|
Critical Care Amy Butler, DVM, MS, DACVECC Ohio State University Approach to the Emergency Patient The term "triage" was developed during World War I in response to advances in battlefield medicine. From the French word "Trier", meaning "to sort" a new system for patient classification was born. Patients were divided into three categories: those who were likely to die regardless of intervention, those who were likely to live regardless of intervention, and those who were more likely to live if immediate intervention was performed. It is the last category we are concerned with identifying. Before a triage exam is started, a very brief medical history should be obtained. This includes the patient signalment (age, breed, sex) and a very brief history of the current medical condition and major illness. This is intended to be only a few sentences at most. In brief, patients with pale mucous membranes, tachycardia, difficulty breathing, seizuring, recumbency or non-responsiveness should be taken immediately to a treatment area. The triage exam is a rapid physical examination that addresses the most life-threatening conditions first. The triage exam is divided into two parts: The primary and secondary surveys. It is different from a general physical exam in that if a serious problem is found during the primary assessment, that problem is immediately addressed before going on the rest of the physical examination. It is also performed in a very different order than a general physical exam. The Primary Survey 1) Airway and Breathing Is the patient breathing? If no, immediately move onto circulation. If the answer is still no, start CPCR. If it still has circulation, intubate and begin ventilation. Is the rate normal? Normal respiratory rate for dogs and cats is 8-12 bpm. However, respiratory rates of up to 40 bpm may be considered normal. Panting can occur at rates up to 200-300 bpm, but does not effect an increase in true ventilation since panting is primarily dead space ventilation. Is the respiratory pattern normal? Many different respiratory patterns exist, and the origin of disease can often be determined by the pattern.
2) Circulation Can the heart be ausculted? If the patient is alive and breathing, check the pulse rate. Reasons to not be able to auscult the heart include pericardial effusion, pleural effusion, diaphragmatic hernia or thoracic masses. It may also be difficult to auscult the heart in large breed, obese dogs, especially when the patient is in lateral recumbency. Is the rate normal? Normal heart rate in the dog is 80-120 bpm. Larger dogs tend to have slower heart rates, and small dogs have higher heart rates. A heart rate greater than 140 bpm in a large/giant breed dog or greater than 160 in a small dog should be of concern. A heart rate less than 60 is also cause for concern. Cats tend to get bradycardic when ill, thus a heart rate < 160 bpm in a sick cat is concerning. Is the rhythm normal? This part of the exam is not intended to diagnose an arrhythmia, but to see if one is present. The heart should be ausculted at the same time that pulses are felt to determine if pulse deficits are present. Pulse deficits occur when there is the sound of a heart beat, but no corresponding pulse wave. Common arrhythmias that can ready be picked up during the primary survey include ventricular arrhythmias and atrial fibrillation. Is there a murmur? Again, this stage of the exam is not meant to localize or diagnose the murmur, only to determine if one is present. Rather than the crisp "lub-dub" of the normal heart beat, listen for a slurring on the heart sound "shhhh-dub" or "dub-shhh" depending on whether the murmur is systolic or diastolic in origin. How is the pulse quality? Femoral pulses are the easiest to palpate, and can be located in the femoral triangle. Poor quality pulses (often called "weak" or thready") indicate poor forward flow. This may be due to low blood pressure, vasoconstriction or heart failure. Absent pulses indicate severe hypotension or obstruction to flow, such as with saddle thrombus in the cat. Bounding pulses can be caused by patent ductus arteriosus, aortic insufficiency and sepsis. What is the mucus membrane color?
3) Neurologic Exam What is the mentation? There are many categories of mentation. What is the posture? Opisthotonus describes the posture with the forelimbs rigidly extended and the neck flexed dorsally. Decerebrate rigidity affects all four limbs, causes opisthotonous and stuporous to comatose mentation. This indicates a severe brainstem lesion. Decerebellate rigidity has a similar posture, but with flexed rear limbs and intact mentation. It indicates a severe cerebellar lesion. Schiff-Scherrington posture can look similar to opisthotonous, but the neck is not as rigidly extended and mentation is normal. Schiff-Sherrington posture indicates a severe thoracolumbar lesion. Is nystagmus present? Animals with vestibular disease normally have nystagmus, a rhythmic movement of the eyes. This can be horizontal, vertical or rotary. The eyes normally move rapidly away from the side of the lesion in cases with horizontal or rotary nystagmus. Vertical nystagmus is associated with central vestibular disease. What is the pupil size? The normal pupil size is mid-range and responsive. Pinpoint pupils indicate moderate cerebral injury. The most severe cerebral injuries produce dilated, non-responsive pupils. These patients will have altered mentation as well. Normal dogs with severe iris atrophy may have dilated, poorly responsive pupils. Is there deep pain? This is frequently mistaken for the withdrawal response, but these are two very different pathways. Deep pain is present when a hemostat squeezed across the phalanges elicits a painful response (crying, whining, biting). The presence of withdrawal does not indicate intact deep pain. If the animal is comatose, deep pain cannot be evaluated. 4) Abdomen Only a brief abdominal palpation should be performed looking for three key findings: Fluid wave: A fluid wave can be best palpated with the animal standing, although any positioning will work if there is a large volume of effusion. To palpate a fluid wave, place your hands on either side of the abdomen. Tap one hand firmly against the abdominal wall, and feel for a fluid wave to translate to the opposite hand. In dogs, fluid waves can occur secondary to accumulation of blood (neoplastic, coagulopathy, trauma); peritonitis (septic, bile, sterile); right sided heart failure, neoplastic effusion and uroabdomen. In the cat, abdominal effusions are usually caused by neoplasia, right sided heart failure, FIP and peritonitis. Tympany: Tympany is a clinical finding most often associated with GDV in dogs, although it can also be caused by gastric dilatation without volvulus or mesenteric torsion. The tympany associated with GDV is usually located under or immediately behind the ribs. To find tympany, place the hands on either side of the abdominal wall and tap with one or both hands. A sound similar to tapping on a drum is indicative of tympany. Pain: Many different abdominal emergencies can present with pain. Pain localized to one section of the abdomen can indicate different disease processes. Pain localized to the cranial abdomen can indicate GDV, gastric distension, foreign bodies, liver lobe torsion or abscesses, or pancreatitis. Pain localized to the mid-abdomen can indicate splenic torsion, splenic masses, intestinal foreign bodies, mesenteric volvulus, pyelonephritis, ureteral obstruction or adrenal masses. Caudal abdominal pain usually indicates urinary tract obstruction, prostatitis, prostatic abscesses, uroabdomen, or aortic thromboembolism. Treatment During the primary survey, any abnormalities should prompt quick treatment. If respiratory distress is present, supplemental oxygen should be delivered. An IV catheter should be placed. IV fluid therapy is recommended for shock states, unless cardiogenic shock is suspected. Pain medications are always indicated in trauma patients as pain can worsen the signs of shock. Since analgesics can interfere with the neurologic exam, the primary survey should be completed first. Point of care diagnostics should also be gathered. These include ECG, pulse oximetry, blood pressure, PCV/TS and glucose. Additional blood should be saved for CBC/Chemistry and blood gas testing. The Secondary Survey Thoracic auscultation: This is intended to localize murmurs and fine tune the original assessment of the chest. The "Not Brain" neurologic exam: This includes problems such as weakness, abnormal proprioception, loss of spinal reflexes, and peripheral nerve injury. In trauma patients, the spine and neck should be palpated for obvious fractures. Full abdominal palpation: This is meant to identify the major organs, assess size, presence of pain, and localize any abnormalities. Musculoskeletal exam: Palpate all long bones and flex/extend joints, looking for areas of instability, crepitus or swelling. Also examine the patient for painful areas of bone, joint or muscle. Open wounds: Quickly cover open wounds with sterile lubricant and a sterile wrap to prevent further contamination. Open wounds are rarely life-threatening, but hospital-acquired infections can be serious and difficult to treat. The standing exam: Stand the patient up and have them walk. Assess for limping, abnormal limb movement or paresis. Critical Care Monitoring This lecture will discuss some of the most common modalities used for monitoring the critically ill patient. We will review use, indications, limitations, and interpretation of data received from these monitors. Systemic arterial blood pressure Measurement of blood pressure is routinely done in small animal practice. Most of the information presented here comes the ACVIM consensus statement (J Vet Internal Med, 2007) covering the subject. Indications:
Materials: Three ways are routinely used to measure blood pressure in the ICU: oscillometry (using a Cardell® (Figure 1), DinaMap, or the PetMAP®, doppler ultrasonography (aka sphyngomanometry-Figure 2) or direct blood pressure (arterial catheter and a pressure transducer linked to in a monitor). See the table below for the pros and cons of each method. Obtaining a measurement: To obtain reliable values in the measurement of BP, it is important to follow a standard protocol. BP may be affected by stress or anxiety associated with the measurement process and these changes may result in a false diagnosis of hypertension. The following protocol has been recommended by the ACVIM consensus statement.
Normal systolic blood pressure is around 140 mmHg with a diastolic of 80 mmHg and a mean of 100 mmHg in dogs. Note that sighthounds (e.g. Greyhounds) have a BP 10-20 mmHg higher that other breeds. Cats may have a slightly lower systolic BP 130/80 with a mean of 100 mmHg. The table below discussed pros and cons of each method: 
Trouble shooting:
The pulse oximeter is a very commonly used monitoring tool. It is a continuous, non-invasive measurement of a patient's arterial oxygen saturation. Indications and Limitations:
The pulse oximeter sensor contains two light emitting diodes (LED) that transmit specific wavelengths of light which are received by a photodetector. Pulsatile flow must be present. Oxygenated blood absorbs light differently than depleted blood. Thus the amount of light absorbed by the blood can be used to calculate the ratio of oxygenated hemoglobin to total hemoglobin in arterial blood. The monitor displays this ratio as percent that is usually labeled SpO2. Normal values: SpO2 of 97-98% is normal in dogs and cats breathing room air. If provided oxygen supplementation, 98-100% is normal. If patient is receiving oxygen supplementation, it is very important to know the inspired oxygen (FiO2) by using an oxygen analyzer. How to obtain a measurement: Select a site on the patient that has unrestricted blood flow and can remain immobile as possible to reduce or eliminate movement artifact (e.g. lip, tongue, ear, prepuce or vulva). Choose a site in sufficient perfusion to avoid false saturation values and/or low signal. Pulse oximeter are affected by motion, skin pigmentation, tissue thickness (i.e. area the device is placed), ambient light, low-perfusion state or cardiac arrhythmias and abnormal hemoglobin, but not by anemia or icterus. It is accurate at +/- 4 percentage points, which may be significant at the steeper part of the curve. The strength of the signal is usually displayed on the monitor, and is probably the most reliable way to assess accuracy. You can also use the sound display and make sure that heart rates from the machine and the patient match. The pulse oximeter is inaccurate with SaO2 less than 80%. Troubleshooting:
An overview of ECG is beyond the scope of this handout, however, basic guidelines about placing and interpreting an ECG tracing are provided. Indications and principle: The ECG is a representation of the electrical activity of the electrical activity of the heart. It provides an overview of heart rate, and is crucial to the diagnosis of brady/ tachyarrhythmias as well as pulse variations. On the other hand, ECG doesn't provide any information on myocardial performance, contractility, cardiac output or blood pressure. Normal values: The following table presents normal values for heart rate, intervals between complexes, durations of P-QRS-T complexes, and heights of complexes. 
ECG Placement: Only two electrodes are required for a functional ECG, one cranial and one caudal to the heart. Three leads are better because there are more options to view the tracing. A three lead ECG is sufficient in emergency situations. - Black lead => Left arm - White lead => Right arm - Red lead => Left leg Many mnemonics exist, but some (such as "grass and snow on the ground") only work when the patient is in right lateral recumbency. ECG interpretation step-by-step:
Lactate is an end product of anaerobic metabolism and s formed by conversion of pyruvate to lactic acid. Principles: Lactic acid is produced during normal physiologic activity (i.e., exercise) and by pathologic processes. Lactate can be elevated with or without marked acidosis (hyperlactatemia vs. lactic acidosis), but severe hyperlactatemia will typically cause lactic acidosis. Major lactate producers are skeletal muscle and GI tract, with skin, red blood cells, brain, white blood cells and platelets also producing significant amounts. When tissue oxygen delivery is inadequate, hypoxic areas must switch to anaerobic metabolism. Anaerobic glycolysis causes far less ATP to be produced than during aerobic glycolysis. This causes energy deficits in the cell that eventually leads to cell death as important biochemical processes can no longer be maintained. Lactate is one of the single best markers of global perfusion. The degree of hyperlactatemia and severity of lactic acidosis closely reflect the severity of tissue hypoxia. Indications
Venous lactates are typically slightly higher than arterial lactates. The reference range established by one study is 0.3-2.5 mmol/L for venous samples. Analyzers test for the presence of L-lactate, the isomer produced by mammalian tissues. D-lactate is produced by some bacteria and is present in IV fluids (i.e., lactated ringers solution). L-lactate will not cross-react with D-lactate, therefore, therapy with LRS will not affect results. Limitations of Lactate Measurement:
Technical aspects Only a drop of blood is required for the portable analyzer. The machine is easy to use, requires only minimal upkeep (about the same as a glucometer), and takes 60 seconds for one reading. Lactate meters are readily available through a variety of sources. Machines typically cost $250-350. Strips cost $1.60-2.20 apiece, depending on the quantity ordered. Anesthetic Death - What to Do When the Worst Happens Most times, luckily, anesthesia is a routine procedure. However, patients can and do arrest, even in a previously healthy patient. This talk is aimed at allowing technicians to recognize the causes of cardiopulmonary arrest, the signs of impending arrest, and what to actually do if it happens. Causes of Arrest Cardiopulmonary arrest is almost always caused by decreased delivery of oxygen to the brain and heart. A number of causes can contribute. Hypoxia: Hypoxia means that tissues are not receiving enough oxygen. This can be caused by either not enough oxygen in the blood or not enough red blood cells to carry oxygen. Anemia will contribute greatly to decreased carrying capacity of oxygen. A rapid decrease in PCV can be more serious than a lower (i.e., mid-20s) PCV that is stable. Consider blood transfusions if the PCV is less than 18-20%. Hypoventilation occurs when the patient is not breathing with enough volume. It will increase PaCO2, but without much increase in the ETCO2. Reduced Cardiac Output: Occurs when the heart is not putting enough blood forward. This can be due to several causes. Hypovolemia can occur from blood loss, dehydration, or third space losses. IV fluid boluses can be given to correct hypovolemia. Decreased cardiac contractility occurs with many anesthetic agents such as Dexdomitor (dexmedetomidine), isoflurane, halothane, and Propofol. Arrhythmias contribute to poor forward flow. These may be due to primary cardiac disease, electrolyte disturbances, or can be disease related. Sinus bradycardia is one of the most common anesthetic complications. In many patients, it is related to excessive anesthetic depth, hypothermia and hypoxia. Simply turning down the inhalant concentration and administering atropine can prevent an arrest. Hypotension: Is defined as a systolic BP < 90 or MAP < 60 mmHg. This is another serious and common complication of anesthesia. When under anesthesia, the patient lacks normal compensatory responses to low blood pressure, meaning that the body is unable to maintain blood pressure as it normally would when the patient is awake. This can be caused by decreased CO2, which will cause decreased catecholamine response. Additionally, many anesthetic drugs will most commonly cause hypotension. Acepromazine, Dexdomitor, Propofol and inhalants will cause vasodilation and blunt the normal response to hypotension. Fluid boluses are frequently used to expand vascular volume. Hypothermia: This is an extremely common consequence of anesthesia. Small patient size, open body cavities, convective losses and the cool temperatures common in the operating room contribute to development of hypothermia. As hypothermia worsens, the decreased metabolic rate will lessen amount of anesthetic drug needed. This makes it much easier to overdose the patient or create a too deep plane of anesthesia. Signs of Impending Arrest Usually, arrest is preceded by a number of clinical signs. The technician paying close attention to the patient can detect these signs and take action prior to arrest occurring. Hypotension is often one of the first signs noted. A reflex tachycardia may occur. Tachycardia alone also signals that something is wrong. Tachycardia can also indicate that the patient is too light, so further investigation is necessary. Bradycardia is a more serious sign and should be promptly addressed. The onset of cardiac dysrhythmias (such as ventricular premature contractions) signals that the myocardium is not receiving enough oxygen. Falling End-tidal CO2 is an excellent indicator of impending arrest. As blood flow to the lungs decreases sharply, the patient will breathe off the remaining CO2 and the ET CO2 will decrease. Poor oxygenation (pulse oximeter < 90%) is often a late sign, and may not actually decrease much (and sometimes not at all) until after arrest has occurred. What to do if you don't have lots of monitoring equipment? Even without equipment, an observant anesthetist is the best defense against anesthetic arrest. The following parameters should be monitored no more than every 5 minutes, and more frequently in sick patients. Respiratory rate should be carefully monitored. Make sure that the patient is breathing, but also make sure that it is taking adequate breaths. Surgical manipulation in the abdomen can cause minor movements of the rebreathing bag, so ensure that chest excursions are adequate. Heart rate and rhythm should be assessed, either through taking pulses, ausculting the chest, or by placement of an esophageal stethoscope. Mucus membranes can indicate cardiovascular status. Pale mucous membranes indicate anemia or poor perfusion (either vasoconstriction or poor cardiac output). If a patient with a normal PCV becomes pale, hypotension should be suspected. Cyanosis occurs at PaO2 < 40 mmHg or if > 5g/dl unsaturated Hgb. This change will occur very late in patients breathing 100% oxygen. Finally the patient should be monitored carefully for inappropriate anesthetic depth. Eyes that are central indicate that the patient is either too light or too deep. Always err on the side of caution and assume that the patient is too deep. Eyes that are positioned ventromedial indicate an appropriate plane of anesthesia. What do you do if you suspect an arrest? First, turn off the gas! It's easier to re-anesthetize a patient than to perform successful CPR! Reverse any drugs that you can ASAP! Naloxone will reverse most opioids, Flumazanil will reverse benzodiazepines, and Antisedan is the reversal for Dexdomitor. There is no reversal agent for ketamine or acepromazine. Verify the arrest by direct pulse palpation and thoracic auscultation. Never trust your ECG - electrical activity can occur long after arrest. If you don't feel a pulse and can't auscult a heart beat, trust it over your ECG. If there is no heart beat, skip directly to CPCR. Evaluate breathing - is the patient hypoventilating? Give several deep breaths, and note the presence of a reading on the ET CO2 monitor if you have one. If there are no chest excursions when the bag is squeezed, look for an airway obstruction. Re-intubate if necessary. There may be pleural space disease - pneumothorax can occur if the pop-off valve was left closed accidently. Perform thoracocentesis if in doubt. Evaluate the heart rate - bradycardia can potentially be reversed with anti-cholinergics, rewarming or reversing drugs. The emergency dose of atropine is 0.04 mg/kg IV or 0.08 mg/kg IT (1 ml per 20# if you are using standard dose atropine). Give ½ and reassess. Evaluate ECG or pulses - if irregularly irregular, assume arrhythmias are occurring. Treat with lidocaine 2-4 mg/kg bolus, then CRI. If no pulse, skip to the next section (get ready for CPCR!). If pulses are present, suspect hypotension. Give fluid boluses (start with 22 ml/kg in the dog and 10 ml/kg in the cat) and reassess. Obtain a blood pressure if you have blood pressure monitoring equipment. Consider increasing cardiac output (dobutamine or dopamine) or increasing vascular tone (ephedrine, norepi, phenylephrine, and epinephrine). Don't forget that catecholamines will sensitize the heart to arrhythmias. Actively rewarm the patient if it is cold. The abdomen (if open) can be lavaged with warmed fluids. Do not heat fluids to more than 103F. If the abdomen is closed, fluids can be given intraperitoneally at 10-20 ml/kg. Initiating CPCR The goal of CPCR is to maximize myocardial and cerebral circulation. First, do not panic. The patient is already dead, and there is nothing you can do to kill it any deader than it already is. So relax. You can only help. As we discuss the steps below, remember that CPCR runs in cycles lasting 2-3 minutes each. During a cycle, compressions should not be stopped for any reason (including assessing for ROSC). At the end of each cycle, you may stop for a few seconds to auscult the patient or check the ECG. Compressions Begin compressions first! Adequate chest compressions will effect an adequate tidal volume, meaning that unless the animal died for hypoxemic reasons, you may not need to breathe for them. With that said, the animal should be intubated as CPCR progresses (if not already intubated), but it is not the top priority. The first rule of compressions is to "keep it physiologic". That means matching the animals' normal heart rate. In the dog, aim for 80-120 compressions per minute (more on this in a moment), and in the cat, 180 compressions per minute. Yes, it is possible to meet these rates easily. You can sing of the following songs and do compressions to the beat Dog: "Stayin' Alive" by the BeeGees - 103 bpm "Another One Bites the Dust" by Queen - 100 bpm Cat: "Footloose" by Kenny Loggins - 175 bpm "Livin' La Vida Loca" by Ricky Martin - 180bpm The second rule of compressions is to make your compressions count. Use appropriate technique. In medium-large breed dogs, the patient should be lateral recumbency. The hands should be placed flat or in a fist over the heart (where the elbow meets the costochondral junction). Keep your elbows straight and use your back muscles to compress. If you are using your upper arm muscles, you will fatigue much more rapidly and your compressions will be less effective. Unless you have a lift table, you will likely need to stand on a stool to effectively "put your back into it". In the cat or small breed dog, the hand should be wrapped around the chest over the heart and the chest compressed between the flats of the fingers (not just the fingertips). For any size animal, you should compress the chest by 25-35% of thoracic width. Allow for complete chest recoil, as this improves venous return to the heart. Studies have shown that compressions become less effective after just 2 minutes. Switch compressors at the end of each cycle. The third rule of compressions, and the most important, is to NOT interrupt compressions. Every time you halt compressions, the cardiac output is zero. The most common reasons for interrupting compressions are: intubation, catheter placement, drug administration and attempted defibrillation. There is no reason to stop compressions for any of these. Wait until the end of the cycle to briefly (few seconds) halt compressions. Airway and Breathing Once compressions have started, an airway can be established and ventilation begun. Place an appropriately sized endotracheal tube, and remember to tie it in place and inflate the cuff. Do not withhold compressions during intubation. The only rule of ventilation is to "keep it physiologic". Ventilation rates should be 8-12 bpm. Higher ventilation rates are associated with worse outcome. Avoid barotrauma by not ventilating to pressures > 20 cmH2O. If the patient died from hypoxemic causes or you suspect alveolar disease (pneumonia, pulmonary contusions, heart failure), consider providing positive end-expiratory pressure (PEEP). To do this, partially close the pop-off valve and hold pressure on the bag so that the manometer does not drop below 5 cmH2O. This will help to prevent alveolar collapse at end expiration from dilution of surfactant with alveolar fluid. Ambu-bags are unable to deliver PEEP. Drugs Asystole is the most common arrest rhythm. It is a complete cessation of electrical and mechanical activity, and is the least likely to convert. The treatment of choice is epinephrine, even though epinephrine has not been proven to be helpful in asystole. The dose of epinephrine is controversial. High dose epinephrine (1:1000) 0.1ml/kg IV (or 1ml per 10 kg or 20 lbs) is associated with a higher rate of ROSC, but also a higher rate of re-arrest. Low dose epinephrine (1:10,000) is associated with a lower rate of ROSC, but a lower rate of re-arrest. Overall, there is no evidence that one dose is better than the other; however, most human emergency departments have switched to low dose epinephrine. You can either purchase 1:10,000 epinephrine, or dilute 1:1000 epi at a 1:10 dilution in bacteriostatic saline. If the animal fails to convert after one cycle with epinephrine, consider use of vasopressin. Vasopressin is a powerful vasoconstrictor mediated through V1 receptors in the vascular smooth muscle, and has the added benefit of not causing post-resuscitative tachycardia like epinephrine. Currently, there is no evidence that vasopressin is superior to epinephrine for treatment of asystole. The dose of vasopressin is 0.8 u/kg IV. Atropine is also considered controversial for treatment of asystole. It has a clear benefit for bradycardia, but does not increase rate in the non-beating heart. Its use is associated with post-resuscitative tachycardia, similar to high dose epinephrine. The bottom line is that if the animal did not arrest from a vagal cause (vomiting, coughing, defecation), then atropine is not likely to be useful and may be harmful. The dose of atropine is 0.02-0.04 mg/kg IV, or 1 ml per 10kg or 20 lbs. If IV access is not available, the following drugs can be given via the intratracheal route: naloxone, atropine, vasopressin, epinephrine and lidocaine (NAVEL). The dose for IT administration should be doubled or tripled. A long red rubber catheter should be used for drug delivery into the lungs rather than the drug being trickled down the endotracheal tube. IV administration is preferred if available. Remember that circulation during CPCR is very sluggish with even the best compressions, so it will take the entire 2-3 minute cycle for it to reach the heart. Do not stop compressions to administer drugs or to gauge effectiveness until the end of the cycle. Large (6-30ml, depending on patient size) flush volumes may be used to help improve drug return to the heart. It the drug is injected into a cephalic or saphenous catheter, elevate the limb to improve flow time. Fibrillation The only treatment for ventricular fibrillation is defibrillation. Defibrillation does not start the heart, but instead, stuns it and allows normal electrical activity to take over. With that said, it is possible to shock the heart into asystole. Defibrillation is more likely to be successful if at least one cycle of CPCR has taken place prior to defibrillation. To defibrillate, place the patient in dorsal recumbency and apply the paddles firmly to either side of the thorax. Electrical conducting gel should be used to improve contact with the skin, and hair can be clipped if time allows. Do not use alcohol to improve contact as you may set your patient on fire. Administer ONE shock of 2-4 J/kg (monophasic) or 1-2J/kg (biphasic), and resume compressions immediately. Do not stop to see if the defibrillation has been successful until the end of the cycle. Will it work? Out of all causes of arrest, anesthetic death has the best recovery rate. However, one study showed that CPCR lasting longer than 15 minutes was unsuccessful in almost all cases. Severe neurological deficits were seen in dogs with CPCR lasting greater than 12 minutes. No cats survived if CPCR was > 17 min. Faster resuscitation = better outcome. Neonatal Care Neonatal Physiology Development of puppies can be divided into four distinct time periods: the neonatal period (birth - 2 weeks); the infant period (2 - 4 weeks); the pediatric period (4 - 12 weeks) and the juvenile period (12 weeks - puberty). This talk will focus exclusively on the neonatal period. At birth, the hepatic, renal, immune and cardiopulmonary systems are not fully developed. The hepatic (liver) system is unable to respond to normal feedback mechanisms that maintain blood glucose within the normal range. In the adult, periods of starvation incite the liver to create new glucose. In the neonate, there is a lower capacity to store glucose precursors, manufacture fresh glucose and a decreased ability to respond to hormonal signals that create glucose. This makes the neonate especially susceptible to hypoglycemia. Additionally, hepatic biotransformation of drugs is impaired, lowering or altering dose requirements of many medications. The renal system of the neonate is unable to conserve water (and part of the reason why they seem to urinate constantly). Neonatal kidneys are unable to concentrate or dilute urine in response to fluid gains and losses. This makes the neonatal puppy extremely susceptible to dehydration. Adult values are not seen until at least 10 weeks of age, and kidney function increases linearly with age for the first year of life. The cardiopulmonary system is also not fully developed in the neonate. Due to a small thorax to abdominal size ratio, lung capacity is proportionally smaller than in the adult. Additionally, surfactant production is significantly lower in the neonate, meaning that the functional units of the lungs, the alveoli, are not as effective at gas exchange. The heart contains less contractile elements than the adult heart, meaning that the heart cannot pump "harder" in response to hypovolemia. Finally, the sympathetic nervous system (the "fight or flight" system) cannot adequately respond to stressors such as hypoglycemia or hypotension (low blood pressure). Because the body is unable to adequately respond to these, the neonate is more prone to decreased tissue perfusion. The immune system is poorly developed at birth. In humans, most immunity is passed from mother to baby in utero. Puppies receive > 95% of their immunity from colostrum within the first 24 hours of birth. Antibodies are passed via milk and absorbed from the GI tract. After 24-48 hours, the neonatal GI tract becomes impermeable to preformed antibodies, and further colostrum administration is futile. Very little immunity is passed from the bitch to the puppy transplacentally. If the puppy is unable to feed for the first 24 hours, subcutaneous injections of pooled plasma have been shown to be effective in transfer of antibodies. Neonatal "normals" Body temperature is significantly lower in the neonate than the adult. This is due to inadequate fat stores, a high surface: body mass ratio, an immature thermoregulatory system, lack of shivering response and poor peripheral vasoconstriction. Normal body temperatures are listed below:
Weight and weight gain: Puppies should gain 5-10% of their birth weight daily. Twice daily weights obtained on a gram scale are a good way to recognize non-gaining puppies, and an early indicator of disease. Birth weight is an important prognostic indicator. Puppies that weigh >25% less than their littermates are at higher risk of hypothermia, hypoglycemia, sepsis and pneumonia. Hydration is difficult to assess in the neonate. Skin turgor, due to the high water and low fat content of the skin, is not a sensitive measure. Neonates are 75% water, compared with 60% in adults. Neonates are particularly sensitive to dehydration due to the immature renal system discussed above. Hydration can be assessed by the dryness of the oral mucous membranes and/or eyes. The GI tract is sterile at birth, but is rapidly populated by bacterial flora in the environment and from the dam. The meconium, a soft, yellow-brown stool, should be passed in the first 48 hours. Normal neonatal feces are pasty yellow-tan, but should not be observed if the dam is cleaning the puppies normally. Overfeeding typically results in green or yellow watery stool. Canine Herpesvirus infection may cause bright yellow watery stool, and intestinal parasitism (especially Coccidia) or sepsis may cause blood tinged stool. Blood pressure is significantly lower in neonates than adults. In one study, blood pressure was 49 mmHg at 2 months of age, compared with 94mmHg at 9 months of age. This is thought to be due to immaturity of the muscles in the blood vessel walls. Urine production by the kidneys is linearly dependent on blood pressure in the neonate, making hypovolemia and hypotension a serious cause of renal damage. The nervous system is slow to develop in the newborn. They sleep at least 90% of the time. For the first 5 days of life, flexor tone is predominant. From 5 - 21 days, extensor tone tends to be dominant, although positional changes occur. Important reflexes to assess are the righting, rooting and suckle reflexes. The righting reflex is accomplished by placing the puppy on its back. It should turn over vigorously. The rooting reflex is accomplished by placing the muzzle in the circle made by your thumb and forefinger. A healthy puppy should push forward vigorously. The suckle reflex, measured by placing a finger in the mouth, should be strong. Eyes and external ear canals typically open at 10-14 days. Despite closed ear canals, puppies can hear from birth. Once the eye opens, the cornea will remain cloudy for 24-48 hours. The menace reflex, which is not truly a reflex but a learned response, is not typically present until at least 3 weeks of age. Care and feeding of neonates Most puppy milk replacers provide 1.0 - 1.3 kcal/ml formula. Many sources recommend diluting formula with water by at least 25% for the first 2 weeks to avoid diarrhea. More concentrated formulas can promote diarrhea because the high osmolarity of these solutions can pull water into the GI tract. Various formulas are recommended including:
Where 30ml = 1 oz; These should be divided into at least 4 feedings per day; some sources prefer feedings every 2 hours for the first 2 weeks of life. Do not prepare more formula than is required to feed for a 48-hour period. Divide the formula into portions that are required for each feeding and store in the refrigerator, rather than repeatedly heating and cooling the same formula. Before feeding, warm the formula to body temperature. All equipment must be kept scrupulously clean. Bottles are the preferred method of feeding. The nipple hole should be large enough that when inverted, a drop of milk should slowly ooze from the bottle. The bottle should never be squeezed while in the mouth to avoid aspiration pneumonia. Syringe/force-feeding is not recommended in the sick neonate, again because of the risk of aspiration. Tube feeding is preferred for the sick neonate. However, an inaccurately placed tube will result in aspiration and likely death. If you have never tube fed, make sure to have a veterinarian train you in this practice and monitor your first feeding attempts. Ensure that the feedings are administered to the stomach by measuring and marking the tube. Feedings should be administered slowly (over at least 2 min) to avoid rapid distension of the stomach. The Sick Neonate Overall, mortality rates range from 11-34%, although some report losses as high as 40%, in the first 12 weeks of age. Approximately 90% of these losses occur in the first 2 weeks of life. Unfortunately, most sick neonates look the same on physical exam, making diagnosis of the underlying problem difficult. Common signs of sickness in neonates include: weakness, anorexia, constant crying, abdominal distention or pain, poor weight gain, poor nursing, restlessness and isolation. On physical exam, the ill neonate is usually weak or limp with poor reflexes and appears dehydrated. Diarrhea may or may not be evident depending on the attentiveness of the dam. The same triad of clinical signs appears in almost all sick neonates: hypoglycemia, hypothermia and dehydration. All of these must be assessed in order to successfully treat the patient. For the mild to moderately affected puppy: (crying, poor nursing, restlessness) Hypothermia and dehydration should be addressed first. Feeding should NOT be attempted until fluid requirements and body temperature have been corrected. Passive warming, including using warmed blankets or water bottles, circulating warm water blankets or heated bags of rice can be used. Use caution with any focal heat source, especially electric heating pads or heat lamps. A gradient must be established such that the puppy can move away or towards the heat source. A weak puppy may not be able to get away from the heat source. Breathing warm, humidified air is a rapid way of increasing body temperature, and can be accomplished by bringing the puppy into a bathroom with the shower running. A thermometer can used to monitor the ambient temperature. Overheating is rarely a problem but panting with hyperemic membranes and skin is a clue. The puppy should be turned every 15-20 minutes and its temperature monitored. The warming process is essential prior to attempted feeding. Below a body temperature of 94°F, GI motility decreases and the suckle reflex becomes ineffective. Below 85°F there is gastrointestinal stasis, a decrease in heart rate, and hypoglycemia. Once below 70°F, the neonate appears dead, with a very slow heart rate of 40-60 bpm and an occasional chest excursion. A healthy newborn without an external heat source can only maintain a body temperature 12°F warmer than its surroundings. Hypothermic patients should be rewarmed slowly (1-2 hours) to a temperature of 98°-99°F. Warming increases the respiratory and heart rates; increases effectual nursing and swallowing reflex; increases GI movements; and mobilizes glucose stores. Dehydration can be corrected by use of subcutaneous fluids or orogastric intubation. Administration of subcutaneous fluids can be taught by a veterinarian, and is easy to perform. A dose of 3-5 ml per 100g should be sufficient to correct mild to moderate dehydration. Water or electrolyte solutions, warmed to body temperature, can be administered via tube feeding. Do not force the sick neonate to drink (i.e., use of an eyedropper or syringe) due to the risk of aspiration pneumonia. Hypoglycemia typically occurs within 24 hours of fasting in the healthy neonate, but more quickly in the toy breed or sick neonate. It occurs due to higher glucose requirements, lower ability to synthesize new glucose and less glucose stores than in adults. In the sick neonate, hypoglycemia is one of the most common problems. Acute blindness or other visual problems, nystagmus, incoordination, lethargy, depression, muscle tremors, seizures, coma, and death can all occur with hypoglycemia. Unfortunately, these symptoms can also be associated with numerous other common and uncommon neonatal illnesses. If the neonate is conscious and able to swallow, oral dextrose supplementation with a few drops of Karo syrup, honey or Nutri-cal can be attempted. Isotonic glucose (no more than 5% dextrose) can be given subcutaneously. Solutions with greater than 5% dextrose or hypertonic solutions should not be administered under the skin due to the high risk of skin sloughing. If the animal is unconscious, immediate veterinary attention is necessary. The moderately to severely ill neonate: This includes the severely dehydrated, unconscious, seizing or severely pothermic neonate (Body temp < 85 F). Very ill neonates should be treated by veterinarian familiar with neonatal conditions. Vascular access, through intraosseus or IV catheters, should be obtained. Warmed fluid boluses of 45ml/kg should be initiated, followed by fluid rates of 100-180 ml/kg/day. LRS is the preferred crystalloid since neonates can use the lactate as an energy substrate. Dextrose supplementation (up to 5% in peripheral IVs) and potassium supplementation may be necessary as dictated by careful monitoring. Active warming with warmed IV or peritoneal fluids can be performed. Passive rewarming is best achieved with a circulating warm water blanket and an infant incubator. Once hypothermia is corrected and is bowel sounds are present, tube feedings can be administered. Hypoxia (low oxygen levels in the blood) may occur in neonates from difficult whelping, pneumonia, lung atelectasis or aspiration of pneumonia. If hypoxia is suspected or if the puppy is cyanotic, then oxygen supplementation is indicated. Specific neonatal syndromes Fading puppy syndrome is not a specific disease process, but encompasses a large number of diseases than can cause death in the neonatal period. Sick neonates often look the same regardless of the underlying condition, and most of the diseases as lumped together under the title of fading puppy syndrome. Because of the similar nature of the clinical signs, a specific disease etiology is rarely diagnosed. Diseases such as Brucellosis, low grade bacterial sepsis, viral infections (especially herpes virus) and toxoplasmosis have been incriminated in the fading syndrome. Other factors such as maternal neglect or trauma, environmental problems, poor colostral intake or inadequate milk production, and congenital defects including inborn errors of metabolism have been proposed. Recent evidence shows that puppies dying of fading syndrome have below normal surfactant production (the substance that helps keep the lungs open and filled with air). Why this occurs is not known. Timely necropsy performed by a trained pathologist is the best bet for a specific diagnosis to prevent major losses in the litter. Even then, special tests are needed to for culture of bacteria and viral testing. Dead puppies should be refrigerated (never frozen) and necropsied as soon as possible after death. Septicemia is a common disease in puppies. Remember that puppies born sterile, and develop a bacterial flora based on what is carried by the dam and in the environment. The developing immune system is not able to fight off bacterial and viral threats as efficiently as the adult immune system. Bacteremia is the presence of bacteria in the blood, whereas septicemia is the host response to infection, characterized activation of the immune, coagulation and endothelial systems. Points of entry include the GI, respiratory, umbilical, urinary and dermal systems. The signs of septicemia vary with the severity and underlying cause of the condition. Most clinical findings are not specific for septicemia and may be overlooked on initial physical exam. Per-acute death with any clinical signs can occur occasionally. More common clinical signs include: vocalization, restlessness, weakness, hypothermia, dehydration and shock. Petechial hemorrhages may be present. In severe cases there may be discoloration and/or sloughing of extremities. Keeping the whelping box scrupulously clean is imperative. A soiled whelping box will greatly increase bacterial loads, and exposure to other sick neonates or a sick dam will spread disease. Skin infections, especially umbilical infections, caused by unsanitary conditions can rapidly become systemic without proper care. Septicemia may be compounded by lack of colostrum intake. Neonates should be treated with antibiotics, fluids, and supportive care. Post-Operative Monitoring and Management The postoperative period is also a very important time for patient monitoring. Although advanced skills are required to ensure patient safety during anesthesia and through the operative period, vigilance is also required when the patient emerges from anesthesia and begins the recuperative phase. Numerous complications can arise in the postoperative period. Attentive care during this period can identify these complications at an early phase when therapeutic intervention is often more likely to be successful. Vital Sign Monitoring The most crucial factor in identifying postoperative complications is frequent and complete assessment of the patient's vital signs. These include temperature, pulse rate and quality, respiratory rate and effort, and blood pressure. For any patient who is not "doing well" after surgery, the above vital signs, plus a PCV/TS and blood glucose, are the first things that should be checked. Increased Temperature Regardless of cause, an increase in body temperature causes an increase in cellular metabolism, an increased oxygen demand and therefore a higher cardiac output to meet the demand. Significant cardiovascular changes occur with increases in body temperature such as tachycardia and decreased afterload as a result of peripheral vasodilation. At core temperatures greater than 105.5-106ºF delivery of sufficient oxygen to cells begins to fail and widespread cellular injury occurs. Massive endothelial cell injury results in disseminated intravascular coagulation. Acute renal failure, hepatic failure and respiratory injury are also common sequelae. Elevation of patient temperature has two important causes: pyrexia and hyperthermia. Pyrexia occurs when circulating inflammatory mediators cause the patient to have a fever response. In this condition, the hypothalamic setpoint is increased because of production of prostaglandins. The broad rule-outs for pyrexia are: infection, inflammation, CNS disease, and neoplasia. In the very immediate post-operative period (<8 hours), surgical site infection is uncommon. Pyrexia is a normal physiologic response to tissue damage or microbial invasion. It is appropriate to treat the patient's fever by administering antipyretic drugs and attempting to cool the patient. It is not appropriate to attempt to cool the patient without administering antipyretic drugs as this is the equivalent to opening the doors and windows on a cold winter day when you have the thermostat on your furnace set to 80ºF. The furnace (body) in that situation responds to the attempts to cool by increasing its heat production to maintain the temperature set on the thermostat. Antipyretic drugs such as NSAIDs should be administered to stop the prostaglandin production that is elevating the setpoint. The type of patient cooling that is administered is very important. When the patient's temperature is above 105.5-106ºF, cooling efforts applied to the patient's periphery (alcohol, cool water, ice, fans) can have a detrimental effect. In such situations, the patient is relying on conductive heat losses from widespread vasodilation. Cooling the limbs, head or neck in such situations can vasoconstrict the patient and lock the heat into the patient's core where it may cause severe injury. In such situations, core cooling techniques should be employed first to cool the patient from the inside out until the temperature falls into a safer zone. One core cooling technique that is very effective is to aseptically prepare the skin to the right and cranial to the umbilicus and administer room temperature isotonic crystalloids into the abdominal cavity through an over the needle intravenous catheter. Up to 20 mL/kg can be administered safely. If more is required, then attempt to allow some of the fluid to drain from the abdomen and replace it with fresh fluid. A second method involves administration of room-temperature isotonic crystalloid fluids. In all cases, a vigilant search for a possible infection should take place to determine the source of the fever. Hyperthermia is the second cause of elevation of patient temperature. It is different from pyrexia because no change in the patient's hypothalamic temperature set point occurs. The elevation in temperature occurs because the patient is producing heat faster than it can be dissipated, or because of warm environmental conditions. Most commonly this occurs in two situations. Excessive muscle activity from tremoring or seizures, or from increased respiratory muscle workload can increase the patient's body temperature. Airway obstruction can also result in an impaired ability to dissipate heat efficiently. Dogs in particular rely on the ability to pant as a very important heat dissipation mechanism and are particularly sensitive to airway obstruction. Brachycephalic patients are exquisitely sensitive to airway obstruction in the postoperative period and thus can become hyperthermic very quickly. Treatment of patients with hyperthermia should be aggressive cooling attempts as described above. The same temperature points should dictate whether peripheral or core cooling efforts should be utilized. Antipyretic drugs should not be utilized when the clinician is convinced that the patient is hyperthermic and not pyrexic. Remember that opioids in cats can cause hyperthermia, with reported body temperatures up to 106 F. Decreased Temperature Hypothermia is common in the postoperative, post-anesthetic period. Heat loss during the surgical period can be extensive, particularly for small patients. Hypothyroid patients are also particularly vulnerable to hypothermia because of their inability to increase metabolic rate and heat production effectively. Numerous physiological changes occur when body temperature is decreased. Initially, peripheral vasoconstriction occurs in an attempt to preserve temperature of core structures. In addition, all enzyme systems slow down. As the core temperature continues to drop, the myocardium continues to lose strength and at severe temperature drops, arrhythmias are the most common cause of death. Just as peripheral cooling can potentially be detrimental to a patient with a severe elevation in body temperature, so too, can peripheral warming be detrimental to a patient with hypothermia. If significant vasoconstriction has occurred for a long enough duration, then the lack of blood supply causes anaerobic metabolism to occur and waste products of cellular metabolism are not removed. If warmth is applied to the peripheral tissues, vasodilation results. The resulting blood that is returned to the heart is still colder than the core temperature and contains high concentrations of waste products. Thus, at core temperatures lower than 92-95ºF, particularly if the patient has been at that core temp for several hours, core rewarming should take place prior to peripheral warming techniques are applied. Core rewarming can be accomplished in a similar fashion to cooling described above. The temperature of the fluids should be approximately 102ºF. Fluids can be microwaved, mixed well, and 3ml removed through puncture of the bag. Withdraw the syringe plunger, and place a patient thermometer in the fluid. This can be repeated until the fluids reach the appropriate temperature. Increased Heart Rate Tachycardia can have many causes. The definition of tachycardia differs depending on the size of the patient and their normal resting heart rate. It is different between breeds and sometimes between individuals within a breed depending on their level of athleticism. Tachycardia should be treated because it reduces cardiac output by not allowing sufficient time for diastolic filling, and it increases myocardial oxygen demands. Over time, a hypoxic myocardium will become predisposed to arrhythmias and possible fibrillation. Ventricular arrhythmias are frequent causes of tachycardia in the postoperative patient, and should be differentiated from supraventricular tachycardia by ECG. Sinus tachycardia is the most common cause of tachycardia in the postoperative patient. Potential causes include: hypoxemia, pain and anxiety, hypovolemia, anemia, electrolyte disturbances and primary cardiac diseases. In the tachycardic patient, the following treatment algorithm can be followed. First, pain should be treated if the animal appears painful on gentle palpation or manipulation of the surgical site. A response to analgesics, such as a bolus of fentanyl 2-5 mcg/kg IV, hydromorphone 0.1-0.2 mg/kg IV or methadone 0.2-0.5 mg/kg IV can help to determine if pain is responsible for the tachycardia. Next, a bolus of crystalloids at ¼ of the total shock dose can be administered. Patients with open abdominal or thoracic procedures can have huge evaporative fluid losses, and it is very easy for these patients to become hypovolemic even with adequate fluid rates during anesthesia. If the heart rate decreases during fluid administration, then slowly increases as the fluids redistribute into the interstitial space, a second bolus may be necessary (either crystalloids or colloids). The anxious patient should respond to administration of anxiolytic drugs such as phenothiazines, benzodiazepines, or alpha-2 agonists. If there is no response to the above treatments, provide supplemental oxygen with a face mask or nasal cannula. Finally, a PCV/TS should be checked. Significantly anemic patients will respond to red blood cell transfusions or hemoglobin based oxygen carrying fluids (HBOC) such as Oxyglobin. If there is still no response to therapy, a search for an underlying cardiac cause should be performed. Ventricular tachyarrhythmias are common following splenectomy or GDV surgery. VT should only be treated if is causing cardiovascular instability (either hypotension or tachycardia), or if there is a high potential for fibrillation (multifocal or R-T phenomenon). I follow the above treatment algorithm first when treating VT, and also monitor electrolytes for severe hypomagnesemia, hypocalcemia or hypokalemia. Lidocaine is the drug of choice for treatment in dogs. A 2 mg/kg bolus followed by a CRI of 50-80 mcg/kg/min is usually helpful in treatment. Decreased Heart Rate Bradycardia is almost always caused by a conduction disturbance within the myocardium. Various forms of heart block can be diagnosed using an electrocardiogram. Several factors can contribute to the development of sinus bradycardia. Some patients develop alterations in sympathetic and parasympathetic tone following major surgery. Excessive parasympathetic tone, especially when it is combined with the bradycardic effects of some drugs such as opioids and alpha-2 agonists that are routinely utilized in the postoperative period, can result in significant bradycardia. Provided the patient is resting comfortably, is experiencing no syncopal symptoms, and has adequate blood pressure then severe bradycardia generally has no adverse effects. Large breed athletic dogs in particular can have resting heart rates during sleep of 35-40 beats per minute without consequence. Vagally mediated bradycardic events are a frequent source of cardiopulmonary arrest in the intensive care unit. Most often, these events occur during vomiting, defecation, or coughing events that are predominantly parasympathetically controlled. Frequently, such events take place so rapidly that prevention or intervention is not possible. Periodically, vagal events in patients who are being monitored with an electrocardiogram can be detected and treated with parasympatholytic drugs prior to complete cardiopulmonary arrest. Another rare cause of bradycardia to consider in patients with intracranial disease and with an increased risk for developing intracranial hypertension is the Cushing's reflex or Cushing's response. This response occurs due to a decrease in perfusion to the sympathetic center in the brainstem. A massive sympathetic output occurs to attempt to increase the mean arterial blood pressure, thereby increasing the cerebral perfusion pressure by increasing the differential between intracranial pressure and mean arterial pressure. The elevation in blood pressure causes a reflex bradycardic response from the carotid baroreceptors. Patients with the Cushing's reflex typically have alterations in mental status, significant hypertension (systolic > 180 mmHg) and concurrent bradycardia. Treatment for the intracranial hypertension with hypertonic solutions such as mannitol usually causes resolution of the Cushing's reflex and the associated bradycardia. Increased Respiratory Rate or Effort An increase in respiratory rate and/or effort can accompany many potential postoperative complications. In general, respiratory rate is tightly regulated to control carbon dioxide concentrations in the blood. Patients with severe metabolic acidosis will have an increase in respiratory depth and effort before the respiratory rate will increase noticeably. It is important to identify the dysfunctional anatomic contributors in order to provide effective intervention. Most commonly, postoperative patients will experience parenchymal or pleural space disease, or upper airway obstruction. Patients with symptoms of parenchymal disease (inspiratory/expiratory effort, crackles or wheezes) should have thoracic radiographs if they are stable. If there is evidence of pulmonary infiltrates present, then cardiogenic and non-cardiogenic causes should be eliminated if possible. Common non-cardiogenic causes include aspiration pneumonia and acute lung injury from the systemic inflammatory response syndrome (SIRS-see below). A complete blood count is also often helpful in determining the underlying cause. If aspiration pneumonia is suspected, then a transtracheal wash to obtain secretions for cytology and bacterial culture and sensitivity should be considered if the patient is stable. Broad spectrum antibiosis should be initiated until the culture and sensitivity results have been obtained. Arterial blood gas analysis and pulse oximetry are appropriate ways of determining when oxygen supplementation is needed for such patients. Sedation may be helpful for patients experiencing significant respiratory distress accompanying their underlying disease. Butorphanol (0.05 mg/kg IV) or morphine can be used for sedation. Patients with pleural space disease (inspiratory/expiratory effort, dull or absent lung/heart sounds) should have a diagnostic/therapeutic thoracocentesis performed. Causes for pneumothorax following surgery include: excessive ventilation/high pressure bagging, closed pop-off valve, pre-existing lung disease, and a discontinuous diaphragm (i.e., nicking the diaphragm while performing a gastropexy). When the pleural space has been evacuated as completely as possible, thoracic radiographs should be performed. If the pneumothorax is continuous or recurrent, a chest tube should be placed. Pleural effusion as a post-operative complication is rare, and tends to be limited to overhydration in cats with cardiac disease. Upper airway obstruction is a very common postoperative problem, especially in brachycephalic breeds. Swelling or injury due to endotracheal intubation is frequent. As a result, significant obstruction can occur and the patient that had very little reserve can decompensate quickly. Patients with upper airway obstruction will have a marked abdominal component to their breathing pattern and will have stridorous airway noises. As they become hypoxic, more frantic efforts to breathe result in a vicious cycle of worsening airway distress. If the patient is experiencing anxiety, then sedation is an important component of management. If the patient is sedated and will tolerate large bore oropharyngeal tube placement without chewing on the tube, then placing a tube past the redundant soft palate but not into the larynx may provide an improved airway. If neither of these results in rapid relief of the airway obstruction then induction of anesthesia and reintubation may be required. Common sedatives include acepromazine (in the cardiovascularly stable patient) 0.02-0.05 mg/kg IV or butorphanol (for the patient not on other opioids) 0.05 mg/kg IV. An increase in respiratory rate and effort that is not accompanied by any abnormal auscultatory findings may be due to high levels of circulating catecholamines. Common causes of such problems include: pain, anxiety, shock syndrome or anemia and should be investigated promptly. If all of these can effectively be ruled out, then the patient should be evaluated for the possibility of a pulmonary thromboembolism. Decreased Respiratory Rate or Effort There are very few reasons for a patient to experience a decrease in respiratory rate or effort. Some considerations include: excessive sedation from drugs such as opioids, benzodiazepines, alpha-2 agonists or other anesthetic agents. Neurologic injury of the cervical spinal cord or neuromuscular disease that affects diaphragmatic function can also produce a decrease in respiratory efforts. Arterial blood gas analysis is warranted in all such patients to determine if intervention is warranted. Patients with carbon dioxide retention should be observed carefully for worsening condition or the need for mechanical ventilation. Increased Blood Pressure Catecholamine-inducing conditions such as pain or anxiety are the most common causes of hypertension in otherwise healthy patients. Another common cause is inappropriate use of blood pressure monitoring equipment that results in falsely elevated pressure. A rare cause of hypertension is the Cushing's reflex described previously. Patients with preexisting hypertension can create a challenge. As hypertension increases in such patients, the natural zone of autoregulation increases. A decrease in mean blood pressure from 150 to 100 mmHg in such patients is the equivalent of a decrease of 100 to 60 mmHg in a normal patient with the same consequences. As a result, known hypertensive patients should be monitored vigilantly to prevent ischemic consequences. Such patients are also likely to experience hypertensive crisis when their preexisting hypertension is exacerbated by postoperative pain or anxiety. It is also important to remember that alpha-2 agonist medications often result in mild hypertension. Decreased Blood Pressure Hypotension is a common but severe finding in postoperative patients. It is important to verify a finding of hypotension several times due to the inaccuracies inherent in blood pressure measurement. Remember that Doppler blood pressures will trend towards the mean pressure in hypotensive patients; however, there is significant variation in where that change occurs. A mean arterial pressure of 60 mmHg and/or a systolic blood pressure of 90 mmHg are considered minimally acceptable. Primary rule outs for hypotension include: medication induced, hypothermia, shock, and vasodilation. First, analgesic and sedative medications should be investigated for a possible cause. Acepromazine, dexmedetomidine and other ?-2 agonists are the most likely to cause hypotension. Opioids and benzodiazepines tend to be very cardiovascular sparing, although in very high doses they may cause mild hypotension. If blood pressure falls below acceptable limits, medications should be reversed if possible. If the blood pressure does not increase, then the following steps should be taken. Hypovolemia (especially when combined with hypothermia) is another common cause of hypotension. A fluid challenge of 10-22 ml/kg (dog) or 10ml/kg (cat) of isotonic crystalloids should be administered. If the blood pressure temporarily increases, another dose of crystalloids or a dose of colloids (5ml/kg) should be given, up to a total shock dose. If hypothermic, the patient should be actively rewarmed as described above. Hypothermia blunts the sympathetic nervous systems response to catecholamines and results in decreased vascular tone. Almost all hypotensive patients will have a shock syndrome. Appropriate intervention for the type of shock thought to be present should be titrated to effect for each patient's condition. Volume resuscitation, inotropic and vasopressors medications and thrombolysis or surgical intervention may all be appropriate depending on the underlying mechanism of cardiovascular dysfunction. Increases in the packed cell volume (PCV) and total solids (TS) It should be noted that PCV for two main reasons: 1) to estimate the oxygen carrying capacity of the patient i.e. the red blood cell count and 2) as an indication of the hydration status of the animal. Remember that the PCV is a ratio of red blood cells to the plasma volume; therefore it may be altered if there is a change in either of these parameters. The total solids are an indication of the concentration of plasma proteins and a very rough estimate of the colloid oncotic pressure. These two parameters tend to trend in the same direction in the post surgical period. There are very few reasons that a patient demonstrates an increase in the PCV and TS in the postoperative period. The most common cause is due to hemoconcentration or in other words a loss of free water. This may occur if the evaporative losses during surgery were extensive, the pre-operative resuscitation was inadequate or if the animal has a fever or is hyperthermic. However, hemoconcentration is not a requirement in making a diagnosis of dehydration. It should also be noted that the sensitivity and specificity of these two parameters are not equal. An alteration in the total solids is more sensitive and specific in making a diagnosis of dehydration than are changes in the PCV. An increase in PCV with concurrent decrease in TS is commonly seen postoperatively in patients with sepsis or SIRS. If these alterations are noted in the postoperative period, then volume resuscitation is indicated. The fluid plan should include stabilization of the intravascular volume (titration of boluses of fluids to specific hemodynamic end points) and then rehydration of the tissues. Decreases in the packed cell volume and total solids There are several reasons why the PCV and TS is low in the post-operative phase. The most common is due to crystalloid administration during the surgical procedure. The animal has undergone a relative salt and water gain, has therefore diluted out the PCV/ TS and the kidneys have not yet had a chance to excrete this excess fluid. Please note that the only way the oxygen carrying capacity of the blood can alter in this scenario is if there are actually loss of red blood cells (discussed below) and not just an alteration in the PCV. In the majority of cases the patient is able to excrete this excess in the next several hours and their vital signs tend to be within normal range. Serial PCV and TS are performed in order to rule out the presence of ongoing hemorrhage. The second most common cause is post-operative hemorrhage. However, since whole blood is being lost the 2 parameters, which make up the PCV (RBC and plasma) are both equally affected. The ratio between the two remains relatively the same and it is only when fluid shifts from the other body compartments (tends to take 4 to 6 hrs to occur) or exogenous fluids are administered is a decrease in the PCV noted. However, splenic contraction can complicate the matter by increasing the PCV but not the TS. Therefore, in the post-operative period several parameters are utilized to identify the presence of ongoing hemorrhage; vital signs, the blood pressure, the degree of change in serial PCV's and TS, the difference between the PCV and TS and the type of surgery that was performed. A relative decrease in TS with only a mild decrease in PCV is an indicator of ongoing hemorrhage in the dog. Therapy consists of stabilization of the intravascular volume by the administration of packed red blood cells, colloids, crystalloids and or whole blood. The end-point to this fluid resuscitation is to normalize the vital signs, blood pressure and allow oxygen delivery to the tissue without causing further hemorrhage. There are other complications associated with administration of large volume of crystalloids; activation of the inflammatory/coagulation cascade (see below), dilution of coagulation factors and platelets, and increased permeability to the endothelium. Postoperative complications can lead to a Systemic Inflammatory Response (SIRS) Why do we spend so much time and money monitoring our ICU patients? We are concerned that if the tissues do not get enough oxygen, they cannot make enough energy to survive. Obviously, if this occurs to enough cells the organism cannot live and this is not an ideal outcome. In evolution there has been the development of two closely connected pathways that are able to judge this - the inflammatory and coagulation systems. These pathways are initially involved in the healing process and recovery, however if the damage hits a critical point, or is severe or a second incident has occurred, these pathways switch from being protective to causing severe injury. The pathways consist of the inflammatory cascades (white blood cells, arachandonic acid, complement, cytokines, reactive oxygen species and inflammatory mediators, to name a few) and the coagulation cascade. In vivo these systems are so closely intertwined that if one is active, so is the other. This process is called the Systemic Inflammatory Response Syndrome (SIRS). There are a number of triggers which result in activation of this response; tissue trauma, transfusion reactions, burns, pancreatitis, reperfusion injury, post CPCR resuscitation, hyperthermia, hypothermia, immune mediated diseases and infections. If the initiating trigger is due to an infection, be it viral, protozoal, fungal or bacterial, the process is called sepsis. However, the exact same pathways and processes are being activated if no infectious agent is involved. The clinical criteria for SIRS are based upon an adaptation of human SIRS criteria. Unfortunately, depending on the criteria used, the sensitivity is only 77-97% and the specificity is only 64-77% in dogs meeting SIRS criteria. In order to meet SIRS criteria, two or more of the following must be met in the dog: There are some sources that argue that tachypnea in the dog should be considered at a RR > 40 bpm and/or a PaCO2 < 30 mmHg, instead of 20 bpm. The reasoning behind this is that many dogs have a normal respiratory rate up to 30 bpm, so making the SIRS criteria more stringent would make the likelihood of truly diagnosing SIRS a lot greater. SIRS criteria in the cat are slightly different than the dog and the cat must have two or more of the following in order to meet SIRS criteria:   |