Stabilization of the Emergency Patient

8/2/2019 Stabilization of the Emergency Patient

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Sta bilization of the Emergency Patient Massey University Seminar May 2006

Philip R Judge 2006 2

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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Stabilization of the Emergency Patient

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