Emergency NursingCHAPTER 33 PART 2
2Clinical Signs of Pain
Vocalization
Depression
Anorexia
Tachypnea
Tachycardia
Abnormal blood pressure
Pale mucous membranes
Aggression
Abnormal postures
Hypersalivation
Dilated pupils
3Abdominal Pain
Classic “praying” or “play bowing” position
Hypersalivation
Inability to lay down or sleep
4Untreated Pain
Causes stress
Triggers harmful physiological changes that prolong recovery
Signs not always obvious
Monitor for absence of normal behavior
5DIC
Definition A syndrome
The natural balance between clot formation and clot prevention/resolution is altered
6DIC
Consequences Massive activation of coagulation
Coagulation overwhelms body’s normal regulatory function
Systemic clot formation begins on a widespread scale
Clot formations will set up multiple-organ microthrombosis
Subsequent multiple organ failure
7DIC
Causes Vascular injury
Severe trauma
Severe inflammation
Sepsis
Toxins
Poor perfusion
8DIC
Pathogenesis Patient commonly moves from a hypercoagulable to a
hypocoagulable state
Die from thrombotic or hemorrhagic episodes
9DIC
Common physical examination findings Petechia
Ecchymosis
Cold extremities
Abnormal mentation
Abnormal body temperature
Increased respiratory effort
10Treatment of DIC
Primary goal Remove the stimulus initiating intravascular coagulation
Treat the primary disease
11Treatment of DIC
Secondary goal Prevent secondary complications
Maintain organ perfusion
Fluids
Blood products
Anticoagulants
12Shock
Definition Poor blood flow creating impaired oxygen delivery to the
tissues
13Categories of Shock
Compensatory or hyperdynamic Earliest phase of shock
Clinical signs
Increased heart rate and respiratory rate
Rapid capillary refill time
Brick red mucous membranes
Bounding pulses
14Categories of Shock
Uncompensated or hypodynamic shock Second phase of shock
Blood flow is shunted vital organs (brain, heart) at the expense of other tissues
Clinical signs
Weak pulses
Rapid heart rate
Increased capillary refill time
Pale mucous membranes
Hypothermia
Dull mentation
15Categories of Shock
Shock can be further divided based on underlying cause Hypovolemic shock
Distributive shock
Cardiogenic shock
Septic shock
16Hypovolemic Shock
Most common form of shock
Primary perfusion failure
Results from a reduction in circulating blood volume Bleeding
Dehydration
Effusive fluid loss
17Distributive Shock
Maldistribution of blood flow associated with vasodilation Consequent decrease in effective blood volume
Regardless of intravascular volume or cardiac output
Common causes
Trauma
Heatstroke
Envenomation
Anaphylaxis
18Cardiogenic Shock
Associated with decreased cardiac output
Can occur from heart failure Cardiomyopathy
Valvular disease
Cardiac arrhythmias
19Septic Shock
Caused by massive systemic infection or primary infectious diseases Opportunistic infections can also trigger septic shock
Typically associated with severe tissue damage Trauma
Heatstroke
Envenomations
Pancreatitis
20SIRS
Systemic inflammatory response syndrome
Parallels septic shock
Triggered by systemic inflammation
21SIRS
Similar to shock in that there is an early hyperdynamic phase followed by uncompensated or hypodynamic phase
Clinical signs Abnormal temperature fluctuations
Depression
Tachypnea
DIC
22SIRS
Primary treatment Oxygen therapy
Aggressive fluid therapy
“Shock” doses
90 ml/kg/hr dog
45-60 ml/kg/hr cat
Fluid administration goal oriented!
Correction of underlying problem
23Reperfusion Injury
Cellular injury that develops as blood flow returns to an area or tissue previously deprived of perfusion
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
24Reperfusion 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
Oxygen-free radicals and inflammatory mediators cause inflammation and vessel injury leading to thrombosis and edema
25Vessel Injury
Leads to thrombosis and edema
DIC, SIRS, and multi-organ dysfunction can develop