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