Transcript Clinical Signs of Pain - Dr. Roberta Dev Anand

Emergency Nursing
CHAPTER 33 PART 2
Clinical Signs of Pain
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
Vocalization

Pale mucous membranes

Depression

Aggression

Anorexia
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Abnormal postures
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Tachypnea
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Hypersalivation
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Tachycardia
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Dilated pupils

Abnormal blood pressure
Abdominal Pain
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Classic “praying” or “play bowing” position
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Hypersalivation
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Inability to lay down or sleep
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Untreated Pain

Causes stress

Triggers harmful physiological changes that prolong
recovery

Signs not always obvious

Monitor for absence of normal behavior
4
DIC
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Definition


A syndrome
The natural balance between clot formation and clot
prevention/resolution is altered
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DIC
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Consequences
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Massive activation of coagulation

Coagulation overwhelms body’s normal regulatory function

Systemic clot formation begins on a widespread scale
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Clot formations will set up multiple-organ microthrombosis

Subsequent multiple organ failure
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DIC
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Causes
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Vascular injury
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Severe trauma
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Severe inflammation
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Sepsis
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Toxins

Poor perfusion
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DIC

Pathogenesis
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Patient commonly moves from a hypercoagulable to a
hypocoagulable state
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Die from thrombotic or hemorrhagic episodes
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DIC
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Common physical examination findings

Petechia
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Ecchymosis
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Cold extremities
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Abnormal mentation
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Abnormal body temperature

Increased respiratory effort
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Treatment of DIC
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Primary goal
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Remove the stimulus initiating intravascular coagulation

Treat the primary disease
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Treatment of DIC
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Secondary goal
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Prevent secondary complications
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Maintain organ perfusion
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Fluids

Blood products

Anticoagulants
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Shock

Definition

Poor blood flow creating impaired oxygen delivery to the
tissues
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Categories of Shock
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Compensatory or hyperdynamic
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Earliest phase of shock
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Clinical signs
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Increased heart rate and respiratory rate
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Rapid capillary refill time
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Brick red mucous membranes
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Bounding pulses
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Categories of Shock
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Uncompensated or hypodynamic shock
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Second phase of shock
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Blood flow is shunted vital organs (brain, heart) at the
expense of other tissues
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Clinical signs
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Weak pulses
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Rapid heart rate
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Increased capillary refill time
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Pale mucous membranes

Hypothermia
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Dull mentation
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Categories of Shock

Shock can be further divided based on underlying cause

Hypovolemic shock
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Distributive shock
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Cardiogenic shock
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Septic shock
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Hypovolemic Shock

Most common form of shock

Primary perfusion failure

Results from a reduction in circulating blood volume

Bleeding

Dehydration

Effusive fluid loss
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Distributive Shock

Maldistribution of blood flow associated with vasodilation
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Consequent decrease in effective blood volume


Regardless of intravascular volume or cardiac output
Common causes
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Trauma
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Heatstroke
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Envenomation
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Anaphylaxis
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Cardiogenic Shock
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Associated with decreased cardiac output
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Can occur from heart failure
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Cardiomyopathy
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Valvular disease
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Cardiac arrhythmias
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Septic Shock
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Caused by massive systemic infection or primary infectious
diseases
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
Opportunistic infections can also trigger septic shock
Typically associated with severe tissue damage

Trauma
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Heatstroke
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Envenomations
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Pancreatitis
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SIRS
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Systemic inflammatory response syndrome

Parallels septic shock
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Triggered by systemic inflammation
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SIRS

Similar to shock in that there is an early hyperdynamic
phase followed by uncompensated or hypodynamic
phase
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Clinical signs

Abnormal temperature fluctuations

Depression

Tachypnea
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DIC
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SIRS
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Primary treatment
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Oxygen therapy
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Aggressive fluid therapy
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“Shock” doses
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90 ml/kg/hr dog
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45-60 ml/kg/hr cat
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Fluid administration goal oriented!
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Correction of underlying problem
Reperfusion Injury

Cellular injury that develops as blood flow returns to an
area or tissue previously deprived of perfusion
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Poor perfusion causes oxygen-starved tissues to develop
an anaerobic metabolism and become depleted of
cellular energy stores

These conditions alter certain enzyme systems, which
destabilize white blood cell membranes
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Reperfusion Injury

Once perfusion is restored, altered enzyme systems
generate harmful molecules called oxygen-free radicals

Simultaneously, membrane-damaged white blood cells
release inflammatory mediators that contribute to a
reactive environment
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Oxygen-free radicals and inflammatory mediators cause
inflammation and vessel injury leading to thrombosis and
edema
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Vessel Injury
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Leads to thrombosis and edema

DIC, SIRS, and multi-organ dysfunction can develop
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