stabilization of the emergency patient
TRANSCRIPT
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Sta bilization of the Emergency Patient Massey University Seminar May 2006
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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
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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
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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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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
Barrel-shaped thorax
Inspiratory +/- expiratory effort increased
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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. Tick Paralysis2. Elapid Snake Envenomation
3. Botulism
4. Polyradiculoneuropathy
5. Myasthenia Gravis
6. Muscle relaxants
Pulmonary Parenchymal Disease
1. Pneumonia2. PIE
3. Neoplasia
4. Pulmonary edema
5. Pulmonary interstitial disease
Central Nervous System Disease
1. CNS disease causing depression of
respiratory drive
a. Head trauma
b. Neoplasia
c. Drugs/medications
d. Toxicity
e. Seizures
f. Infection/inflammation
g. Cerebral edema, increased
intracranial pressure
Hypoventilation
1. Shock
a. Hypovolemic shock
b. Hemorrhagic shock
c. Septic shock
d. Cardiogenic shock
e. Non-cardiogenic shock
2. Pleural space disease
3. Sepsis
4. Mediastinal disease
5. Pain
Table 2: Interpretation of Pulse Oximetry Readings
SaO2 PaO2 Interpretations
>95%
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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 andbronchioles. 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
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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 s tress, 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. Increased heart rate beta-1 adrenergic receptor stimulation
b. Increased myocardial contractility beta-1 adrenergic receptor stimulation
c. Increased cardiac output
d. Increased peripheral vascular resistance mediated by alpha-adrenergic arterial
construction of skin, voluntary muscle, abdominal viscera, and kidneys
e. 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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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.
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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 myocardialcontractility, 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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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.
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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.
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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 intra-
operative 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.
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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 (DO2) = 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. The patient requires a functional respiratory tract
2. The patient requires adequate cardiac output
3. The patient requires adequate hemoglobin concentrations
4. The patient requires appropriate vascular tone to ensure oxygenated blood is received by the tissues
5. 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. Immediate intravascular volume resuscitation
VII. Immediate restoration of normal blood hemoglobin concentration
VIII. Immediate restoration of colloid oncotic pressure
IX. Rehydration
X. 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 pressuresiv. Central venous pressure of 5-10cm water
v. Normal blood gas analysis
vi. Establishment of normal or supra-normal urine output
b. Fluid therapy for Rehydration administer isotonic crystalloid solutions such as
Hartmans solution to replace hydration deficits over 6-12 hours
c. 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 bi-
product 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 mosteffective 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 g/kg/min this dose is titrated
according to the patient s tatus. 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 isused at a starting dose of 1-3 g/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 anti-
arrhythmic 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
g/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 38.0-
39.20C.
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, orpotentially 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 patients 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 andoxygen 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 Secure a patent airway
o Provide oxygen by flow past system
o Orotracheal intubation reduces the chances of aspiration of gastric and oral secretions
and blood
Breathing
o Assess mucous membrane color
o If patient comatose, intubate and provide supplemental oxygen
o 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 Airway and breathing as above
o Auscultate heart, determine heart rate, assess pulses
o Determine patient temperature
o 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, pulsecharacter, 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 externalstimuli, 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 Ensure the patient has a patent airway.
o Provide oxygen by flow-past, mask, or endotracheal tube or catheter.
o Avoid nasal oxygen - sneezing increases intracranial pressure.
o 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 PaCO2 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 s everity
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 Secondary Encephalopathy Abnormal Osmotic States
1. Neoplasia primary or
secondary Abscessation
2. Hemorrhage
3. Concussion, hematoma4. Cerebral edema
5. Contusion - brain stem
6. Infarction - cerebral,
brainstem
7. Degenerative disease
8. Hydrocephalus
9. Lysosomal Storage Diseases
10. Lissencephalopathy
11. Status Epilepticus
12. Canine distemper virus
13. Rabies
14. Feline infectious peritonitis
15. Fungal, protozoal and
bacterial infections
16. Granulomatous
meningoencephalitis
1. Renal disease (uremia,
acidosis)
2. Liver disease (hypoglycemia,
hyperammonemia)3. Pancreatic disease -
Insulinoma, diabetes
mellitus, hypoglycemia
4. Myocardial disease
ischaemic. Cardiomyopathy
5. Hypertension
6. Bacterial embolism
7. Feline ischemic
Encephalopathy
8. Anoxia
9. Pulmonary disease
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
Hyper-osmolar states
1. Hyperglycemia
2. Diabetes mellitus
3. Hypernatremia4. Diarrhea
5. Diabetes insipidus
6. Severe water loss
Hypo-osmolar states
1. Water intoxication
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Clinical Signs in Coma
L oc at ion of Les ion Mot or Func tion Pupillar y L ight Reflex Ey e Mov ement s
Diffuse Cerebral Disease tetraparesis, may have
locomotor movements but
posturalr eactions are
abnormal
normal normal but no visual
following
Metabolic/Toxic
Encephalopathy
tetraparesis, reflexes may
be depressed
may be normalor abnormal
depending on etiology
normal or abnormal
depending on etiology
Bilateral Tentorial
Herniation
tetraparesis, increased
extensor tone
(decerebrate rigidity)
dilated or mid-position
unresponsive
bilateral ventrolateral
strabismus
poor vestibular eye
movements
Unilateral Tentorial
Herniation
hemiparesis or
tetraparesis, increased
extensor tone on affected
side
dilated ipsilateral ipsilateralventrolateral
strabismus
poor vestibular eye
movements
Brainstem Hemorrhage tetraparesis with
decerebrate rigidity
bilateralmidposition no vestibular eye
movements
may have bilatera l
ventr olateral str abismus
Location of Lesions Causing Stupor and Coma
Location of lesion Possible Clinical Signs
Cerebrum Seizures
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 Neurological Signs
Ischemia Neoplasia
Hemorrhage Encephalitis
Trauma Granulomatous meningoencephalitis
Granulomatous meningoencephalitis Thiamine deficiency
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3. Proulx, J., Energy Metabolism in Sepsis, IVECC Proceedings, 2000, P 493-498.
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