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Stabilization of the Emergency Patient

Massey University Seminar – May 2006

Stabilization of the Critical Patient
Philip R Judge BVSc, MVS, MACVSc Senior Veterinarian Animal Emergency Centre Melbourne

Introduction
Critically ill patients often have multiple life-threatening problems, and can present a challenge, to even the most experienced clinician. Prioritization of treatment in these patients should be directed at the most immediate life-threatening problems, followed by a full body systems review to enable effective treatment to be directed at the underlying cause of the patients illness. When a traumatized, or critically ill patient arrives at the Emergency Centre, the patient is managed in most instances in a manner consistent with the following general principles. 1. 2. 3. 4. 5. 6. 7. 8. 9. Perform and Primary Survey and Triage Classification Emergency Management of Airway Restore Normal Pleural Pressure Restore and Maintain Normal Ventilation Provide Fluid Therapy to Improve Tissue Oxygenation and Cardiovascular Function Provide Supportive Care for the Neurological System Perform Full Body Systems Examination Definitive Management of the Underlying Disorder Supportive Management of Each Body System

 Perform a primary survey - a primary survey is a rapid clinical examination designed to assess the  patient for the presence of any life-threatening abnormalities. The examination should take no longer than 1 minute to perform. Life threatening abnormalities in patients are most commonly associated with disorders of the airways (obstruction), breathing (airway obstruction, pleural space disease, pulmonary parenchymal disease, thoracic wall disease, and respiratory paralysis) cardiovascular system (shock - hemorrhagic, septic, hypovolemic) and neurological function (seizures, depression, coma, paralysis)  Perform triage - triage is necessary when there is more than one patient presenting to the  emergency centre at the same time. Accurate triage will ensure that the patients with the most severe injuries are seen first, while those with less severe injuries are seen at the next earliest opportunity. There are several triage systems in use in emergency rooms, An example is as follows

© Philip R Judge 2006

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Stabilization of the Emergency Patient

Massey University Seminar – May 2006

 Class I - most urgent, these patients must receive treatment immediately, within seconds.  Examples include traumatic respiratory failure, cardiorespiratory arrest, airway obstruction, and ALL unconscious animals  Class II - are those patients that require treatment within minutes. Examples include all  patients suffering multiple injuries, shock, or bleeding, but have ‘adequate’ ventilatory function.  Class III - are those patients with serious injury requiring attention within an hour - these  patients may have fractures, open wounds etc, but without active bleeding, shock, or altered mentation  Class IV - are those patients that require attention within a few hours and include those  patients that present several hours following trauma, with lameness, anorexia etc

Management of Life-Threatening Abnormalities
Just as the primary survey, and triage classification are performed with systems oriented priorities, so is resuscitation. Airway disruption and blockage are the highest priority. Respiratory system difficulties not directly associated with airway obstruction are the next priority. Life-threatening cardiovascular emergencies are the third priority, and neurological function follows.

Airway Management Priority 1: Secure a Patent Airway
Management of Airway Obstruction Etiology of airway obstruction  Brachycephalic upper airway obstruction syndrome   Pharyngeal trauma, basilar skull fractures, pharyngeal hematoma, or allergic reaction to an insect  bite or sting resulting in pharyngeal edema  Laryngeal edema   Laryngeal paralysis   Foreign body in pharynx, larynx, or major airway   Neurological disorders (central or peripheral) may lead to loss of laryngeal tone and gag and swallow  responses, resulting in airway obstruction  Encroachment on proximal airway lumen by an extra-mural mass or foreign object   Blood clots or mucus present in the larynx, trachea, main-stem bronchi. The source of bleeding can  be the lungs (results in bubbles or foam seen in the trachea), trachea, larynx, or oral cavity. Aspiration of saliva, and/or gastric and esophageal contents may also result in airway obstruction. A liquid aspirate of about .25ml/kg with pH of 2.5 can produce a fatal obstructive bronchospasm, and acute chemical pneumonitis, direct trauma to larynx induces laryngo-spasm, trauma to airways, foreign body © Philip R Judge 2006

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Stabilization of the Emergency Patient

Massey University Seminar – May 2006

Clinical signs of airway obstruction  Prolonged inspiratory phase, inspiratory dyspnea. (Note: if obstruction is present in the thoracic  trachea, or bronchi, there is usually an expiratory component to the dyspnea) extended neck, lips drawn back (accessory muscles of respiration are activated)  Cyanosis - is a late and unreliable sign of airway obstruction. The presence of cyanosis demands  immediate action to secure the patient airway and restore ventilation Note: with complete airway obstruction, no breath sounds are heard on thoracic auscultation.  Partial obstruction may not give rise to clinical signs until over 75% of the airway is compromised  Treatment of airway obstruction  Provide supplemental oxygen therapy at all times while evaluating respiratory function, until it is  confirmed that the patient does not require supplemental oxygen  Gently extend the head and neck, pull the tongue forward, and clear the mouth of blood, mucus and  vomitus  Suction the larynx if required   Intubation (laryngoscope preferred to minimize damage to the airway during intubation)   Sedation/anesthesia for intubation – patients with airway obstruction are hypoxic and hypoxemic, and  are EXTREMELY sensitive to the effects of anesthetic and sedative agents frequently used in veterinary medicine. In general, the safest anesthetic to use in the emergency is the anesthetic with which you are most familiar. However, some anesthetics are safer than others are. The authors preference is to sedate any patient in which intubation cannot be achieved without chemical restraint, using an intravenous bolus of diazepam at 0.1-0.3 mg/kg. If diazepam alone is insufficient to allow endotracheal intubation, addition of ketamine to effect (1-5 mg/kg IV), or fentanyl (1-4 micrograms/kg IV) are preferred agents  If orotracheal intubation is not possible, perform an emergency tracheostomy 

© Philip R Judge 2006

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Stabilization of the Emergency Patient

Massey University Seminar – May 2006

Procedure for Tracheostomy  Make a ventral midline incision from the manubrium (anterior sternum) to the laryngeal cartilages   Part the sternohyoid muscles on the midline by blunt dissection   Continue blunt dissection down to the tracheal rings   Blunt dissect around the circumference of the trachea, and elevate the trachea using artery forceps  placed around the trachea  Make an ‘H’ incision through the tracheal rings, or transverse incision between tracheal rings   Place stay sutures through the tracheal rings - one on each side of the incision   Insert the tracheostomy tube. The tube should be 2/3 to 3/4 the diameter of the trachea, and  should have a high volume/low pressure cuff. Only inflate the cuff if positive pressure ventilation is required, or if it is necessary to prevent aspiration of oropharyngeal contents.  Fasten the tube to the patient by tying it around the patients’ neck with umbilical tape or gauze 

Airway Management Priority 2: Restore Normal Intra-pleural Pressure
Pleural Space Disease - pneumothorax, tension pneumothorax, hemothorax and diaphragmatic hernia
Pleural space disease occurs commonly following catastrophic trauma. In addition, intrathoracic neoplasia, congestive heart failure, cardiac tamponade, and emphysematous bulla and all lead to the presence of pleural space disease in non-traumatic patients. The presence of pleural space disease decreases effective pulmonary reserve, and interferes with normal gas exchange and tissue perfusion and oxygenation. Animals suffering from pleural space disease appear anxious, and may have an exaggerated respiratory effort, frequently with prolonged expiration, or biphasic expiration with an abdominal grunt at the end of expiration.

Pneumothorax is the most common pleural space disease encountered in patients with multi-system trauma. A description of the approach to pneumothorax follows

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Stabilization of the Emergency Patient

Massey University Seminar – May 2006

Pneumothorax Etiology of pneumothorax  Trauma with rupture of alveoli secondary to increase in intra-thoracic pressure against a closed  glottis  Direct penetration of thoracic wall (sharp objects, rib fractures)   Rupture of major airway. Note that major airway rupture will also cause pneumomediastinum  Pathophysiology of pneumothorax  The pleural space is normally at sub-atmospheric pressure, with a small amount of fluid forming a  cohesive bond between the lungs and parietal pleura. If air enters the pleural space, the cohesion is lost and the lungs collapse.  The initial response of the patient is tachypnea, leading to decrease in blood carbon dioxide, and  increasing blood pH. Hyperventilation increases the efficiency of gas exchange BUT it does increase patient energy needs, and compounds cellular hypoxia.  As a pneumothorax becomes worse, compensatory mechanisms fail, and the patients develop  hypercapnea, acidosis and death  It is interesting to note that dogs and cats can increase the degree of chest wall expansion by 2.5-3.5  x normal during compromised pulmonary function Definitions  Open pneumothorax – A pneumothorax in the presence of an open chest wound   Closed pneumothorax – A pneumothorax in the presence of an intact thoracic wall; tears in visceral  pleura and pulmonary tissue result in pneumothorax  Valvular pneumothorax – is a form of closed pneumothorax, in which air enters the pleural cavity  chest during inspiration. This causes a tension pneumothorax. Causes include traumatic lung injury, emphysematous bulla rupture, lung granulomas, and lung cysts.  Tension pneumothorax - results in a progressive increase in intra-pleural pressure, resulting in  impaired chest expansion, and collapse of intra-pleural blood vessels, elimination of the thoracic pump of venous return, decreased cardiac output, and rapid patient decompensation and death

Clinical signs Clinical signs of pneumothorax include some or all of the following  Tachypnea   Anxiety   Restlessness   Cyanosis   Pale mucous membranes   Mouth breathing  © Philip R Judge 2006  Barrel-shaped thorax   Inspiratory +/- expiratory effort increased 

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Stabilization of the Emergency Patient

Massey University Seminar – May 2006

The approach to the patient with pneumothorax  A respiratory rate of 45-60 breaths per minute, or the presence of supportive clinical signs indicates  thoracocentesis is required  Thoracocentesis - NOTE: be prepared to evacuate the entire pleural space at the first attempt at  thoracocentesis. Thoracocentesis – The Procedure Clip and prep intercostal spaces 5-11 on both sides of the chest, infiltrate lignocaine into intercostal space 6-7. Insert a 22 g needle attached to 3-way stopcock extension set and 10ml - 20ml syringe, into chest cavity, at the level of the rib 6-7 intercostal spaces. If air is suspected in the pleural cavity, insert the needle at the junction of upper and middle 1/3 of the rib cage; if fluid is suspected in the pleural space, the needle should be inserted at the junction of middle and lower 1/3 of the rib cage ALWAYS, ALWAYS DRAIN BOTH SIDES of the chest cavity, due to compartmentalization of the thoracic cavity with mediastinal anatomy in dogs and cats. Drops of saline or lidocaine placed in hub of needle prior to introducing into chest cavity can serve as indicator of entering chest cavity, and the presence of a tension vs. a closed pneumothorax  When to Consider Placement of a Chest Drain   Insert chest drain 10-20fr tube at the 7th intercostal space if indicated using the following  criteria  If thoracocentesis is required more than 4 times during the first 4 hours of admission to  hospital  Air +/- blood is being aspirated on repeated thoracocentesis attempts   Patients status is not significantly improving despite adequate oxygen therapy, fluid support,  and the continued presence of active pleural space disease  Vacuum cannot be established using simple aspiration via thoracocentesis   If pneumothorax is failing to resolve in 36 hrs, consider thoracotomy to evaluate problem  If the patient does not respond to therapy for pneumothorax, or continues to deteriorate despite therapy, a major air leak in a bronchus, or thoracic trachea is suspected; or thoracic or abdominal bleed (indicated by blood in thoracic or abdominal cavity, or failure of improvement in cardiovascular function despite appropriate fluid therapy). Further diagnostic evaluation, including thoracic and abdominal ultrasound, DPL, +/- radiography is warranted. In some instances, emergency surgery may be indicated to locate and rectify the problem, so that effective respiration and cardiovascular performance can be established.

© Philip R Judge 2006

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Stabilization of the Emergency Patient

Massey University Seminar – May 2006

Airway Management Priority 3: Restore and Maintain Adequate Ventilation and Tidal Volume  Administer oxygen with a mask, intranasal, or via endotracheal tube, or trans-tracheal (16-20g needle  percutaneously into trachea if complete upper airway obstruction is present - prior to tracheostomy if required)  Initiate positive pressure ventilation if indicated (See Table 1). It is important to note that  oxygenation assessment using pulse oximetry can be misleading. Table 2 may be used as a guide to determine when ventilatory assistance is required. We consider ventilation in any patient that is receiving oxygen supplementation that has a reliable pulse oximetry reading of less than 90-94%. Table 1: Indications for the Provision of Positive Pressure Ventilation (PPV) Disorders of the Neuromuscular Junction 1. 2. 3. 4. 5. 6. 1. Tick Paralysis Elapid Snake Envenomation Botulism Polyradiculoneuropathy Myasthenia Gravis Muscle relaxants Central Nervous System Disease CNS a. b. c. d. e. f. g. disease causing depression of 1. Shock a. b. c. d. e. 2. 3. increased 4. 5. edema, Sepsis Mediastinal disease Pain Hypovolemic shock Hemorrhagic shock Septic shock Cardiogenic shock Non-cardiogenic shock respiratory drive Head trauma Neoplasia Drugs/medications Toxicity Seizures Infection/inflammation Cerebral intracranial pressure Hypoventilation 1. 2. 3. 4. 5. PIE Neoplasia Pulmonary edema Pulmonary interstitial disease Pulmonary Parenchymal Disease Pneumonia

Pleural space disease

Table 2: Interpretation of Pulse Oximetry Readings SaO2 >95% <89% <75% PaO2 >80% <60% <40% Interpretations Normal Serious Hypoxemia Lethal Hypoxemia

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Massey University Seminar – May 2006

A Note about Pulmonary Contusions Pulmonary contusions are detrimental to the patient, because they impair the oxygenating ability of the lungs. Contusions result from a compression-decompression insult to the thoracic wall, and lead to direct pulmonary capillary disruption, and alveolar damage. Pathophysiology Pulmonary contusions result in intra, and extra pulmonary hemorrhage. Hemorrhage into the alveoli causes interference with the gas exchange unit, causing hypoxia, and increased ventilatory rate and effort mediated via chemoreceptors and the respiratory centre in the brain. Bronchospasm occurs due to pulmonary trauma, and the presence of blood and mucus in the larger conducting airways. The combination of bronchospasm, and fluid in airways reduces airflow within the larger airways and bronchioles. In addition, the presence of blood and cellular debris in the distal airways dilutes surfactant, and results in flooding and collapse of alveoli. The net result is areas within the lung of low and no ventilation, ventilation-perfusion mismatching, and a reduced ability of the lungs to oxygenate blood. Concurrent traumatic injury to the myocardium, the presence of circulatory shock, and intra-pleural diseases (hemorrhage, effusion, pneumothorax, fractured ribs, diaphragmatic hernia, and flail chest) may also interfere with gas exchange and respiration. Within the lung tissue, a secondary inflammatory reaction occurs in response to extravasation of blood, concussive trauma to the lungs, and tissue hypoxia. This reaction is progressive over the first 24-48 hours of injury, and further impairs the ability of the lungs to oxygenate effectively Treatment The management of pulmonary contusions is based on the principles of improving tissue oxygenation, improving pulmonary function and gas exchange, and general supportive care.  Fluid therapy, correction of shock – fluid therapy in the patient with pulmonary contusions has  long been controversial, due to the desire of clinicians not to “flood” the lungs with large quantities of intravenous fluid, which could potentially translocate into the pulmonary parenchyma and airways. To date, there are only limited numbers of studies that have evaluated the ideal fluid resuscitation plan in patients with pulmonary contusions. Two retrospective studies of clinical human patients found no correlation between the nature of fluid resuscitation, and the severity of pulmonary lesions found in patients. Currently there is very little evidence to make a strong recommendation regarding appropriate fluid therapy in patients with pulmonary contusions. However, an understanding of the pathophysiology of pulmonary contusions does justify a conservative approach. We currently recommend a carefully titrated fluid plan, to achieve adequate cardiac output and tissue perfusion, while avoiding excessive venous pressures.  Flow past oxygen, nasal oxygen 

© Philip R Judge 2006

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Massey University Seminar – May 2006

 Mechanical ventilation – a discussion of ventilation therapy is beyond the scope of this  presentation, however, ventilation therapy using lung-protective ventilation techniques, +/addition of positive end-expiratory pressure (PEEP) may be recommended in patients that remain hypoxemic despite oxygen therapy.  Drainage of pleural fluid, stabilization of flail chest  Complications Complications of pulmonary contusions may include pulmonary or systemic infection, the development of lobar cysts, lung lobe torsion, and spontaneous pneumothorax For the remainder of this tutorial, we will concentrate on fluid dynamics during shock, and tissue oxygen delivery.

Pathophysiology and Treatment of Shock
Shock is a condition of severe hemodynamic and metabolic dysfunction, characterized by reduced tissue perfusion, impaired oxygen delivery, and inadequate cellular energy production. Many common disorders lead to shock, including those associated with severe heart failure, hypovolemia, peripheral vasoconstriction, thromboembolism, sepsis, hypoxia (caused by anemia, methemoglobinemia, carboxyhemoglobinemia), heat stress, severe hypoglycemia, and cyanide poisoning.

Patient acute response to circulatory failure or shock fall into the following phases Multiple afferent stimuli, including arterial and venous pressure and volume, osmolality, pH, hypoxia, pain and anxiety, tissue damage, and sepsis, are all integrated by the hypothalamus, which sends signals to the sympathetic nervous system, and adrenal medulla. At the same time, the anterior pituitary initiates a cascade of hormone release in response to the injury. 1. Activation of the autonomic nervous system – sympathetic autonomic neural activity stimulation is immediate, and has the following effects a. b. c. d. e. Increased heart rate – beta-1 adrenergic receptor stimulation Increased myocardial contractility – beta-1 adrenergic receptor stimulation Increased cardiac output Increased peripheral vascular resistance – mediated by alpha-adrenergic arterial construction of skin, voluntary muscle, abdominal viscera, and kidneys Increase in alveolar ventilation – mediated by beta-2 adrenergic receptor stimulation

These effects serve to maintain blood pressure, and increase heart, lung, and brain perfusion.
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Massey University Seminar – May 2006

2.

Release of epinephrine and norepinephrine from the adrenal glands – further augments cardiorespiratory stimulation, and causes hyperglycemia, and elevation of plasma free fatty acids, which serve as an energy source during stress.

3.

Activation of the Renin-Angiotensin-Aldosterone System (RAAS) – release of renin from the juxtoglomerular apparatus occurs in response to decrease pressure in the renal efferent arterioles, and adrenergic stimulation of the juxtoglomerular cells. Renin acts on a serum globulin called angiotensin, converting it to angiotensin I. Angiotensin I is in turn converted to angiotensin II by angiotensin converting enzyme (ACE) in the lungs. Angiotensin is a potent arteriolar constructor. Angiotensin also stimulates the release of aldosterone from the adrenal glands, which increases sodium and water reabsorbtion from the distal tubules in the kidneys, and also augments adrenaline secretion and stimulates ADH release.

4.

Release of Antidiuretic Hormone and Adrenocorticotrophic Hormone – occurs in response to altered serum osmolality, baroreceptors stimulation and physiologic stress response mediated by the limbic system. Water retention and corticosteroid release follows.

5.

Tissue hypoxia – occurs as a result of tissue vasoconstriction and reduced tissue perfusion, mediated by the neurohormonal responses mentioned above. Tissue hypoxia results in decreased ATP production, cell swelling, and the release of the metabolites of arachadonic acid, lysosomal enzymes, phospholipases and proteases, and oxygen free radicals. Complement and immune system activation may also occur in response to tissue invasion by bacteria or their toxins. These compounds produce a wide variety of effects, including significant pulmonary vasoconstriction, systemic vasodilatation, and increased capillary permeability. They are also associated with disruption of capillary endothelial integrity, platelet activation, and the development of disseminated intravascular coagulopathy.

6.

Cell and organ death – occurs secondary to decreased tissue oxygen delivery, and tissue hypoxia. As shock progresses, marked decreases in systemic arterial blood pressure and cardiac output occur, forcing more tissues into anaerobic metabolism and lactic acid production. Microthrombi form in tissue vascular beds, slowing blood flow through tissues, leading to hyperviscosity of blood, hypercoagulation, and organ anoxia and death.

Shock – Effects on Organ Systems Shock produces different effects on different organ systems. The progression of the patient from apparent compensation to decompensation is accompanied by marked alterations in vital organ function – these alterations are outlined below.

© Philip R Judge 2006

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Stabilization of the Emergency Patient

Massey University Seminar – May 2006

Heart Prolonged shock of any cause leads to a decrease in cardiac function associated with the following  Decreased coronary perfusion   Myocardial hypoxia   Reduced cellular ATP production   Metabolic acidosis   Intracellular influx of calcium, and interference with diastolic and systolic function  As myocardial function and compliance reduce, end diastolic pressures rise, further reducing coronary perfusion. Sympathetic activation of the heart increases myocardial oxygen demand in the face of reduced oxygen delivery. Peripheral vasoconstriction further increases left ventricular outflow impedance (preload). The end result is myocardial ischemia, decreased myocardial output, decreased myocardial contractility, and the development of arrhythmias. Lung Hyperventilation is common in patients with shock, and initially results from catecholamine-mediated stimulation. Hyperventilation initially produces a respiratory alkalosis. As shock progresses, hyperventilation occurs secondary to metabolic acidosis. Pulmonary blood flow decreases in untreated shock due to decreased venous return of blood to the heart, and contributes to decreased oxygen transfer at the level of the alveoli and predisposes the lungs to atelectasis. Respiratory failure in untreated shock is multifactorial, and is thought to arise from respiratory muscle fatigue secondary to ischemia and lactic acidosis, failure of the respiratory centre, and the development of pulmonary edema and acute respiratory distress syndrome (ARDS), characterized by interstitial and alveolar edema. Multiple pathologic factors are involved in the development of ARDS, including the following  Increased alveolar capillary membrane permeability   Cardiac failure leading to increased capillary hydrostatic pressure in the lungs   Reduced Colloid Oncotic Pressure due to extravasation of plasma proteins resulting from  increased capillary permeability  Reduced pulmonary lymphatic function due to decreased lung compliance, and the development  of atelectasis  Decreased surfactant production due to hypoxia   Loss of type I alveolar cells (gas exchange), and replacement by type II alveoli resulting in  thickened alveolar septa and impaired gas exchange  Complement activation, cell damage, and lysosomal enzyme release.   Reduced pulmonary compliance, ventilation – perfusion (V/Q) mismatching, and right to left  intrapulmonary shunts

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Stabilization of the Emergency Patient

Massey University Seminar – May 2006

Clinical signs include tachypnea, inspiratory crackles, hypoxemia, and depression Kidneys Initial compensation for decreased renal blood flow is provided by efferent arteriolar constriction, mediated by angiotensin II, which helps to maintain glomerular filtration rate, and through redistribution of intra-renal blood flow to deep cortical nephrons, which is mediated by prostaglandin E 1. However, in untreated shock, continued afferent arteriolar constriction, renal ischemia and necrosis will occur, and is characterized by injured tubular epithelium, interstitial edema, tubular collapse and tubular obstruction with casts and cellular debris Gastrointestinal tract Liver vasoconstriction and ischemia result in centrilobular necrosis, compromised

reticuloendothelial cell function, allowing entry of bacteria into the systemic circulation. Intestine - vasoconstriction and ischemia produce intestinal mucosal hypoxia and necrosis. Hemorrhage and pooling of fluid in the gastrointestinal tract lumen occurs. Damage to the intestinal myenteric plexus results in gastrointestinal tract stasis, which enhances translocation of bacteria and their toxins from the intestinal lumen. Pancreas - intense vasoconstriction in the pancreas causes cell necrosis, release of vasoactive peptides, and other mediators of inflammation Central nervous system Vasodilatation of cerebral afferent vessels occurs in response to central nervous system hypoxia and hypercapnea. Hypoxia occurs secondary to reduced blood flow and oxygen delivery; hypercapnea occurs secondary to increased cerebral metabolic rate, and decreased cerebral perfusion during sustained shock. Cerebral blood flow remains relatively constant until systemic arterial pressure drops below 60mmHg, but becomes directly dependant on systemic blood pressure below this blood pressure. Note that this constant blood flow mechanism ceases to exist in patients with severe hypoxia, hypercapnea and cranio-cerebral trauma.

© Philip R Judge 2006

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Stabilization of the Emergency Patient

Massey University Seminar – May 2006

Specific responses for specific shock states
Hemorrhagic shock
Significant blood loss results in the following  Decreased arterial blood pressure initially, followed by peripheral vasoconstriction and a return to  normal arterial blood pressure  Decreased cardiac output   Decreased central venous pressure   Decreased blood volume reduces perfusion of the lungs, brain and heart   Increased systemic vascular resistance, heart rate, and oxygen extraction by tissues  Physiologic responses increase myocardial contractility, heart rate, and peripheral vasoconstriction. If blood volume is not restored, poor tissue perfusion and inadequate tissue oxygenation lead to metabolic acidosis, increased lactate levels, and base deficits. The initial compensatory response includes increasing heart rate, and myocardial contractility, through the sympathoadrenal axis, and increasing systemic vascular resistance. This tends to maintain arterial pressure in the presence of decreasing blood flow, together with increased oxygen extraction ratios, which improve tissue oxygenation when blood flow is reduced. If blood loss continues, arteriolar vasodilatation caused by local decreases in pH due to lactic acidosis, and falling arterial blood pressure occur. Persistent venular constriction, sludging of blood in capillary beds, and rapid leakage of plasma into the interstitial compartment also occur.

Cardiogenic shock
Acute heart failure from causes other than heart block produce the following  Hypotension   Elevated heart rate secondary to increased sympathetic neural stimulation   Elevated central venous pressure   Elevated oxygen extraction   Decreased cardiac output   Activation of renin-angiotensin -aldosterone system; hypervolemia and edema  An improvement in survival in these patients is dependant on improving stroke volume and cardiac output, and hence improving tissue perfusion.

© Philip R Judge 2006

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Stabilization of the Emergency Patient

Massey University Seminar – May 2006

Traumatic shock Traumatic shock is often complicated by hypovolemia, and sepsis. Traumatic injury on its own produces hemodynamic changes similar to those produced by stress and exercise.  Increased sympathetic activity - increased heart rate, cardiac contractility.   Increased blood pressure (especially if hemorrhage is not present)   Decreased central venous pressure (CVP)   Decreased systemic vascular resistance   Decreased oxygen extraction   Increased respiratory rate, hypocapnea and respiratory alkalosis   Progression to decompensation occurs due to tissue injury, tissue hypoxia, release of systemic mediators  of inflammation, sepsis, or continued hemorrhage (if present) The surgical operation represents a controlled form of trauma, and has been used extensively in human patients to study the temporal (time) patterns of circulatory dysfunction and shock. In a large study involving 356 high-risk elective surgical patients, survivors and non-survivors were found to have mean arterial blood pressure measurements and heart rates within the normal range. Peripheral vasoconstriction by the adreno-medullary stress response is an initial response to pain and blood loss that maintains blood pressure in the presence of falling blood flow. However, this vasoconstriction is uneven, and leads to unevenly distributed microcirculatory flow about the body. In non-survivors, prolonged stress and vasoconstriction preceded the development of post-operative organ failure. In the presence of continued hypovolemia, the stress response may lead to poor tissue perfusion, tissue hypoxia, covert clinical shock, and organ dysfunction and failure. Lethal circulatory dysfunction begins in the intraoperative period, but becomes more apparent as organs fail in later post-operative stages. Septic shock Sepsis usually has a more subtle and insidious time of onset than, for example, traumatic or hemorrhagic shock. Sepsis may be the primary disorder, or it may be a complication of the traumatic, post-operative, urologic, respiratory or internal medicine patient. The initial response to sepsis includes  Increased cardiac output, tachycardia, increased cardiac contractility   Decreased systemic vascular resistance (warm shock)  Regardless of origin, septic shock causes maldistribution of blood flow that results in decrease in cerebral, renal and coronary blood flow, and effective circulating blood volume. Compensatory mechanisms include neurohormonal responses that increased myocardial contractility, heart rate and alveolar ventilation, and activation of humoral and compliment immune systems. Systemic dissemination of mediators of inflammation such as cytokines, nitric oxide, bacteria and their toxins, and platelet-activating factor, play a crucial role in the progression of sepsis to organ failure and death. In several human studies of patients with sepsis, cardiac output, oxygen delivery, and oxygen consumption were higher than normal in both survivors and non-survivors. Non-survivors had values that were lower than survivors, and these

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values fell abruptly only within the last 24 hrs prior to death. This highlights the difficulty of predicting survivability using methods of blood pressure and blood gas determinations, and stresses the need for having a high index of suspicion that sepsis will occur in a given patient. In early stages of sepsis, several human studies have documented improved survivability in patients aggressively treated early in the course of sepsis with intravenous fluid therapy and dobutamine to improve cardiac output. No improvement in outcome was noted in patients when this treatment was started in the middle and late stages of sepsis. Similar results were noted when plasma transfusions were given in early, middle and late stages of sepsis, with a greater improvement noted in patients when transfused early in the disease course.

Decompensation of the Patient in Shock
The initial physiologic response to shock is that of compensatory increases in cardiorespiratory function in an attempt to maintain tissue perfusion and ventilation and oxygenation. As mentioned earlier, the end result is the uneven distribution of blood flow to microcirculatory bed. When there is disparity between the metabolic demands of tissue or illness that overwhelms the capacity of the circulatory system to meet these demands, decompensation occurs. Decompensation is more likely to occur in those patients where there is pre-existing cardiac, pulmonary or other organ impairments. Tissue oxygen debt resulting from reduced tissue perfusion is the primary underlying physiological mechanism that subsequently leads to organ failure and death Arteriolar and venular constriction in renal, mesenteric, and hepatic circulation causes ischemic injury in these organs, cellular hypoxia, anaerobic metabolism, lactic acidosis, and release of cellular and bacterial mediators of inflammation. Sustained venuloconstriction, arteriolar dilation (caused by decreased pH, release of local vasodilator substances) increases capillary hydrostatic pressure, and contributes to regional extravasation of fluid into the interstitial space. Continued activation of immunologic mechanisms, activation of arachadonic acid cascade and increased release of other mediators of shock, including histamines, kinins, bradykinin, seratonin, oxygen free radicals, and lysosomal enzymes, perpetuate maldistribution of blood flow away from central circulation, and contribute to loss of intravascular fluid volume, and tissue hypoxia and death. Disruption to vascular wall integrity causes activation of clotting cascade, resulting in the deposition of fibrin thrombi throughout the vascular system, contributing to further ischaemia, hypoxia and acidosis. The coagulation activation eventually consumes clotting factors, resulting in systemic fibrinolysis and continued hemorrhage; symptoms of disseminated intravascular coagulopathy (DIC). Following fluid therapy, patients with postoperative, post traumatic, and volume-depleted states, including dehydration, may remain hypovolemic, have increased interstitial water, decreased intracellular water, and increased total body water. This may or may not be manifested as peripheral or pulmonary edema. © Philip R Judge 2006

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What Does the Patient in Shock Look Like?
Symptoms of shock are indicative of decreases in tissue blood flow, exaggerated sympathetic autonomic responses, and the presence of circulating mediators of shock Symptoms of Patients with Circulatory Dysfunction  Tachycardia   Dry, clammy, pale, cold mucous membranes; mucous membranes may also be red and warm   Cyanosis due to low oxygen saturation, sluggish capillary blood flow   Slow capillary refill time due to vasoconstriction, and reduced blood volume   Initial euphoria mediated by increased sympathetic tone, followed by mental depression due  to hypoxia and hypotension  Rapid pulses, becoming weak (decreased cardiac output)   ECG changes include S-T segment slurring; ventricular premature depolarizations or  ventricular tachycardia, especially following blunt chest trauma. Sinus tachycardia progressing to bradycardia is a poor prognostic sign  Reduced urine output, reduced urine sodium, acute renal failure   Depressed liver blood flow is characterized by centrilobular necrosis, with leakage of liver  cytosol enzymes, and increasing blood clotting times

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Goals of fluid therapy in Small Animal Medicine
The primary goal of fluid therapy in illness is the delivery of oxygen to tissues The rationale for this goal is that oxygen delivery to tissues, and oxygen consumption are measurable parameters that determine whether a patient lives or dies. This has been proven in several multi-center randomized studies in human medicine. Time is the major factor that determines the outcome of intervention and therapy in patients with shock. When early, or primary events are ignored, temporal patterns are lost, and therapy is then directed to the consequences of, rather than the causes of, circulatory dysfunction. In order to evaluate underlying circulatory mechanisms, it is necessary to describe the time course, or sequence of events that has occurred in a given patient, and to differential primary events from secondary or tertiary events Intravenous fluid therapy and circulatory support is aimed at achieving the following I. Immediate intravascular volume resuscitation II. Immediate restoration of normal blood hemoglobin concentration III. Immediate restoration of colloid oncotic pressure IV. Rehydration V. Maintenance of fluid balance Although cardiac and respiratory functions are directly measurable, tissue perfusion and oxygenation are not quantifiable. However, tissue perfusion and oxygenation are of greater consequence in terms of outcome. Inadequate tissue perfusion with either low of high blood flow, leads to tissue hypoxia, which, when extensive in degree or protracted time, produces organ dysfunction, multiple organ failure, and death. When the early manifestations of shock are alleviated by therapy that is insufficient to correct poor tissue oxygenation, the resultant oxygen debt may not be recognized until the appearance of organ failure, including ARDS, sepsis, acute cardiac failure, renal failure, hepatic failure, DIC or coma. Tissue oxygen delivery is defined by the following equation

Oxygen delivery (DO 2) = CO x [Hb] x SaO2 x 1.3 + 0.03 x PaO 2 The variables we can alter in this equation are – Cardiac output (CO) is defined by the following equation Cardiac output = stroke volume x heart rate

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Stroke volume is further defined by the following equation Stroke volume = end diastolic volume - end systolic volume
Improving end diastolic volume is achieved by improving the patients’ volume loading. Improving end systolic volume is achieved by improving contractility of the heart using positive inotropes. It is possible to increase cardiac output by as much as 50% by using fluid therapy and positive inotropes. Hemoglobin concentration [Hb] Oxygen delivery is directly proportional to hemoglobin concentration. Hemoglobin concentration is approximately one third of the patients’ hematocrit. Optimal hemoglobin concentrations in dogs and cats have not been established. In humans, a hemoglobin concentration of greater than 12 g/L is considered optimal for patients with shock and critical illness. The optimal hematocrit for cats is 0.35, and for dogs is 0.37. A patient with a hematocrit of lower than 0.20 will suffer from oxygen debt to tissues that is incompatible with normal tissue function. Oxygen saturation (SaO2) Provision of supplemental oxygen may increase the patients’ SaO2 by 10-12%. Effective Use of Fluid and Transfusion Therapy Fluid therapy in small animal practice is usually directed at correcting a maldistribution of blood flow due to many conditions, including hypovolemia, dehydration, vascular space alterations, poor cardiac performance, and sepsis in order to optimize tissue oxygen delivery.

Effective Fluid Therapy
Having considered the determinants of tissue oxygen delivery, a rational approach to fluid therapy can be made with the knowledge that 1. 2. 3. 4. 5. The patient requires a functional respiratory tract The patient requires adequate cardiac output The patient requires adequate hemoglobin concentrations The patient requires appropriate vascular tone to ensure oxygenated blood is received by the tissues The patient requires adequate blood flow through capillary beds to enable oxygenated blood to be extracted into the tissues

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Fluid therapy in small animal practice is usually directed at correcting a maldistribution of blood flow, and the improvement of tissue perfusion, so that tissue oxygen delivery can be optimized. Therapeutic objectives in the therapy of shock are outlined below, in order of temporal priority. At all times, the goals of fluid therapy are the achievement of supra-normal values of cardiac output, and oxygen delivery to tissues.

1. Circulatory support begins by control of internal and external bleeding. Thereafter, the primary method
of circulatory support is fluid therapy (except in cardiogenic shock). Intravenous fluid therapy is typically administered through a large bore venous catheter. Initially, a cephalic or saphenous catheter is used. However, if the patient is expected to remain hospitalized for longer than 24 hours, a jugular catheter may be placed at the earliest opportunity. Intravenous fluid therapy and circulatory support is aimed at achieving the following VI. VII. VIII. IX. X. Immediate intravascular volume resuscitation Immediate restoration of normal blood hemoglobin concentration Immediate restoration of colloid oncotic pressure Rehydration Maintenance of fluid balance

Fluids available for resuscitation and support of the circulatory system include isotonic crystalloid solutions (Lactated Ringers Solution, PlasmaLyte A), hypertonic saline (administered as a 7-7.5% solution), and colloids (plasma, whole blood, dextran 70, pentaspan). Several comparisons between crystalloids and synthetic colloids have shown no difference in survival in human patients suffering from hypovolemic shock. However, colloids do provide superior intravascular volume support and may lead to a decrease in the production of pro-inflammatory cytokines. Interestingly, in experimental models of hemorrhagic shock, resuscitation with colloids and hypertonic saline has been shown to result in reduced oxygen tension and delivery to intestinal and hepatic tissues, when compared to resuscitation isotonic crystalloid fluids, either alone or in combination with dextran 70. Combinations of fluids appear to be the most effective method of providing fluid therapy, especially in early decompensatory (stage II) shock, end stage (stage III) shock, and shock secondary to dehydration and third space losses of fluids. The use of pentaspan or dextran 70 lowers the amount of isotonic crystalloid required by 40-60%.

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So, how much fluid are we going to administer to our patients? This depends largely on the clinical state of the patient, the type of fluid lost, and the presence of shock. a. Fluid therapy for shock: Traditionally, it was suggested that one blood volume of isotonic crystalloid be administered by rapid intravenous infusion to the patient showing clinical signs of shock, within the first hour of patient presentation to provide intravascular support. More recently, the practice of ‘small volume resuscitation’ with fluids has been advocated - that is, titrating the volume of fluid a patient receives, whether it be crystalloid, colloid, blood products, or a combination of these, to achieve a set of end-points. In the patient showing clinical signs of shock, these end-points include i. Normal mucous membrane color ii. Normal heart rate, normal respiratory rate iii. Return of normal pulse pressures iv. vi. b. c. Central venous pressure of 5-10cm water Establishment of normal or supra-normal urine output v. Normal blood gas analysis Fluid therapy for Rehydration – administer isotonic crystalloid solutions such as Hartman’s solution to replace hydration deficits over 6-12 hours Fluid therapy for hospital maintenance – is dictated by the clinical status of the patient. Typically, most critically ill patients require between 1.5 and 4 times their normal daily intake of fluids, in order to cope with fluid losses resulting from their illness 2. Maintenance of optimum hemoglobin concentration. The “ideal” packed red cell mass in critically ill patients is 25-27%. This level of red cell mass provides adequate blood hemoglobin concentrations, while producing a reduction in blood viscosity. In humans, the incidence of thromboembolism in critical patients is lower when patients are mildly anemic. In critically ill animals, packed red blood cells or whole blood should be administered to maintain a hematocrit of approximately 27%. Transfusion to a higher hematocrit does not improve tissue oxygen delivery significantly. The rate of infusion of whole blood or packed red cells should not exceed 20ml/kg/hr unless the clinical state of the patient dictates a faster rate of infusion is required e.g. during exsanguination following arterial laceration. Blood products should not be administered concurrently with calcium-containing fluids as calcium may cause in-line clotting of the blood product. 3. Maintenance of colloid oncotic pressure may be achieved by using plasma products such as fresh frozen plasma, or by using synthetic colloids such as dextran 70 or pentaspan. Administration of synthetic or naturally occurring colloids aids in the maintenance of an effective colloid oncotic pressure within the blood vessel lumen, which, in turn influences circulating blood volume and blood flow, venous return, and cardiac output. 4. Maintenance of cardiac output and tissue blood flow. This is achieved through adequate intravascular volume resuscitation using crystalloids and colloids, and by the use of positive inotropic support after the maximum effect of intravenous fluid administration has been obtained. How do we know when the maximal effect of intravenous fluid therapy has been reached? In most

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emergency patients, we use an assessment of the presence or absence of the clinical signs of shock to determine if we have given sufficient fluid to a patient to restore normal tissue blood flow. In critical patients that have jugular catheter in place, measurement of central venous pressure provides a useful index as to the relative “fullness” of the vascular system. Normal central venous pressure in the dog is between –2 and 2 cm water. In most critically ill patients, we aim to provide mild hyper-volemia, and a central venous pressure of +5-+10 cm water. Central venous pressure should also be interpreted in conjunction with mixed venous lactate concentrations. Lactate is a biproduct of the anaerobic metabolism of pyruvate. Serial measurements of venous blood lactate can be used to assess a return of body tissues to aerobic metabolism – this provides a more accurate measure of the success of out fluid therapy in achieving cardiac output and tissue oxygenation. Regardless of the monitoring technique used, failure of the patient to show signs of improving tissue perfusion despite seemingly adequate amounts of intravenous fluid support indicate that the cardiovascular system requires assistance to improve cardiac output and blood vessel tone. The most effective drug therapy if poor cardiac output is suspected despite adequate fluid therapy is the use of the positive inotropic agent dobutamine. The starting dose is 2 µg/kg/min – this dose is titrated according to the patient status. Dobutamine produces marked increased in cardiac output and stroke volume, as well as decreases in systemic and pulmonary vascular resistances, and venous flow pressures. Hypotension can occur in patients that are inadequately volume resuscitated prior to commencement of therapy. If this occurs, the dobutamine infusion should be stopped, and the patient given a bolus of intravenous fluids. Dopamine also has positive inotropic properties, as well as being a potent vasopressor. Administration of a vasopressor such as dopamine will produce greater increases in blood pressure than dobutamine; however, dopamine does not improve tissue oxygen delivery to the same extent as dobutamine. For this reason, dobutamine is preferred over dopamine in the therapy of shock and circulatory dysfunction. How do we as clinicians decide when we have restored adequate cardiac output, tissue perfusion, and oxygen delivery? Without the use of pulmonary arterial catheters as are widely used in intensive care units in human medicine, we as veterinarians rely on measurements of clinical parameters such as heart rate, respiratory rate, neurological function, blood lactate levels, blood gas analysis, urine output and central venous and arterial blood pressure . 5. Maintenance of pulmonary function and adequate gas exchange involves the provision of oxygen supplementation by nasal catheter or oxygen-enriched air. Ensuring the patient has an optimal hemoglobin level is also critical in ensuring adequacy of gas exchange in the lungs. Mechanical ventilation is indicated in those patients where oxygen supplementation fails to increase SpO2 above 90-95%, or in patients where excessive work of breathing is present. Strenuous use of the accessory muscles of respiration can increase oxygen consumption by 50-100%, and decrease cerebral blood flow by as much as 50%. In addition, any increase in the work of breathing creates a greater negative pressure within the thorax during inspiration, which results in an increase in impedance to ventricular ejection. Ventilation of these patients is critical in reducing oxygen demand, and improving cardiac output – it could make the difference between life and death.

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6.

Maintenance of adequate mean arterial blood pressure. Hypotension is defined as a mean arterial pressure below 70 mm Hg, and diastolic pressures less than 50 mm Hg. How do we treat hypotension in the critical patient? The short answer is to administer intravenous fluid therapy until the patient is volume replete, and to administer a vasopressor if hypotension persists in the face of adequate volume resuscitation. However, alpha-adrenergic vasopressors must be used with caution, because they may intensify the uneven vasoconstriction produced by neural mechanisms, sepsis and critical illness. Vasoconstriction produced by vasopressors does raise blood pressure, but may further exacerbate the uneven microcirculatory flow present in patients with shock and circulatory dysfunction. The effect of vasopressors such as dopamine isoproterenol, and epinephrine, because they also have inotropic actions that improve cardiac performance, is a balance between favorable increase in blood pressure, and unfavorable uneven maldistribution of blood flow. If the decision is taken to use a vasopressor, the smallest doses needed to maintain satisfactory blood pressure should be used, because no amount of vasopressor can make up for inadequate blood volume. Dopamine is used at a starting dose of 1-3 µg/kg/min.

7.

Maintenance of cardiac rhythm and the synergy of cardiac conduction and contraction. Cardiac dysrrhythmias are common in emergency and critically ill patients. Cardiac rhythm may be abnormal in patients due to a wide variety of causes, including the presence of cardiac disease, myocardial contusions, hypovolemia, pain, electrolyte and acid-base balance abnormalities, and systemic circulation of mediators of inflammation, infectious organisms. In all cases, a search for, and management of the underlying disease process that has lead to the abnormal cardiac rhythm is the most effective means of managing the abnormal rhythm. Many anti-arrhythmic drugs have toxic or undesirable side effects if they are administered inappropriately to patients. Prior to starting antiarrhythmic therapy, it is therefore recommended that all patients have normal intravascular volume and hydration, electrolyte and acid-base status, analgesia, and adequate management of the underlying disease process (e.g. sepsis, infection, heart failure etc.). In addition, it is wise to document that the abnormal cardiac rhythm is causing hemodynamic compromise to the patient prior to starting anti-arrhythmic therapy, so that an assessment of the effectiveness of therapy can be made, using clinical parameters as well as ECG parameters.

8.

Maintenance of adequate urine volume is achieved through management of hypovolemia and maldistribution of blood flow as outlined above. Oliguria or anuria are managed by the addition of furosemide at 2-4 mg/kg IV, mannitol at 0.5 – 1.0 gm/kg IV over 10 minutes, and dopamine at 1-3 µg/kg/min IV. The goal is urine output of 2-4 ml/kg/hr.

9.

Body temperature control is achieved through normal tissue perfusion, and the provision of warm humidified air, and warming of intravenous fluids. The goal is a normal rectal temperature of 38.039.20C.

10. Manage sepsis through ensuring adequate tissue perfusion and tissue oxygen delivery as outlined above. Selection of antibiotics should be based on culture and sensitivity from isolated organisms. 11. Maintain normal blood glucose, electrolyte, and acid-base balance – electrolyte balance is essential to ensure normal tissue metabolism, cell function, normal cardiac rhythm and vascular tone. Supplementation of intravenous fluids with electrolytes such as potassium magnesium, and glucose is usually based on measurement of serum levels. However, because most body potassium and

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magnesium is located within the intracellular space, serum measurements poorly reflect total body levels. Supplementation of potassium and magnesium may be based on expected urinary losses, or based on urinary electrolyte measurement. The Patient That Does Not Stabilize – What to Do? Failure of a patient to show clinical signs of improvement following adequate intravenous fluid therapy, or stabilization of the patients clinical signs for only a short period of time indicates the presence of one or more of the following, and warrants immediate attention  Greater than 40% blood loss   Undetected ongoing hemorrhage – e.g. into fracture sites, pleural cavity, abdominal cavity, fascial  planes etc  Pneumothorax/hemothorax   Aspiration pneumonia   Pericardial effusion   Cardiomyopathy   Cardiac dysrrhythmias   Hypothermia   Acidosis   Hypocalcemia   Myocardial contusion   Severe Sepsis   Hypoglycemia 

The clinician should immediately mount a systematic search for the cause of the poor response to therapy. Use a systematic body-systems approach, beginning with the respiratory system, cardiovascular system, neurological system, urinary, gastrointestinal, Hematological and skeletal and muscular systems, in accordance with the patients clinical signs, underlying disease. Catastrophic hemorrhage is an immediate life-threatening abnormality and results in vascular collapse, decreased oxygen delivery to the tissues, and loss of blood into an anatomical area where space occupation by blood causes secondary cardiovascular or neurological malfunction (e.g. cardiac tamponade, intracranial bleeding). Cardiovascular collapse from exsanguination hemorrhage results in insufficient blood flow to the brain, and profound vasodilatation from persistent hypoxemia and hypercapnea, decreased cellular energy production, and metabolic acidosis. Animals with catastrophic hemorrhage may rapidly develop hypotension, bradycardia, coma, and death. The compensatory response to catastrophic hemorrhage depends on the rate of bleeding. Rapid hemorrhage in a short period of time leads to a ‘blunting’ of the normal compensatory response. The normal response to hemorrhage is a centrally mediated sympathetic nervous system stimulation of contraction of venules, and splenic vessels, allowing ‘mobilization’ of red blood cells pooled in these

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areas. This response is depressed with rapid hemorrhage, due to hypoxia of the respiratory and vasomotor centers in the brain. In addition, species differences in splenic capacity also impact on the extent of the compensatory response to catastrophic hemorrhage. Dogs are able to store up to 10-20 ml/kg of blood in the spleen, vs. 5 ml/kg in the cat. Irrespective of the degree of compensation present, ongoing hemorrhage in traumatized patients will manifest itself in the following manner  Progressive delay in capillary refill time   Increased heart rate and respiratory rate (early hemorrhage)   Decreased heart rate and respiratory rate (late hemorrhage)   Apprehension, fright   Progressive decrease in body temperature   Progressive decrease in patient mentation   Severe abdominal pain if hemorrhage is occurring into the peritoneal cavity   Dyspnea, and respiratory distress with both intrapleural of intra-abdominal hemorrhage.  A clinically useful rule of thumb in patients with severe trauma is as follows “If hemorrhage is unapparent in animals presented following a history of recent trauma, it should be assumed that these animals have serious ongoing internal hemorrhage until proven otherwise” Obviously, external hemorrhage is easily diagnosed. However, internal hemorrhage is hidden from sight, and may occur within the thorax, peritoneum, retro-peritoneum, osseofascial compartments of the cervical area, or at fracture sites. In traumatized patients manifesting shock without evidence of severe external hemorrhage, these areas must be investigated for evidence of blood accumulation. The management of catastrophic hemorrhage and the shock syndrome that accompanies it is outlined below using four basic principles  Volume resuscitation - using blood, plasma, synthetic colloids, and hypertonic or isotonic  crystalloids. The volume of fluid administered will vary depending on the individual patient requirements. Most authors currently recommend low volume resuscitation with a combination of blood products, synthetic colloids, and crystalloid solutions in order to reduce the chances of further bleeding from these patients, as their blood pressure increases following fluid therapy. Following definitive control of hemorrhage, patients are resuscitated to a normo or slightly hypertensive state. In patients with severe blood loss, restoration of intravascular blood volume is ideally obtained with whole blood transfusions, auto-transfusion of pooled thoracic or abdominal blood, or packed red blood cells and plasma/synthetic colloid.  Rapid surgical exploration of the thorax, abdomen, or limbs - and internal control of hemorrhage  by occlusion of the arterial blood supply leading to the site of hemorrhage  Identification, ligation/repair of bleeding vessels. A brief outline of a suggested approach to the  patient with an acute hemabdomen is presented below

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Surgery of the Patient with Acute Hemabdomen A thorough and systematic approach to exploration of the abdominal cavity should be performed. Techniques of various surgeons vary - the following is a guide  Uncontrollable arterial bleeding can temporarily be stopped by compressing the aorta cranial to the  celiac artery. During suctioning, the entire abdominal cavity should be packed with surgical towels or laparotomy pads. This will control venous hemorrhage.  The towels or pads are removed one at a time until the source of the bleeding is located. Once  located, the source can be ligated, or affected organ, or segment of affected organ removed. It is best to preserve as much of a bleeding organ as possible unless it is severely injured, is infected, or potentially neoplastic  Once hemorrhage is controlled, each quadrant of the abdomen is carefully examined. Tissues found  to be injured should be isolated with moist laparotomy pads prior to definitive surgical repair.  Tissue and fluid samples should be obtained for both aerobic and anaerobic culture and sensitivity,  and biopsies taken from liver, pancreas, kidney, stomach, small intestine, mesenteric lymph node, and abdominal muscle as indicated by the patients condition  Once surgery is complete, lavage the abdomen with copious amounts of warmed 0.9% NaCl. Ensure  complete suctioning of lavage fluid  Placement of a jejunostomy tube, or gastrotomy tube to allow post operative feeding if a prolonged  convalescence is anticipated, or if the patient has sepsis, or was malnourished prior to presentation

Neurological Assessment Following stabilization of airway, respiratory function, and cardiovascular function, a complete neurological assessment of the patient should be carried out, and a coma score evaluation completed. Particular attention should be given to the patient’s level of consciousness, ocular responses, and ability to effectively guard its airway and prevent aspiration of gastric, esophageal, and oral secretions. In addition, a complete evaluation of spinal reflexes, presence of superficial, and deep pain, anal tone, and bladder function should be carried out and repeated if results are inconclusive at presentation. Subsequent neurological assessment should be scheduled every 6-12 hours. 1. Patients that present with seizures and status epilepticus – patients that are in status epilepticus present a unique challenge to the emergency clinician. A protocol for management of seizures is included (Appendix A) 2. Patients that present with Stupor and Coma – are managed in accordance with the protocol in Appendix B

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Supportive Care of the Critically Ill or Traumatized Patient During and following stabilization of the critically ill patient, the patient must be adequately supported to ensure recovery. In many instances of illness and severe trauma, pro- and anti -inflammatory cytokines, vasoactive mediators of inflammation, and infectious organisms will impact on patient recovery several days following the initial trauma. These mediators of systemic inflammation and sepsis cause maldistribution of blood flow, arteriovenous shunting of blood flow through organs such as the gastrointestinal tract; increased capillary permeability, and third space loss of intravascular fluid. The net result is decreased tissue blood flow and tissue oxygen delivery to the tissues, resulting in organ dysfunction and eventually organ failure. Every effort should be made to ensure that tissue oxygen delivery remains adequate through maintaining adequate blood pressure, central venous pressure, heart rate and rhythm, urine output, control of infection, and maintenance of colloid oncotic pressure and hemoglobin concentrations. General nursing care, including pain management, prevention of aspiration pneumonia, decubital ulcer prevention, and management of intestinal ileus and gastroparesis is critical in the management of these patients. Early provision of nutritional support in critically ill patients has been shown to reduce mortality and morbidity, infection rates, and hospital stays in numerous human studies. There are currently a large number of human and veterinary products available for enteral nutrition in critically ill patients.

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Appendix 1: Protocol for the Management of Seizures P.R. Judge, Animal Emergency Centre 37 Blackburn Rd Mt Waverley, VIC 3149 Definition A seizure is a manifestation of an excessive discharge of hyper-excitable cerebrocortical neurons. The appearance of seizures varies with the location and extent of seizure activity. Seizures are generally classified according to their clinical manifestations. Generalized seizures have widespread onset within both cerebral hemispheres, and manifest in the following manner  Loss of consciousness   Recumbency   Generalized motor signs, including convulsions, tonic (sustained) or clonic (repetitive) muscle  contractions, limb paddling, and trembling.  Jaw chomping and facial twitching.   Autonomic hyperactivity including pupillary dilatation, salivation, piloerection, micturition, and  defecation.  Occasionally, atonic seizures occur, which must be distinguished from syncope and narcolepsy cataplexy. Partial seizures have a focal onset in one cerebral hemisphere, and limited spreading within the brain. Their occurrence indicates the presence of acquired structural deformity. Partial seizures may be either simple or complex, depending on whether consciousness is disturbed. Simple partial seizures manifest in the following manner  Unilateral motor signs such as facial twitching, tonic or clonic movements of one or both limbs  on one side, spasmodic turning of the head to one side. Movements are contra-lateral to the side of the lesion or seizures focus. Complex partial seizures spread to allocortical areas, and consciousness is either lost or impaired. Other symptoms of complex partial seizures include  Contra-lateral or bilateral asymmetric or symmetric motor signs, usually limited to a particular  area of the body; for example twitching, jaw chomping, tremor of the neck.  Bizarre behaviors, growling, hissing, circling, panic, or attacking real or imaginary objects.   Consciousness is diminished or lost, however, seizure motor activity is usually not sufficient to  cause recumbency.  Presence of aura. Aura corresponds to the onset of a simple partial seizure before it evolves into  a complex partial seizure or generalized seizure.

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 Localized post-ictal motor deficits may occur in partial seizures, and occurs on the contra-lateral  side to the seizure focus. Pathophysiology  Seizures result from an imbalance between the normal excitatory and inhibitory mechanisms of  nervous tissue in the brain. Idiopathic seizures result from a functional disturbance in the neurons. Primary intra-cranial causes of seizures usually result from lesions that irritate the surrounding neurons, for example neoplasia, glial scarring following trauma. Extracranial causes of seizures alter brain biochemical homeostasis in favor of excitation.  Seizures cause increased cerebral metabolic rate, increasing the rate of oxidative metabolism.  This causes elevated carbon dioxide production, potentiating CNS acidosis and resultant CNS edema due to local vasodilatation. Increased cerebral metabolism results in decreasing PO2 and oxygen deficiency. Neuronal calcium concentrations increase, and arachadonic acid metabolites, prostaglandins, and leukotrines lead to brain edema and cell death. Elevated CSF pressure may also result  Systemic signs – Sympathetic nervous system activation and adrenal release of catecholamines  result in hyperglycemia, hypoglycemia, hyperthermia, dehydration, lactic acidosis, cardiac arrhythmias, pulmonary hypertension, edema, and hemorrhage. Management  Airway  o o o Secure a patent airway Provide oxygen by flow past system Orotracheal intubation reduces the chances of aspiration of gastric and oral secretions and blood  Breathing  o o o Assess mucous membrane color If patient comatose, intubate and provide supplemental oxygen If patient is semi-comatose, anesthetize with thiobarbituate or propofol, intubate and ventilate; provide supplemental oxygen. o If patient is conscious, provide oxygen if ventilating adequately; if not, consider anesthetizing and ventilating  Patient Assessment  o o o o Airway and breathing as above Auscultate heart, determine heart rate, assess pulses Determine patient temperature Observe the seizure - symmetrical and generalized vs. focal and asymmetrical. Lateralizing signs (head tilt, turning to one side, unilateral twitching or clonus) are suggestive of secondary epilepsy.

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 Circulation and Data Collection   Place cephalic catheter and begin fluid therapy with LRS to replace intravascular  volume deficits.  Administer diazepam at 0.1-0.5 mg/kg IV (t1/2 = 15-60 min); may be repeated 2-3  times over 5-10 minutes.  If an intravenous line cannot be established, administer diazepam at 0.5 mg/kg per  rectum via a tomcat catheter.  Draw blood for CBC, glucose (stat) PCV/TP, electrolytes and biochemistry profile, and  anticonvulsant levels (if patient is already current receiving medication).  Obtain and ECG tracing from the patient   Patient Management Post-Diazepam   If diazepam is ineffective in controlling seizures, give and anticonvulsant dose of  phenobarbital - 5mg/kg IV, and repeat every 30-40 minutes for up to 3 doses. Phenobarbital will take approx. 20-30 minutes to reduce seizure activity.  If seizure clustering or status epilepticus continues, one of the following regimens may  be used  Midazolam 0.5 mg/kg IV bolus, followed by constant rate infusion is the  preferred agent to use in combination with phenobarbitone and/or propofol  Thiopental given as 2-4 mg/kg IV boluses to effect, up to 10-20 mg/kg,  endotracheal intubation, isoflurane anesthesia. Pay attention to ventilation and circulation.  Propofol given as 1-2 mg/kg IV boluses to effect, followed by a CRI of propofol  at 0.1-0.2 mg/kg/min IV.  Pentobarbital given as IV bolus of 2-6 mg/kg   Diazepam CRI at 1-2 mg/kg/hr in a 5% dextrose solution  NB: focal seizures can lead to life threatening hyperthermia if they are not controlled, and should be managed as for status epilepticus  Correction of Underlying disease and/or Secondary Effects   Metabolic acidosis - will usually correct once seizures stop and with fluid and oxygen  support.  Hypoglycemia - treat with 0.5 g/kg of 50% dextrose, diluted to a 10% solution, and given  slowly IV over 10 minutes. Avoid hyperglycemia as this may exacerbate toxic brain damage.  Hypocalcemia - give 15 mg/kg of 10% calcium gluconate IV slowly over 30 minutes.   Thiamine deficiency in cats – thiamine is administered at 2 mg/kg IM if diet or history  (anorexia, treatment with antibiotic therapy, etc. suggestive of deficiency.

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 Hyperthermia - cold ice packs on trunk, inguinal, axilla regions, moist towels, cool fan.  Cool body temperature to 39.5o C - hypothermia will rapidly develop if patients are actively cooled beyond this point.  Gastric lavage and colonic enema for ingested toxins   Increased intra-cranial pressure – usually the result of a structural brain disease;  manage with intravenous fluid therapy, adequate ventilation strategies, followed by mannitol 1 g/kg IV PRN, furosemide 2 mg/kg IV, +/- methylprednisolone sodium phosphate 10 mg/kg IV  Monitoring the patient - pay close attention to the following   Airway patency   Ventilation - SpO2, blood gases, mucus membrane color   Tissue perfusion - mucus membrane color, thermoregulation, blood pressure, pulse  character, ECG rhythm.  Electrolytes, PCV/TP   Neurological status - evidence of raised intracranial pressure, lateralizing signs, and  abnormal inter-ictal signs.  ARDS, neurogenic pulmonary edema.  Further diagnostic testing is advised for the following patients  Animals under 1 year of age, or older than 5 years of age   Abnormal neurologic behavior in the inter-ictal phase   Animals with systemic disease, animals with focal seizures  Further diagnostic tests include  Serum bile acids   Ammonia tolerance test   Abdominal ultrasound   Thoracic radiographs   CSF analysis   Intracranial imaging (CT or MRI) 

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Appendix 2: Protocol for the Management of Stupor and Coma Philip R Judge Animal Emergency Centre 37 Blackburn Rd Mt Waverley VIC 3149

Definitions Stupor and coma are pathological abnormalities caused by an interruption in the structural, metabolic, and/or physiological integrity of the cerebrum or brainstem. Coma is characterized by an unconscious state from which the animal cannot be aroused by any external stimuli, including those that are noxious. Stupor is clinically similar to coma, except that the animal can be aroused by external stimuli, but may quickly relapse into its sleep-like state as soon as the stimuli are withdrawn. Management  Airway  o o o o Ensure the patient has a patent airway. Provide oxygen by flow-past, mask, or endotracheal tube or catheter. Avoid nasal oxygen - sneezing increases intracranial pressure. Intubation reduces the chances of aspiration of gastric and oral secretions and should be performed if the patient has depressed gag reflexes.  Breathing   In comatose patients, intubate, and provide supplemental oxygen.   If patient is semi-comatose, anesthetize, intubate, and ventilate; provide supplemental  oxygen.  If patient is conscious, provide oxygen if ventilating adequately; if not, consider  anesthetizing and ventilating.  Ventilate to achieve P aCO2 of 30-37 mmHg.   Circulation   Place a peripheral intravenous catheter - avoid struggling and stress.   Do not occlude jugular veins.   Begin administration of isotonic crystalloid solution (LRS initially) until blood test results  available, at rate of 40-60 ml/kg/hr for patients that are hypovolemic.  Elevate the head no more than 30 degrees from horizontal to aid in increasing venous  drainage from the brain, and reduce intracranial pressure

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 Data Collection - draw blood for the following tests - do not occlude the jugular veins - use  peripheral vein for blood collection  PCV/TP/Glucose - test immediately   Electrolyte levels, full biochemical profile, CBC   Determine serum osmolality   Treatment - begin therapy for specific abnormalities as indicated by blood test results, for  example hypoglycemia, hyperglycemia, hypocalcemia. If the patient is not hypernatremic, administration of hypertonic saline and pentaspan or dextran 70 as intravascular replacement fluids may improve blood flow through microvascular beds, and reduce extravasation of administered fluids.  Management of Cerebral Edema - Conduct a neurologic examination, and determine the  following  Level of consciousness, pupil responses, pupil position   Cranial nerve assessment   Respiratory pattern   Motor responses   Response to noxious stimuli   Oculocephalic reflex   Localize lesion and determine severity   Record the results   Following intravascular volume replacement therapy, treat cerebral edema using the following   Furosemide at 1-2 mg/kg IV followed in 10 minutes by   Mannitol 0.5 g/kg IV given over 5-10 minutes. Contraindication to mannitol administration is  hyper-osmolality. Indications include a declining level of consciousness, evidence of brainstem lesion, and craniotomy.  If poisoning is suspected cause, perform a gastric lavage, +/- activated charcoal administration  (1-2g/kg) PO and colonic irrigation, and provide specific antidotes as indicated.  Perform Coma Scale q 30 minutes during stabilization   Patient Monitoring   Turn the patient every 2-4 hours   Eye lubricant   Soft bedding   Insert urinary catheter and connect to closed collection system   Elevate head no more than 30 degrees above horizontal   Maintain blood pressure at 100 - 120 mmHg   Monitor LOC every 2 hours, perform coma score   Control seizures with diazepam at 0.5-2 mg/kg IV - (caution in hepatic encephalopathy, as  these patients are more sensitive to benzodiazepines)  Control body temperature in low normal range 

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 Monitor renal, hepatic, and gastrointestinal function   Monitor PCV/TP/ACT   Nutritional support is indicated if patient comatose for >12 hours   Avoid tight cervical, thoracic, abdominal dressings  Differential Diagnosis of Stupor and Coma

Primary Brain Disease 1. 2. 3. 4. 5. 6. 7. 8. 9. Neoplasia – primary or secondary Abscessation Hemorrhage Concussion, hematoma Cerebral edema Contusion - brain stem Infarction - cerebral, brainstem Degenerative disease Hydrocephalus Lysosomal Storage Diseases

Secondary Encephalopathy 1. 2. 3. Renal disease (uremia, acidosis) Liver disease (hypoglycemia, hyperammonemia) Pancreatic disease Insulinoma, diabetes mellitus, hypoglycemia 4. 5. 6. 7. 8. 9. Myocardial disease – ischaemic. Cardiomyopathy Hypertension Bacterial embolism Feline ischemic Encephalopathy Anoxia Pulmonary disease

Abnormal Osmotic States Hyper-osmolar states 1. 2. 3. 4. 5. 6. 1. Hyperglycemia Diabetes mellitus Hypernatremia Diarrhea Diabetes insipidus Severe water loss Water intoxication

Hypo-osmolar states

10. Lissencephalopathy 11. Status Epilepticus 12. Canine distemper virus 13. Rabies 14. Feline infectious peritonitis 15. Fungal, protozoal and bacterial infections 16. Granulomatous meningoencephalitis

10. Coagulopathies 11. Nutritional deficiency (thiamine) 12. Anemia, blood loss 13. Carbon monoxide poisoning 14. Hypoadrenocorticism 15. Hypothyroidism 16. Post-ictal depression 17. Toxicity – ethylene glycol, lead, barbituates, cannabinoids, alcohol

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Clinical Signs in Coma

Location of Lesion Diffuse Cerebral Disease

Motor Function tetraparesis, may have locomotor movements but postural reactions are abnormal tetraparesis, reflexes may be depressed tetraparesis, increased extensor tone (decerebrate rigidity) hemiparesis or tetraparesis, increased extensor tone on affected side tetraparesis with decerebrate rigidity

Pupillary Light Reflex normal

Eye Movements normal but no visual following

Metabolic /Toxic Enc ephalopathy Bilateral Tentorial Herniation

may be normal or abnormal normal or abnormal depending on etiology depending on etiology dilated or mid-position unresponsive bilateral ventrolateral strabismus poor vestibular eye movements ipsilateral ventrolateral strabismus poor vestibular eye movements no vestibular eye movements may have bilateral ventrolateral strabismus

Unilateral Tentorial Herniation

dilated ipsilateral

Brainstem Hemorrhage

bilateral midposition

Location of Lesions Causing Stupor and Coma

Location of lesion Cerebrum  Seizures 

Possible Clinical Signs

 Normal or constricted pupils that respond to light   Roving eye movements   Cheyne-Stokes respirations  Midbrain  Hyperventilation   Loss of oculocephalic response   Negative caloric test   Pinpoint or dilated pupils that do not respond to light  Medulla  Irregular respiration pattern   Cardiac arrhythmias, or irregular heart rate and rhythm 

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Diagnostic Approach to the Patient with Stupor and Coma

Stupor and coma

History and physical examination

No trauma

Trauma

CBC, biochemistry, urinalysis

Pursue evaluation

Normal

Normal

Abnormal

Extracranial possibilities Intracranial possibilities Diabetes mellitus Uremia Hypoglycemia Hepatic Encephalopathy Toxins Hypothyroidism Hepatic Encephalopathy

No neurological signs Ischemia Hemorrhage Trauma Granulomatous meningoencephalitis

Neurological Signs Neoplasia Encephalitis Granulomatous meningoencephalitis Thiamine deficiency

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32. Creteur, J., Sun, Q., Abid, O., De Backer, D., Van der Linden, P., Vincent, J.L., “Normovolemic hemodilution
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34. Duffy, T.C., Kirby, R., Rudloff, E., “Critical Role of the Vascular Endothelial Cell in Health and Disease: A Review
Article” In Journal of Veterinary Emergency and Critical Care, 2004, June, 14(2): 84-99. 35. Quesnel, A.D., “Seizures” In Textbook of Veterinary Internal Medicine, 5 Edition, W.B. Saunders Co., 2000, P 148151. 36. Podell, M., “Seizure Management in Dogs” In Bonagura (Ed), Current Veterinary Therapy XIII, Small Animal Practice; W.B. Saunders Co., 2000, P 959-962. 37. Ganong, W.F., In “Circulation Through Special Regions” In Review of Medical Physiology, 19th Edition, Appleton and Lange, 1999, P 582-591. 38. Parent, J., Poma, R., “Single Seizure, Cluster Seizures, and Status Epilepticus” In Wingfield/Raffe (Ed), the Veterinary ICU Book, Teton New Media, 2002, P 871-879. 39. Shell, L., “Altered States of Consciousness” In Textbook of Veterinary Internal Medicine, 5th Edition, W.B. Saunders Co., 2000, P 144-147. 40. Schunk, K.L., “Neurological Emergencies” In Veterinary Emergency and Critical Care Medicine, Mosby Year Book 1992, P 288-294. 41. Oliver, J.E., Lorenz, M.D., Kornegay, J.N., “Stupor or Coma” In Handbook of Veterinary Neurology, 3 Edition, W.B. Saunders Co., 1997, P 287-311.
rd th

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