the pulmonary vessels. Cats with this condition often present with respiratory difficulty 1-3 days or so after a stressful event such a declaw or neutering. These cats can often have severe respiratory compromise with generalized increased bronchovesicular sounds or crackles. The heart usually sounds relatively normal. Radiographically, the pulmonary opacities are predominantly interstitial with a diffuse distribution. Echocardiographically, some appear to have a "bright" endocardium. The treatment that we have used for this condition is oxygen supplementation and aggressive diuretic therapy with furosemide. The prognosis is guarded. Upper Airway Disease Upper airway disease may involve the pharynx, larynx, or trachea. Problems in these areas include edema, infection, foreign bodies, neoplasia, as well as neuromuscular and degenerative diseases. The most common upper airway diseases we see in dogs are laryngeal paralysis (typically larger breeds) and collapsing trachea (typically smaller breeds). One of the hallmark clinical signs of upper airway disease is stridor. If a patient presents with stridor, upper airway disease should be strongly considered. This does not preclude the existence of other causes of respiratory distress, but does warrant investigation of the upper airway. Patients with extra-thoracic dynamic airway obstruction (e.g. laryngeal paralysis) will have severe inspiratory difficulty. Collapsing trachea patients may have both inspiratory and expiratory difficulty depending upon the location of the collapsing segments of the trachea. Patients with dynamic airway obstruction such as laryngeal paralysis or collapsing trachea may present in severe respiratory distress. A vicious cycle develops in these patients in which something places a demand on the respiratory system (e.g. exercise) causing greater pressure changes within the upper respiratory tree causing collapse of the affected area resulting in inefficient gas exchange, further stimulating the patient to breath harder. These patients may also develop very high body temperatures causing even greater demands on respiration. To break this cycle, we sedate with acepromazine (30 - 50 ug/kg intravenously or IM), and continue supplementing with oxygen. This is very effective and usually within 15 to 30 minutes the respiratory stress is diminished and the patient is breathing relatively comfortably. We also cool the animal (wetting or spraying water on the fur coat) if the body temperature is greater then 105F. Some patients may benefit from anti-inflammatory doses of corticosteroids because of laryngeal or tracheal edema. It is extremely rare that emergency laryngeal surgery is required in patients with laryngeal paralysis. The above medical therapy is generally quite effective. If a patient is in acute distress, and you are concerned about imminent collapse, anesthesia and intubation will relieve the distress immediately if laryngeal paralysis is the cause. Anesthetic recovery in patients with dynamic upper airway obstruction is extremely difficult. The excitement phase of recovery causes dynamic airway pressure changes resulting in collapse of the affected area of the pulmonary tree, starting the vicious cycle again. Pulmonary Parenchymal Disease Pulmonary parenchymal disease may be due to edema (cardiogenic or noncardiogenic), hemorrhage, infection, or infiltrative processes. Harsh respiratory sounds (increased bronchovesicular sounds) or pulmonary crackles are often heard on auscultation. The location of these sounds may help in the diagnosis. For example, a cranioventral distribution or right middle lung lobe distribution makes aspiration pneumonia a likely possibility, while a perihilar location makes a cardiogenic cause a suspicion. Harsh respiratory sounds or pulmonary crackles in the absence of auscultable cardiac abnormalities make noncardiac pulmonary parenchymal disease the most likely cause of the respiratory distress. A thorough clinical history, thoracic radiographs, bloodwork, tracheal wash, bronchoscopy, or even lung biopsy may be required to definitively diagnose the problem. Some of the more common causes of pulmonary parenchymal disease that we see in our hospital are discussed below. Pulmonary edema due to cardiac disease usually has a perihilar distribution in dogs but can be patchy and diffuse in cats. The majority of dogs will have a loud murmur or persistent cardiac arrhythmia. Most cats will have auscultable cardiac abnormalities such as a murmur or gallop rhythm but auscultable cardiac abnormalities are not as consistently noted in cats compared to dogs. Thoracic radiographs generally show some degree of cardiomegaly in most animals. Cardiac ultrasound often confirms cardiac disease as the cause of the pulmonary edema but this method is not commonly or readily available in a general practice or most emergency clinics. In most instances, cardiac disease as the cause of the pulmonary edema can be inferred from the signalment, history, physical examination, and thoracic radiograph findings. Noncardiogenic pulmonary edema is fluid accumulation in the lungs not due to heart disease. A specific cause of noncardiogenic pulmonary edema is neurogenic pulmonary edema. The four most commonly recognized causes of neurogenic pulmonary edema include upper airway obstruction, head trauma, seizures, and electrocution. This cause of pulmonary edema is characterized by an acute onset (typically within minutes) of respiratory abnormalities after one of the four listed insults. The degree of pulmonary edema can vary from mild to severe involving all lungfields. The typical pattern is interstitial to alveolar with the distribution initially starting in the caudodorsal area. The treatment for this condition is supportive with oxygen supplementation and diuretics (furosemide 2-4 mg/kg IV q6-8h). Some animals require positive pressure ventilation and synthetic colloid support because of the severity of the pulmonary edema and the massive loss of high protein fluid into the lungs. These animals have a poor prognosis and usually die. Most animals with neurogenic pulmonary edema are substantially improved or dead from respiratory compromise within 48 hours of the inciting incident. Spontaneous pulmonary hemorrhage is most commonly due to rodenticide anticoagulant intoxication or thrombocytopenia. Supportive care with oxygen supplementation and specific treatment of the underlying cause are the only options available to treat this problem. Pulmonary thromboembolism (PTE) is challenging to diagnose as well as treat. Diagnosis in veterinary medicine is most commonly arrived at using medical history, recognition of concurrent diseases or drug therapies that are commonly associated with PTE, a history of sudden onset of respiratory abnormalities, and thoracic radiograph findings. Thoracic radiograph findings can vary and many times look completely normal. An animal with severe respiratory distress (not due to upper airway disease) that has normal appearing thoracic radiographs is highly suggestive of PTE. Other radiographic changes sometimes seen with PTE include patchy interstitial pattern, patchy alveolar pattern, and mild pleural effusion. The respiratory signs can vary from just mild tachypnea to severe distress. Treatment is supportive with oxygen supplementation, heparin therapy and specific therapy for the associated cause. Thrombolytic therapy can be used but we have had limited experience with this treatment. ARDS or adult respiratory distress syndrome is recognized in dogs and cats and can cause severe respiratory compromise. It is an inflammatory condition of the lungs characterized clinically by bilateral pulmonary infiltrates (on thoracic radiographs) and hypoxemia with normal heart function. ARDS can be an end stage process secondary to almost any inflammatory condition within the lungs or any inflammatory condition remote from the lungs such as pancreatitis, sepsis, trauma, etc.. Treatment is primarily supportive while the associated cause is treated. "Feline asthma" is an airway hypersensitivity condition in cats that results in bronchoconstriction, pulmonary air trapping, and increased respiratory secretions. The degree of respiratory distress can be mild to life threatening. Many owners describe that their cat is retching or coughing. Some owners incorrectly think that their cat is vomiting. Most cats have a prolonged expiratory phase with end expiratory wheezes heard on auscultation. Rarely, a cat will present with a barrel chest secondary to severe airway trapping with minimal respiratory sounds on auscultation because so little air is moving in the respiratory tract. Emergency therapy for cats with asthma in respiratory distress include oxygen supplementation, corticosteroids (Dexamethasone sodium phosphate 0.2mg/kg IV or IM) and terbutaline (0.01 mg/kg IM or SQ). We have also used inhaled corticosteroids and bronchodilators in some cats. We generally see improvement in respiratory rate and effort within 30 minutes to an hour after terbutaline injection or inhalation therapy. Aspiration pneumonia in dogs is a common cause of respiratory distress at our hospital. This is primarily diagnosed based on the radiographic appearance of interstitial/alveolar infiltrates in the cranioventral and right middle lung lobe areas. Treatment includes oxygen supplementation, nebulization and coupage, maintenance of hydration, broad-spectrum antibiotics (ideally based on culture and sensitivity), and mild exercise (walking) if possible. In addition, diagnostics and therapy should also be directed at the underlying cause of the vomiting or regurgitation. Pulmonary contusions may cause mild to severe respiratory distress. Increased bronchovesicular sounds and/or crackles are often heard or auscultation. Some dogs with severe contusions will have a soft cough at presentation and can also have hemoptysis. Pulmonary contusions tend to get worse over the first twelve hours or so. In addition, radiographic signs will lag behind clinical signs by several hours. Treatment for pulmonary contusions is primarily supportive with oxygen supplementation and judicious fluid therapy, if resuscitation with fluids for other problems (e.g. hypovolemia) is necessary. Respiratory signs tend to start improving after about 36 - 48 hours in most cases. Smoke inhalation is a relatively rare cause of respiratory distress in dogs and cats. Respiratory changes can vary from no clinical signs to severe respiratory distress. The majority of dogs and cats have an increased respiratory rate. Upper airway sounds may occur as a result of mucosal swelling from irritation and thermal injury. Lower airway abnormalities are relatively common and are manifested as increased bronchovesicular sounds, expiratory wheezes and crackles. Oxygen supplementation should be provided to treat hypoxemia and shorten the life span of carboxyhemoglobin if it is present. Corticosteroids are controversial with some studies showing improvement and others showing detriment or no detectable effect. Antibiotics should be given based on detection of infection and culture and sensitivity results. Bronchodilators such as phosphodiesterase inhibitors or the beta-2 agonist terbutaline may help relieve bronchoconstriction if it is present. Most animals with smoke inhalation that make it to the veterinary hospital alive tend to do well and survive to discharge. Dogs and cats that are not worse by the second day and have mild respiratory signs will likely remain in the hospital approximately two days. If they have severe signs and have gotten worse by the second day, most animals either die by 72 hours or remain hospitalized for 6-7 days before being discharged. Extrapulmonary Diseases Thoracic wall abnormalities such as rib fractures or flail chest are relatively easy to diagnose. Diaphragmatic rupture and pleural space abnormalities are not as obvious. Diaphragmatic rupture interferes with respiration via diaphragmatic dysfunction as well as producing a pleural space problem secondary to abdominal contents in the pleural space and/or pleural effusion. Clinical findings include diminished respiratory sounds either unilateral or bilateral as well as well typical signs consistent with a restrictive pulmonary disease (e.g. rapid, shallow respirations). Definitive diagnosis of diaphragmatic rupture requires thoracic radiographs, ultrasound, or contrast radiography (upper GI or intraperitoneal). Definitive treatment of diaphragmatic rupture requires surgery. Accumulation of fluid within the pleural space may be due to a variety of causes including congestive heart failure, neoplasia, pyothorax, vasculitis, hepatic disorders, coagulopathy, pulmonary thrombosis, diaphragmatic hernia, and chylothorax. Clinical signs of a patient suffering from pleural effusion may be a result of the underlying disease process as well as the effects of the effusion itself. Respiratory signs are usually a result of restriction of expansion of the lungs resulting in small, rapid respirations. Effusions may be unilateral or bilateral. Diminished ventral respiratory sounds are detected during auscultation of the chest. If pleural effusion is suspected, thoracocentesis should be performed. As much fluid should be removed as possible. Both sides of the thorax should be aspirated if diminished sounds are detected bilaterally. Fluid analysis should include PCV (if bloody), total solids, cytology, cell count, aerobic and anaerobic culture, and measurement of triglyceride concentration if indicated. Analysis of fluid may be the most important diagnostic clue in patients with pleural effusion. Pneumothorax is a pleural space abnormality that may occur spontaneously or secondary to trauma. Spontaneous pneumothorax most commonly occurs in large breed dogs and is usually secondary to a pulmonary parenchymal abnormality such as a cyst, bullae, bleb, or abscess. These patients often present in severe respiratory distress with bilaterally diminished respiratory sounds dorsally. A large amount of air is often obtained during thoracocentesis. Both sides of the thorax should be aspirated. In cases of tension pneumothorax, a small intercostal incision to rapidly release the air may be necessary if patient collapse is imminent. Air should be removed until a negative result is obtained. If a negative result cannot be obtained then chest tubes should be placed and a constant vacuum applied. Summary Respiratory distress is a common presenting complaint in emergency medicine. Aggressive, yet judicious therapy should be provided to optimize the outcome. Disease categories causing respiratory distress in dogs include cardiac disease, airway disease, pulmonary parenchymal disease, pleural space disease, thoracic wall abnormalities and diaphragmatic rupture. The most common causes of feline respiratory distress are hypertrophic cardiomyopathy, feline asthma, and pleural effusions. Because many of these patients are severely compromised, diagnostic tests may be limited until initial stabilization is provided. Auscultation of the pulmonary and cardiovascular system combined with signalment and a careful medical history may provide important clues to the underlying cause and allow the clinician to provide judicious empirical therapy until definitive diagnostic procedures may be performed. Key Words: laryngeal paralysis, collapsing trachea, pneumonia, pulmonary contusions, smoke inhalation, pneumothorax Emergency Management of the Acute Abdomen INTRODUCTION Animals with an acute abdomen are primarily characterized as having abdominal pain. Vomiting and/or diarrhea often accompany this abdominal pain as well. As with any emergent patient, the basic principles of stabilization of the four major body systems (respiratory, cardiovascular, neurologic and renal systems) should be adhered to when initially assessing and stabilizing these patients (see Approach to the Emergency Patient). After initial stabilization of an animal with an acute abdomen, definitive diagnostic evaluation should be performed to determine the underlying cause as soon as possible so that definitive care can be provided. If the underlying cause can be identified quickly and treated, the chances for more serious complications such as septic peritonitis or systemic inflammatory response syndrome and multiorgan dysfunction syndrome can be minimized. DIAGNOSTIC EVALUATION The list of specific causes of abdominal pain is extensive. Any portion of the abdomen could be a source of pain when examining an animal. Intervertebral disc disease may also simulate a painful abdomen and should be considered in the differential, although this is rarely associated with vomiting and only occasionally associated with loss of appetite. The general causes of abdominal pain include distention of a hollow viscus, stretching of a capsule, ischemia, and inflammation secondary to variety of causes. The clinician has to utilize knowledge of the anatomy of the abdominal cavity to assess the source of pain. The source of pain may be the skin over the abdomen, the subcutaneous tissues, abdominal musculature, peritoneum, retroperitoneum, liver, pancreas, biliary system, stomach, intestines, urogenital system, spleen, and mesentery. One may occasionally locate the specific area of pain, for example, a loop of intestine, the prostate, or the kidneys, and this may help in the diagnostic approach. Many times, a specific area cannot be identified. Diagnosing the cause of abdominal pain requires assimilation of information from a variety of sources including signalment, history, physical examination, bloodwork, radiographs, abdominal ultrasound, radiographic contrast studies, abdominocentesis, peritoneal lavage, response to treatment, and/or exploratory laparotomy. Signalment and History Signalment can be a clue to the cause of abdominal pain or vomiting. For example, young animals commonly swallow foreign bodies or contract infectious diseases. The sex of the patient and whether it is sexually intact may also indicate the source of pain. An older, intact male dog may have a painful prostate. Abdominal pain in an intact female dog with a pyometra should create concern for a possible uterine rupture and septic peritonitis. Young adult German Shepherd dogs are predisposed to intestinal volvulus. String foreign bodies are common in cats. Acute pancreatitis commonly occurs in middle-aged, obese female dogs. Signalment of the patient may be helpful in the eventual diagnosis. An accurate history may be the most important diagnostic clue in the assessment of the vomiting patient. The clinician's first task is to assess whether the animal is vomiting or regurgitating. Vomiting is characterized by hypersalivation, retching, and repeated contraction of the abdominal muscles and diaphragm. Regurgitation is a more passive process. Once it is established that the patient is vomiting, important questions should include the potential for exposure to toxins or dietary indiscretion. Is ingestion of a foreign body a possibility? Are any other animals affected? Has the animal had any major medical problems in the past? Is the patient currently receiving any medications including over the counter drugs such as aspirin or other nonsteroidal anti-inflammatory medications? Is there a possibility of trauma? Could the patient have been exposed to any other animals? Is the patient current on all vaccinations? The clinician should determine when the animal was last normal, what the first abnormal sign was and the progression of abnormal signs since then. The progression of the clinical signs can also help determine the urgency to obtain the diagnosis of the underlying cause. Chronic abdominal pain that has remained relatively static in its progression is not usually an emergency, although at some point, the problem could progress to become an emergency. An animal that has had a chronic problem that has now rapidly deteriorated or an animal with an acute problem that is or is not rapidly deteriorating warrants a more aggressive and expedient approach to define the underlying cause of the painful abdomen. Emergency Clinical Pathology An extended database that includes a packed cell volume (PCV), total solids (TS), dipstick glucose, dipstick BUN, blood smear, venous blood gas, and electrolytes including sodium, potassium, chloride, and ionized calcium helps in rapidly providing a relatively well-rounded metabolic assessment of the patient and can sometimes provide or point towards a diagnosis of the underlying cause. PCV and TS should always be assessed together. Parallel increases in both suggest dehydration and anecdotally seems to be the most common problem in dogs and cats that present with an acute abdomen. A normal or increased PCV with a normal to low total solids indicates protein loss from the vasculature. In an animal with an acute abdomen, this clinicopathologic picture is often associated with protein loss in animals with peritonitis and should alert the clinician of this possibility. Hemorrhagic gastroenteritis (HGE) is associated with a very high PCV( 60-90%) and normal or low total solids. An animal with an acute onset of vomiting and bloody diarrhea with these changes in PCV and TS make HGE the most likely diagnosis. Hemorrhage most commonly results in a parallel decrease in the PCV and TS although in acute hemorrhage, these changes may not be initially recognized until intravenous fluid therapy has been provided. Acute hemorrhage in dogs can sometimes be recognized with a normal or increased PCV and normal or decreased total solids. Splenic contraction in dogs makes total solids a more sensitive indicator of acute blood loss compared to PCV. The most common causes of acute hemorrhage in dogs with acute abdomen are splenic rupture (usually secondary to neoplasia) and severe gastrointestinal hemorrhage from gastrointestinal ulceration. In cats with an acute abdomen, the most common cause of acute hemorrhage is abdominal hemorrhage secondary to hepatic neoplasia. Blood glucose is easily and rapidly obtained by dipstick methods and a glucometer. Packed cell volume may affect the accuracy of these methods. High packed cell volume often causes falsely low glucose measurements. This variation is not consistent from manufacturer to manufacturer; therefore it is best to consult the manufacturer of your dipstick and glucometer regarding this and other effects. Anecdotally, we think that we can improve the accuracy by measuring blood glucose on the plasma or serum instead of whole blood. Increased blood glucose in a dog with an acute abdomen can be associated with diabetes or transient diabetes associated with severe pancreatitis. Blood glucose can rarely be quite high in dogs with extreme hypovolemia secondary to severe abdominal or gastrointestinal hemorrhage. Physical examination findings of extremely poor tissue perfusion are evident and it is clear that the animal may die imminently. We call this the "death glucose" and associate it with massive catecholamine release from the extreme poor tissue perfusion. If perfusion is not corrected quickly in these dogs, they will die. Increased blood glucose in cats may be associated with stress or diabetes. Hyperglycemia in cats is not as useful diagnostically as compared to dogs. Decreased blood glucose is often associated with sepsis and warrants a more aggressive approach to find the underlying cause of the acute abdomen, particularly septic peritonitis. Rarely, extremely low blood glucose may occur as a result of sepsis but more typically the blood glucose is usually in the 40-60 mg/dl range. Low blood glucose in a patient with poor tissue perfusion may also be a result of hypoadrenocorticism. Dipstick BUN (Azostik, Miles Inc., Elkhart, IN) provides an estimate of azotemia in an animal with an acute abdomen. Increased BUN may be due to pre-renal, renal, or post-renal causes. Reliable assessment of a blood smear depends upon on a good quality blood smear. All cell lines should be systematically evaluated including the red blood cells, white blood cells, and platelets. The average number of platelets per monolayer field under oil immersion should be estimated. In normal dogs and cats, there are 11-25 platelets per field; each platelet in a monolayer field under oil immersion is equivalent to approximately 15,000 platelets per microliter. The smear should be screened at low power to search for platelet clumps that may result in a falsely low platelet estimate prior to evaluating the counting area. If there are more than four to five platelets per field then it is unlikely that the bleeding is strictly due to thrombocytopenia. Most patients with spontaneous bleeding due to thrombocytopenia have less than two platelets per oil immersion field. A decreased number of platelets is one of the most consistent findings in animals with DIC. Animals with an acute abdomen may have DIC secondary to the systemic inflammation or massive peritoneal inflammation. The morphology of the red blood cells should be examined. Anisocytosis, macrocytosis and polychromasia indicate regeneration. Schistocytes or fragments of red blood cells suggest DIC. Heinz bodies are often seen in systemically ill cats. The smear should be scanned at lower power to get an estimate of the number of white blood cells and then at higher power to assess the character of the white blood cells. A leukocytosis with a mature neutrophilia suggests an inflammatory or infectious process. Band cells indicate a more severe inflammatory or infectious process. The absence of a leukocytosis or a left shift does not rule out an inflammatory or infectious process. A leukopenia can be due to decreased production or sequestration of white blood cells, a viral infecion such as parvovirus, or immunosuppressive drugs. A venous blood gas provides an evaluation of metabolic acid/base status. Animals that have severe vomiting due to a high gastrointestinal obstruction can have a hypochloremic metabolic alkalosis as well as hypokalemia and hyponatremia. Furosemide administration can cause similar acid/base and electrolyte changes. More often, metabolic acidosis is present due to severe diarrhea or lactic acidosis from hypoperfusion. Abdominal Radiographs Abdominal radiographs should be obtained in a patient that is persistently vomiting or has abdominal pain. The radiographs should be carefully evaluated. Evidence of free gas without prior abdominocentesis or recent abdominal surgery suggests intestinal perforation or the presence of gas-forming organisms within the abdominal cavity. The volume of free abdominal gas can sometimes help in differentiating the cause although this is not 100% specific. A large volume of fee gas in the peritoneal space tends to be more associated with pneumocystography of a ruptured urinary bladder, a ruptured vagina, post abdominal surgery, ruptured gastric dilatation/volvulus, pneumoperitoneography, or extension of a pneumomediastinum. Pneumomediastinum is most often associated with pneumoretroperitoneum although on rare occasions, pneumoperitoneum can occur. A small volume of free gas in the peritoneal space is most often associated with rupture of the gastrointestinal tract or infection with a gas-forming organism. Rarely, we have seen small amounts of gas in the spleen associated with a Clostridia infection in the spleen. Free gas is most commonly detected between the stomach or liver and the diaphragm on the lateral radiograph. A horizontal beam radiograph with the animal in left lateral recumbency and focused at the least dependent area can increase the sensitivity of radiographically identifying free gas in the peritoneal space. Gaseous or fluid distention of the small bowel proximal to an obstruction should prompt the clinician to consider upper gastrointestinal contrast study or exploratory laparotomy. Another option to help determine complete bowel obstruction is to repeat radiographs 3 hours later and see if the localized bowel dilation has changed or not. If the bowel remains distended in the same area, this suggests a bowel obstruction. Generalized small bowel distention suggests generalized small bowel ileus or a very low gastrointestinal obstruction. Loss of abdominal detail may be due to lack of fat in the abdomen (puppies or very thin animals) or due to free abdominal fluid All organs in the abdominal cavity should be evaluated for density, shape, size and location. Abnormalities in any organ may help localize the cause of the acute abdomen. Extra-abdominal structures should be evaluated for completeness of evaluation and further diagnostic clues. The retroperitoneal space should be assessed as well. Loss of detail of the kidneys, a "streaky" appearance, or distention of the retroperitoneal space suggests fluid accumulation, a space occupying mass or sublumbar lymphadenopathy. The structures that make up the abdominal compartment "walls" should be carefully assessed for integrity to rule out herniation or rupture. Abdominal Fluid Analysis: If abdominal fluid is present in an animal with a painful abdomen, it is important to obtain some for analysis. Abdominal fluid analysis can help rule out septic peritonitis and also possibly provide a diagnosis or direct further diagnostic investigation. Free fluid may also be analyzed for creatinine or K+ if urinary tract leakage is suspected and compared to peripheral blood concentrations. Measurement of fluid pH, pCO2, glucose concentration, and lactate concentration may be helpful in diagnosing a bacterial peritonitis. These measurements can be compared to simultaneously collected peripheral blood pH, pC02, glucose and lactate concentrations. Decreasing gradient of glucose from peripheral blood to abdominal fluid and increasing gradient of peripheral blood lactate to abdominal fluid lactate suggests septic peritonitis as the cause of the abdominal fluid. In addition, abdominal fluid with a pH of <7.2, pCO2 > 55mHg, glucose < 50 mg/dl, or a lactate concentration >5.5 mmol/L is suggestive of bacterial peritonitis when there is a gradient of these changes with simultaneously collected blood evaluation (eg. higher blood pH,lower blood pCO2, higher blood glucose, and lower blood lactate concentration). More rigorous evaluation of these parameters is required before they can be used on a routine basis. If bile peritonitis is suspected, abdominal bilirubin concentration will often be higher than simultaneously collected blood bilirubin concentration. A pure transudate is grossly clear and is characterized by a total protein <2.5 g/dl and low cell count (<500 cells/ul). There are few cells present and most are either nondegenerate neutrophils or reactive mesothelial cells. The most common causes of a pure transudate in the abdomen include hypoalbuminemia and a portal venous obstruction. A modified transudate is usually serous to serosanguineous with a total protein between 2.5 - 5.0 g/dl and a moderate total cell count (300-5500 cells/ul). Depending upon the cause there may be variable numbers of red blood cells, nondegenerate neutrophils, mesothelial cells, macrophages, and lymphocytes. This type of effusion is often due to passive congestion of the liver and viscera and impaired drainage of the lymphatics. The most common causes are right-sided heart failure, dirofilariasis, neoplasia and liver disease. An exudate is often cloudy, has a total protein concentration greater than 3.0 grams/dl and a cell count greater than 5000 to 7000/ul. The predominant cell type is the neutrophil although numerous other cells may be present as well. This is the most common type of free abdominal fluid associated an acute abdomen. Exudates can be septic or non-septic and making this classification can be challenging in these patients. Septic exudates are characterized by the presence of intra and extracellular bacteria. In most animals with septic peritonitis, cytological evidence of bacteria can be found, particularly if one has patience and explores numerous microscopic fields and also examines the cytology of the sediment of the abdominal fluid. Rarely, septic peritonitis can be present despite the absence of cytological evidence of bacteria in the fluid. In these instances, the clinician must use all available information that can be obtained quickly to determine if exploratory surgery is warranted including signalment, history, physical examination, clinicopathology, imaging modalities, response to medical therapy, informed discussion with the owner and clinical intuition. Utilizing all this information, the correct decision on whether to perform exploratory surgery or not is usually made. TREATMENT CONSIDERATIONS Antibiotics are not used to specifically treat causes of vomiting or abdominal pain. Indications for antibiotic therapy include loss of the intestinal mucosal barrier due Canine Parvovirus, Panleukopenia virus, or intestinal invasive bacteria. Therapy should be broad spectrum with antibiotics that are particularly effective against gram-negative bacteria and anaerobes. Ampicillin/gentamicin is bactericidal, inexpensive, broad spectrum and effective. One should use aminoglycosides with caution due to their nephrotoxicity, particularly in renal compromised patients (dehydrated and poorly perfused patients). Other antibiotics with gram-negative spectrum include fluoroquinolones, other aminoglycosides (amikacin), Trimethoprim-sulfa, and cephalosporins. Drugs with anaerobic spectrum include penicillins, clindamycin, and metronidazole. A parenteral route should be utilized in the vomiting or critically ill patient. Anti-emetics should be avoided in undiagnosed conditions because they may mask clinical signs of disease progression. If the vomiting is causing compromise of the patient, then anti-emetics are indicated. Critical patients are particularly sensitive to the vagal effects of vomiting and can collapse, develop respiratory arrest, have severe bradyarrhythmias, and even suffer cardiac arrest. Vomiting in a critical patient is a serious problem. Patients with an acute abdomen should not be taken lightly. After stabilization of the respiratory and cardiovascular systems, aggressive attempts should be made to diagnose the cause of the abdominal pain. Rapid evaluation to determine whether the patient requires immediate surgery or not will optimize the chances for a successful outcome. Key Words: painful abdomen, vomiting, septic peritonitis, pneumoperitoneum, bile peritonitis Emergency Management of the Critically Ill Cat with Urethral Obstruction INTRODUCTION Critically ill cats with urethral obstruction present a therapeutic challenge for the emergency clinician. Changes in serum electrolytes and fluid balance can have physiologically devastating effects. Only about 12% of cats present with severe electrolyte and acid/base changes but initial management of these animals can make the difference between life and death. FLUID BALANCE, TISSUE PERFUSION AND INITIAL DATABASE Critically ill cats with urethral obstruction often have severe fluid deficits resulting in hypovolemia and decreased tissue perfusion. The dramatic electrolyte changes that occur with this condition also affect tissue perfusion by their effects on cardiovascular function. When presented with a critically ill cat with urethral obstruction, intravenous access is essential for emergency drug therapy,fluid administration, and collection of blood for an emergency database that includes packed cell volume, total solids, blood glucose, dipstick BUN, sodium, potassium, ionized calcium, and a venous blood gas. A lead II electrocardiogram gives an assessment of any arrhythmias or cardiac conductions abnormalities. ECG abnormalities can also give an indication of the effects of hyperkalemia on cardiac conduction (see below). Initial physical evaluation should be focused on cardiovascular function and tissue perfusion. If there are weak pulses, prolonged capillary refill time and severe dehydration, intravenous administration of balanced electrolyte solutions is extremely important. Although, potassium free solutions such as 0.9% saline are recommended, any balanced electrolyte solution will provide vascular volume support and not contribute substantially to the potassium concentration on an acute basis. There are arguments that 0.9% saline will contribute to the metabolic acidosis, although studies evaluating the efficacy of 0.9% saline and other balanced electrolyte solutions have not been performed in cats with this condition. The dilution provided by 0.9% saline or a balanced electrolyte solution will help to lower the potassium concentration but will not lower it rapidly enough in patients that are affected by the hyperkalemia. We administer 20-30 ml/kg body weight as an intravenous bolus and monitor tissue perfusion status as fluid is being administered. We adjust the dose depending upon the response to this fluid challenge as well as the response to treatment of the electrolyte and acid/base abnormalities. The rapid assessment of the emergency database provides a basis for further therapeutics based on the electrolyte derangements and their physiologic effects on the patient. If the electrolyte changes are severe, yet the patient seems relatively unaffected by these changes, then specific treatment of the electrolyte abnormalities is not attempted. ELECTROLYTE AND ACID BASE CHANGES A variety of electrolyte and acid/base changes occur in critically ill cats with urethral obstruction. None of the changes listed below occur in isolation. Most of the changes occur together. For example, we have found that potassium is inversely correlated with pH, bicarbonate, pC02, sodium, chloride, and ionized calcium, but positively correlated with BUN and creatinine. Ionized calcium can be positively correlated with pH and bicarbonate. Generally, when there is a severe change in one parameter, there are severe changes in all of the parameters. Metabolic Acidosis Metabolic acidosis can be severe in critically ill cats with urethral obstruction. Blood pH can drop below 7.0 in some cats. Severe acidosis (<7.0) can predispose the heart to ventricular arrhythmias, decrease cardiac contractility, and decrease the cardiac inotropic response to catecholamines as well as cause peripheral vasodilation. The irregular rhythm, decreased contractility and peripheral vasodilation may contribute to poor tissue perfusion in the severely affected cat with urethral obstruction. The main treatments for metabolic acidosis in cats with urethral obstruction are relief of the obstruction, fluid diuresis, and bicarbonate therapy. In the majority of cats, the first two are usually all that is required. In the unstable cat with a pH <7.0 due to metabolic acidosis administration of sodium bicarbonate should be considered. The formula often recommended is 0.3 X body weight (kilograms) X the base deficit. This gives an approximation for the total bicarbonate deficit. Administration of one third of this dose slowly intravenously (over about 15 minutes) and the rest placed in the intravenous fluids will correct the metabolic acidosis over several hours. (If blood gas analysis is not available, then 1-2 meq/kg of sodium bicarbonate can be administered slowly). Rapid intravenous boluses of sodium bicarbonate should be avoided because of the production of C02 and its diffusion into the central nervous system making CSF acidosis even worse. In addition, sodium bicarbonate might lower ionized calcium concentration (see below) Hyperphosphatemia The major site of excretion of phosphorus is the kidney. Thus, serum phosphorus increases with urinary obstruction. In severely affected cats, we have observed serum phosphorus increase to 20 mg/dl or greater. The most serious consequences of hyperphosphatemia are hypocalcemia (tetany or seizures as a result), acidosis, and tissue deposition of calcium phosphate salts potentially causing dysfunction of the kidney, heart, and other organs. Therapy for hyperphosphatemia includes relief of the urinary obstruction, intravenous fluid therapy and fluid diuresis. Hyperkalemia Potassium concentration can be normal to extremely high (>10 meq/L) in cats with urethral obstruction. Potassium plays a major role in cell function and neuromuscular transmission. The two tissues of clinical significance that are affected by severe hyperkalemia are muscle tissue (paralysis) and the conducting fibers of the heart. The characteristic ECG changes seen with hyperkalemia are well recognized. These changes include peaking and narrowing of the T wave with a shortened QT interval, widening of the QRS complex, decreased amplitude or loss of the P wave, and as the QRS and T waves merge - a sine wave can be recognized. It has been suggested that specific changes associated with the ECG can correlate with the severity of the hyperkalemia. This relationship is quite variable. We have seen cats with potassium concentrations of 8meq/L with only minor or no ECG changes, while other cats with similar concentrations of potassium have life-threatening ECG changes. This lack of correlation is largely due to other changes that affect the cardiac conduction fibers including the serum calcium concentration (see below), sodium concentration, and acid/base changes. When the constellation of ECG changes are recognized, the potassium concentration is usually quite high and there are often all the other concomittent electrolyte and acid/base changes. Since the severity of the signs does not correlate with the magnitude of the change in the plasma potassium concentration, treatment of hyperkalemia should be guided by its functional consequences by monitoring the electrocardiogram. A cat with high potassium concentration but no functional consequence does not require specific therapy for hyperkalemia. Patients with hyperkalemia that are not suffering from the functional consequences of increased potassium respond well to intravenous fluid therapy and relief of the urethral obstruction. Patients with poor perfusion as a result of cardiac conduction disturbances described above may require more specific therapy directed at the hyperkalemia or its functional effects. Reversing the effects of hyperkalemia can be achieved by direct antagonism of the high potassium's membrane actions and by lowering the plasma potassium concentration. Plasma potassium concentration may be lowered by driving potassium intracellularly or by removal of potassium from the body. Administration of 50 to 100 mg/kg of calcium gluconate intravenously will antagonize the cardiac effects of hyperkalemia. The effects of calcium gluconate administration are immediate. It is for this reason that this is our first drug of choice in cats that have significant cardiac rhythm disturbances due to hyperkalemia. The effects last approximately 20 to 30 minutes. We generally infuse the dose over 2-3 minutes with continuous ECG evaluation. Administration of regular insulin at 0.1 U/kg to 0.25 U/kg IV will promote potassium to move intracellularly. The insulin administration should be followed by a glucose bolus of 1-2 grams per unit of insulin given to prevent hypoglycemia. This regimen will begin lowering plasma potassium concentration within several minutes to one hour. Blood glucose monitoring should be maintained for several hours after the administration of the insulin and the intravenous fluids should be supplemented with glucose to maintain normoglycemia. Sodium bicarbonate administration can lower plasma potassium concentration by raising the pH and driving potassium into the cells. (See "Metabolic Acidosis" above for doses) The effect on the plasma potassium concentration begins within 30 to 60 minutes and may persist for hours. The effects of calcium, insulin and dextrose, and sodium bicarbonate are transient. The administration of these drugs buys the clinician time to remove the urethral obstruction and induce fluid diuresis to correct the underlying problem. Hypocalcemia Severe ionized hypocalcemia may occur in the more critically ill cats with urethral obstruction. Hypocalcemia will make the affects of hyperkalemia on membrane excitability worse. Treatment of severe ionized hypocalcemia is reserved for the patients that have clinical signs of ionized hypocalcemia. Treatment is similar to calcium therapy for hyperkalemia mentioned above (50-100 mg/kg of calcium gluconate intravenously over 2-3 minutes). Continuous ECG monitoring is recommended when administering calcium. CONTINUED CARE After initial stabilization, continued monitoring of physical perfusion parameters, body temperature, mentation, continuous ECG, PCV, TS, dipstick glucose, dipstick BUN, serum sodium, serum potassium, ionized calcium concentration, acid/base status, and urine output should be done. Most cats do well if they remain stable after the first two hours. Post-obstructive diuresis can be profound and can be greater than 120 ml/hour in some cats. Fluid therapy should be adjusted according to the urine output, perfusion parameters, PCV, and TS. The most common electrolyte problem after the initial stabilization is hypokalemia. Many cats require potassium supplementation several hours after initial stabilization. Another complication (but rare) is severe hematuria resulting in anemia. If the urine appears unusually bloody, a PCV should be performed on the urine and the cat's peripheral blood PCV should be monitored closely. We have had to give transfusions in some cats to maintain the PCV. Most of the cats that we have treated for urethral obstruction have the urinary catheter in place for about two days. Our criteria for removal of the catheter are that the urine is relatively free of grit and is not grossly cloudy or bloody. We remove the catheter in the morning on the day of discharge and make sure that the cat can urinate prior to going home. Key Words: hyperkalemia, metabolic acidosis, hyperphosphatemia, ionized hypocalcemia, hypokalemia |
