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Module D

Sepsis, Septic

Shock, and DIC

NUR 203

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Shock

Patho: a response to poor tissue oxygenation

Etiology: Any problem that impairs oxygen delivery to tissues and organs

can start the syndrome of shock; if shock progresses the hypoxia can lead

to multiple organ dysfunction syndrome (MODS) and death

Key Features:

Respiratory Neuro Integumentary Kidney ↑ respiratory rate

Shallow depth of

respirations

↑ Paco2; ↓ PaO2

Cyanosis,

especially around

lips & nail beds

Anxiety

Restlessness

↑ Thirst

Cool to cold

Pale to mottled to

cyanotic

Moist, Clammy

Mouth dry; pastelike

coating present

↓ urine output

↑ specific gravity

Sugar & acetone

present in urine

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Shock Key Features Continued

Cardio GI Late ↓ CO

↑ Pulse Rate

Thready pulse

↓ BP

Narrowed Pulse Pressure

Postural Hypotension

Low CVP (central

venous pressure)

Flat neck & hand veins

in dependent positions

Slow Capillary Refill in

nail beds

Diminished peripheral

pulses

↓ Motility

Diminished or absent

bowel sounds

N & V

Constipation

↓ central nervous

system activity

(lethargy to coma)

Generalized muscle

weakness

Diminished or absent

deep tendon reflexes

Sluggish pupillary

response to light

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Tissue and organ perfusion is related to mean arterial pressure (MAP)

Factors that influence MAP

Total blood volume

Cardiac Output

Size of vascular bed

Sympathetic tone

Types of Shock

Hypovolemic shock – when too little circulating blood vol. causes a MAP ↓ → ↓ O2

Cardiogenic shock –when the actual heart muscle is unhealthy & pumping is impaired

Distributive shock – blood vol. not lost; distribut to interstitial tissues/cannot deliver O2

o Neural induced

o Chemical induced

Anaphylaxis

Sepsis

Capillary leak syndrome

Obstructive shock – caused by problems that impair ability heart muscle to pump

effectively

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Hypovolemic Shock

Pathophysiology: Loss of blood volume from the vascular space;

Decreased MAP; Loss of O2 carrying capacity from loss of circulating

RBC’s; Decrease in MAP of 5-10 mmHg below baseline is detected by

baroreceptors; Compensatory mechanisms can halt the progression; If

MAP continues to fall, cell damage can be so severe that the client cannot

survive

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Stages of Shock

Initial

(Early)

Nonprogressive

(Compensatory)

Progressive

(Intermediate)

Refractory

(Irreversible) MODS

Early shock;

baseline MAP is

decreased by less

than 10 mm Hg;

Compensatory

mechanisms are effective at

returning MAP to

normal perfusion to vital organs;

Lactic acid will

cause

compensation of

sympathetic system;

vasoconstriction

and increased heart rate;

Symptoms are so

mild it is hard to detect shock

When MAP ↓ 10 to

15 mm Hg from

baseline

Kidney and

baroreceptors sense

an ongoing decrease in MAP

and trigger the

release of renin, ADH, aldosterone,

epinephrine and

norepinephrine

Tissue hypoxia

occurs in nonvital organs and in the

kidney, it is not ↑

enough to cause permanent damage

Mild acidosis and

hyperkalemia; ↑ HR/R

Sustained decrease

in MAP of more

than 20 mm Hg

from baseline

Compensatory

mechanisms are functioning but no

longer deliver

sufficient oxygen, even to vital organs

Overall metabolism

is anaerobic:

moderate acidosis

and hyperkalemia; tissue ischemia

Life threatening

emergency; Cold

Severe tissue

hypoxia with

ischemia and

necrosis

Release of

myocardial depressant factor

from the pancreas

Buildup of toxic metabolites

MODS

Death

Sequence of cell

damage caused by

the massive release

of toxic

metabolites and

enzymes Metabolites trigger

small clots to form

Occurs first in the liver, heart, brain,

and kidney

Damage to the

heart muscle is

severe (one cause is the release of

MDF from

ischemic pancreas)

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Shock Assessment

• Assessment

• History

• PE/Clinical manifestations

• Cardiovascular changes

• Respiratory changes

• Kidney/Urinary changes

• Skin changes

• CNS changes

• Skeletal muscle changes

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Shock Psychosocial Assessment

Is it necessary to repeat questions to obtain response?

Does the response answer the question asked?

Does the client have difficulty making word choices?

Is the client irritated or upset by the questions?

Can the client concentrate on a question long enough to answer appropriately, or

is the attention span limited?

Laboratory Assessment

pH—decreased

PaO2—decreased

PaCO2—increased

Lactic acid—increased

Hct—increased with fluid shift and dehydration; decreased with hemorrhage

Hgb—as above

K+--increased

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Best Nursing Practice for Shock

Ensure airway

IV access

Administer supplemental oxygen

Elevate client’s feet

Examine client for overt bleeding

Apply direct pressure to overt bleeding

Administer medications as prescribed

Increase the rate of IV fluids

DO NOT LEAVE CLIENT

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Nursing Interventions for Shock

Nonsurgical management

o Oxygen

o IV therapy (Crystalloids and Colloids)

o Drug therapy: Vasoconstrictors (Dopamine,

Norepinephrine, Phenylephrine); Inotropic Agents

(Dobutamine, Milirinone – Primacor); Agents Enhancing

Myocardial Perfusin (Sodium Nitroprusside – Nitropress,

Nipride)

o Monitoring

Surgical management

Community-based care

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Sepsis and Septic Shock

Patho:

Infection

Sepsis/SIRS – sepsis is a condition in which infectious

microorganisms have entered the bloodstream. As the numbers of

organisms increase, an inflammatory response, known as systemic

inflammatory response syndrome (SIRS), is triggered as a result of

infection escaping local control.

Severe sepsis – the progression of sepsis w/an amplified

inflammatory response.

Septic shock – the stage of sepsis and SIRS when multiple organ

failure is evident and uncontrolled bleeding occurs. Even

w/appropriate intervention, the death rate among patients in this

stage of sepsis exceeds 50%.

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Risk Factors for Shock

(Nursing Focus on the Older Adult)

Hypovolemic Cardiogenic Distributive Obstructive Diuretic therapy;

Diminished thirst

reflex;

Immobility; Use

of ASA-

containing

products; Use of

complimentary

therapies such as

Ginkgo biloba;

Anticoagulant

therapy

Diabetes mellitus;

Presence of

cardiomyopathies

Diminished

immune response;

Reduced skin

integrity; Presence

of cancer;

Peripheral

neuropathy;

Strokes;

Institutionalization

(hospital or

extended –care

facility);

Malnutrition;

Anemia

Pulmonary HTN;

Presence of

cancer

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Changes in Selected Parameters during Sepsis and Septic Shock

Parameter Normal Early Sepsis Late Sepsis

Septic

Shock

Cardiac Output

Normal 3-5

L/min Decreased Increased

Greatly

Decreased

Stroke Volume

Normal 60-80

mL Decreased Increased

Greatly

Decreased

Serum Lactate

(Arterial) < 2 mmol/L

Normal to

slightly increased 2-4 mmol/L > 4 mmol/L

Blood Glucose <110 mg/dL 110-120 mg/dL 120-150 mg/dL >150 mg/dL

Oxygen

Saturation 95-100% <95% < 85% <80%

Serum

Creatinine

0.6-1.2 mg/dL

(men)

0.5 – 1.1 mg/dL

(women)

Normal to

slightly increased

> 2 mg/dL (men)

> 1.4 mg/dL

(women)

> 3.0 mg/dL

(either gender)

Segmented

Neutrophils

55% - 70% of

WBC count Increased Decreased < 10%

Band

Neutrophils

2%-5% of total

WBC count

Normal to

slightly increased > 10% > 20%

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Left Shift

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Interventions – Table 39-6

• Oxygen Therapy

• Drug Therapy

• Antibiotics

• Steroids

• Insulin

• Anticoagulants

• Activated Protein C

• Blood replacement therapy

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DIC (Disseiminated Intravascular Coagulation)

The body’s blood clotting mechanisms are activated throughout the body

instead of being localized to an area of injury

Small blood clots form throughout the body, and eventually the blood

clotting factors are used up and unavailable to form clots at sites of real

tissue injury – Bleeding cannot be stopped

Also called consumption coagulopathy

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Clients at Risk for DIC

Recent sepsis

Injury or trauma

Recent surgery or anesthesia

Complications of delivery (retained placenta)

Leukemia or disseminated cancer

Recent transfusion reaction

Severe liver disease

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Signs and symptoms of DIC

Bleeding from multiple body sites

Clot formation

Hypotension

Bruising and petechiae

Tests for DIC

Fibrin degradation products—increased

PT/PTT—increased

Platelet count—decreased

Serum fibrinogen—decreased

D-dimer—positive

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DIC Treatments

Treat the underlying cause

Improve oxygenation, replace fluids, correct electrolyte imbalances, administer

vasopressor medications

Cryoprecipitate

FFP

Heparin

Activated protein C

Nursing Care for DIC

Be aware of at risk clients

Assess clients thoroughly and frequently for signs and symptoms of DIC

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DIC Things to avoid

Procedures/activities that increase ICP

Medications that interfere with platelet function

Rectal probes/rectal medications

IM injections

High-pressure suctioning

Lemon-glycerin swabs and commercial mouthwash for oral care

Dislodging any clots, including those around IV sites

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DIC Things to DO

Monitor VS closely, including neuro checks, hemodynamics, abdominal

girth, and urine output

Monitor amount of external bleeding carefully—number of dressings

saturated, time to saturate a dressing, pad count in women with vaginal

bleeding

Low-pressure suctioning

Administer oral hygiene carefully—use sponge-tipped swabs with baking

soda rinses

Assess skin q.2h and reposition carefully

Use lamb’s wool between digits

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DIC Things to DO Continued

Auscultate breath sounds q.2h

Monitor edema

Monitor volume of IVF’s, blood products

Administer diuretics as prescribed

Monitor fibrinogen levels

Identify previous coping mechanisms

Explain all procedures in terms the client and family can understand