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11114305
SEPTIC SHOCK
Description
Mind Map on SEPTIC SHOCK, created by Jentoria Dingesa on 28/10/2017.
Mind Map by
Jentoria Dingesa
, updated more than 1 year ago
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Created by
Jentoria Dingesa
about 8 years ago
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Resource summary
SEPTIC SHOCK
ASSESSMENT
Clinical Manifestations of Stages of Septic Shock
Stage I: Compensatory Stage
Activation of SNS to compensate for the hypotension & ↓ cardiac output.
Tachycardia (↑HR >90 beats/min)
pulse present
↑Epinephrine & Norepinephrine= vasoconstriction
BP adequate to provide vital organs)
Normal BP with narrow pulse pressure
Slight drop in BP
↓Renal Blood flow & perfusion
↓Urinary Output
Edema- due to fluid Retention
↓Blood flow to Lungs
Tachypnea (>20 breaths/minute)
↑Ventilation- perfusion mismatch)
Anxious, restlessness, & combative
Flushed Skin
due to systemic vasodilation
Stage II: Progressive/ Decompensated Stage
**Hypotension
SBP ≤ 90mmHg
MAP ≤ 65mmHg
↓SBP of >40mmHg
↓Peripheral perfusion
Weak or Absent pulses
DIstal extremeties ischemia
Hypothermia (core temperature <36 °C)
Cool & Clammy skin
↓Capillary refill (>2sec)
↓Cerebral perfusion
Altered Mental Status
Listless or Agitated
↓Responsiveness to stimuli
Unconciousness
Myocardial ischemia or Infraction
Dysrrhthmia
Acute Respiratory Distress Syndrome
Moist Crackles
Alveolar edema
Tachypnea (>20 breaths/min)
PaCO2 <32mmHg
↓Urinary output
Tacycardia (>90 beats/min)
Stage III: Refractory Stage ***END STAGE (IRREVERSIBLE)
Loss of conciousness
Unresponsive to stimuli
Pupils dilated and unresponsive
Loss of reflexes
Profound Hypotension & Bradycardia
↓CO
↓BP inadequate to perfuse vital organs
Respiratory failure
Hypoxemia
Anuria
Disseminated Intravascular coagulation
Initial stage
Asymptomatic
Adequate perfusion & oxygenation to vital organs
Reversible
Cells switch to anaerobic metabolism due to lack of perfusion caused by vasodilation.
Produce pruvic and lactic acid.
Rise in lactic acid level
presence of sepsis
Fever (Temperature>38.3°C)
Positive blood culture
Rick Factors
Current infection
Pneumonia
Appendicitis
UTI
Endocarditis
Age
Elderly
Decreased functioning of the immune system
Young children/infants
Organ and immunological immaturity and inability to self manage hygiene, more susceptible to UTIs and other infections
Medical History
Indwelling catheter (IV, urinary)
Immunocompromised (AIDS, chemotherapy, immunosuppressive drugs
Recent surgery
Recent childbirth
Malnutrition
Severe Injury
Burns
Large wounds
Gender
Females are more susceptible to UTIs due to shorter urethras
COMPLICATIONS
Multiple organ dysfunction syndrome
Renal
Renal failure
Hepatic
Liver failure
Cardiac
heart failure
Respiratory
Lung injury characterized as diffuse alveolar damage
Neurological
Ischemic stroke resulting from microthrombi
Tissue death in extremities
Gastrointestinal
Intestinal ischmemia or infarction
Post-sepsis syndrome
Insomnia
Hallucinations
Panic attacks
TREATMENTS
Nursing interventions
Airway
Ensure potency
Endotracheal intubation
Natural airway
Breathing
To avoid hypoxemia
Maintain SaO2 at or > 90%. Deliver 100% O2 via
Bag Valve Mask
Non rebreather mask
Mechanical ventilation may be necessary
Decreases metabolic demands of breathing
Circulation
Manage hypotension with fluid resuscitation
Insert 2 large bore IV catheters
Insert urinary catheter
To measure urinary output
Disability
Continuous assessment of end organ perfusion
Neurological function
Assess for altered mental status
Glasgow coma scale for level of conciousness
Renal function
Urinary output is a marker for adequate renal perfusion
Normal adult urinary output is 0.5mL/kg/hour or more
Lab values (BUN, Cr)
Drug therapy
Fluid resuscitation
IV bolus of isotonic crystalloid solution or colloids
Hemodynamic monitoring may be necessary to evaluate large-volume fluid resuscitation
PA catheter or central venous catheter
Arterial pressure monitoring
Antibiotics
Early initiation with broad spectrum antibiotic
Combination therapy with beta-lactam plus an aminoglycoside
Mono therapy with 3rd generation cephalosporin
Culture sample taken to determine causative pathogen
Usually gram negative bacteria
once pathogen is determined, more specific antibiotic regimen is initiated to cover the infecting agent
Vasopressors
Norepinephrine via central catheter; increases vascular tone
Used for hypotension unresponsive to fluid resuscitation
Anticoagulants
Low molecular weight heparin
DVT prophylaxis
Hydrocortisone
Given with vasopressors
Decreases inflammation, reverses capillary permeability
Inotropes (dobutamine)
Nutrition therapy
Hypermetablolism often manifests as protein-calorie malnutrition
Nutritional status assessed by
Serum protein, BUN, serum glucose level, serum electrolytes
Enteral nutrition is initiated within 24 hours
Continuous drip of enteral feedings enhances GI perfusion
Parenteral nutrition is indicated when enteral nutrition is contraindicated
Daily weight measurement used as indicator of fluid status
Large weight gain
Common due to 3rd spacing
Significant weight loss
Dehydration should be ruled out before additional calories are provided
Blood glucose should be maintained at <8.3mmol/L
DIAGNOSIS
Blood Tests
ABG Analysis
HCO3
pH
PaCO2
Blood Culture Test
Gram-Positive Bacteria
Gram-Negative Bacteria
Complete Blood Count (CBC) with Differential
↓ Platelet count
WBC
Leukocytosis ( Elevated WBC level) >10x10^9/L
Indicate presence of infection
Low WBC level)
Leukopenia
↑Creatinine level
Due to decrease Kidney Creatinine clearance
↑Lactic Acid in the Blood >4mmol/L
Indicating Hypoxemia
C-Reactive Protein (CPR) Test
↑ C-reactive protein indicate presence of infammation in the body
Liver Enzyme level
Abnormal PT & PTT
Indicates acute hepatocellular injury due to hypoperfusion.
Electrocardiography (ECG)
ST-segment depression
Inverted T-waves
Arrhythmia resembling myocardial infarction
Other Culture Tests
Sputum Culture
Stool Culture
Urine culture
Urinalysis
Catheter Tip culture
Chest X-Ray
May show evidence of infection, such as consolidation, pleural effusion, or pneumothorax
PATHOPHYSIOLOGY
Infectious agent enters systemic circulation
Widespread leukocyte activation
Release of pro inflammatory cytokines: tumour necrosis factor, IL-1
Peripheral vasodilation and increased capillary permeability
Increased extracellular fluid and decreased intravascular fluid
Hypotension
Maldistribution of circulating blood volume
Hemodynamic collapse
Complement and coagulation cascade activation
Microvascular damage
Micro thrombi formation
Obstruction of microvascular
Local ischemia to vital organs such as kidneys and brain leading to organ dysfunction
Cell hypoxia leading to lactic acid accumulation
Metabolic acidosis
Febrile response
Media attachments
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