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SIRS Systemic Inflammatory Response Syndrome (ETIOLOGY (Drug Reactions,…
SIRS
Systemic Inflammatory Response Syndrome
DESCRIPTION
A syndrome resulting from a dysregulated inflammatory response to an infectious or noninfectious pathogen
Includes 2 or more of the following variables:
Fever greater than 100.4 F or or less than 96.8 F
White blood cell count greater than 12,000/uL, less than 4,000/uL, or greater than 10% immature band forms
Heart rate greater than 90 bpm
Respiratory rate greater than 20 breaths/min or arterial carbon dioxide tension less than 32 mm Hg
STAGE III
PATHOPHYSIOLOGY
Continued cytokine release begins tissue destruction. Circulatory integrity is lost, leading to organ failure, and shock
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Significant systemic reaction occurs if homeostasis is not achieved, which leads to the activation of numerous humoral cascades and the activation of the reticular endothelial system, resulting in a loss of circulatory integrity, leading to end-organ dysfunction
CLINICAL MANIFESTATIONS
Kidney Failure
Respiratory failure, acute respiratory distress syndrome, nosocomial pneumonia
Elevated procalcitonin (greater than 0.15 ng/mL) and lactate level (greater than 280 units/L (SI, 4.68 µkat/L)) may indicate sepsis.
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NURSING DIAGNOSES
Impaired gas exchange R/T respiratory distress
Short-term Goal: The patient will
demonstrate a respiratory rate within 5 breaths of the patient’s baseline throughout the nursing shift.
Long-term Goal: The patient will demonstrate improved ventilation and adequate oxygenation as evidenced by ABG levels within defined limits (pH: 7.35-7.45; PaCO2: 35-45; PaO2: 80-100).
Intervention: Monitor respiratory rate, depth, and ease of respiration. Watch for use of accessory muscles and nasal flaring.
Evaluation: Assess respiratory rate every hour and if respiratory rate remain within 5 breaths of the patients baseline I would consider the intervention effective in preventing negative changes in the patient’s status.
Decreased cardiac output R/T circulatory collapse
Short-term Goal: The patient will maintain a pulse oximetry above 95% and a urine output of 0.5 - 1.0 mL/kg/hr throughout the nursing shift.
Long-term Goal: The patient will verbalize understanding of the prescribed medication regimen prior to discharge.
Intervention: Monitor and report presence of and degree of symptoms including dyspnea at rest or with reduced exercise capacity, orthopnea, paroxysmal nocturnal dyspnea, nocturnal cough, distended abdomen, fatigue, or weakness.
Evaluation: We will consider this intervention effective if patient remain free of the symptoms associated with decreased cardiac output.
Ineffective peripheral tissue perfusion R/T decreased cardiac output
Short-term Goal: The patient will have 2+ peripheral pulses and capillary refill less than three seconds throughout the nursing shift.
Long-term Goal: The patient will demonstrate full range of motion in affected tissue peripheral sites prior to discharge from the hospital.
Intervention: Assess peripheral pulses in the radial, ulnar, dorsalis pedias, and posterior tibialis. Also continuously monitoring capillary refill, skin color and temperature.
Evaluation: We will consider this intervention effective if we are able to prevent complications of SIRS through early identification of peripheral perfusion changes such as diminished peripheral pulses, a capillary refill of less than 3 seconds, cold skin temperatures of the extremities, or pale skin color.
STAGE I
PATHOPHYSIOLOGY
Activation of the inflammatory process: Upon injury to the body, which can be caused by trauma, burns, infection, etc., cytokines are produced on-site, inducing the cellular inflammatory process. At this point in the injury site:
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Tissue repair begins via the reticular endothelial system
Local vasodilation agents such as nitric oxide are released, increasing capillary permeability and causing redness
White blood cells enter interstitial space in an attempt to clear infection, causing swelling
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Local nerve endings are exposed or impacted by inflammatory response, causing pain
Blood flow increases, causing heat
CLINICAL MANIFESTATIONS
Heart rate greater than 90 beats per minute, may see some redness due to vasodilation
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Respiratory rate greater than 20 breaths per minute or PaCO2 less than 32 mm Hg
Hypotension (Systolic and/or
diastolic less than normal baseline)
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Complete blood count reveals WBC count greater than 12,000/µL, less than 4,000/µL, or greater than 10% immature band cells
Blood cultures may reveal infection
C-reactive protein test may be elevated (greater than 1.0 mg/dL.) indicating the presence of inflammation
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Blood glucose level may be elevated
NURSING DIAGNOSES
Acute pain R/T activation of the inflammatory response
Short-term Goal: The patient will maintain a pain level at or below a 3 on the 0-10 pain scale throughout the nursing shift.
Long-term Goal: The patient will no longer require pharmacological pain relief, and will verbalize and apply three methods of pain non-pharmacological pain relief.
Nursing Intervention: Explain to the client the pain management approach, including pharmacological and non-pharmacological interventions, the assessment and re-assessment process, potential side effects, and the importance of prompt reporting of unrelieved pain.
Evaluation: We will consider this intervention effective when the patient requests medication promptly and achieves goal pain level.
STAGE II
PATHOPHYSIOLOGY
Here macrophages and platelets are recruited and growth factor is stimulated, which is an appropriate inflammatory response. NORMALLY pro-inflammatory mediators are decreased in the hopes of regaining homeostasis, however; in SIRS they continue to be released, leading to stage III
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Cytokines are released into the circulation, which leads to growth factor stimulation and the recruitment of macrophages and platelets in an attempt to achieve homeostasis.
Other cytokines stimulate the release of acute-phase reactants such as C-reactive protein and procalcitonin.
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Tissue factor initiates the production of thrombin, thereby promoting coagulation. IL-1 and TNF-α also impair fibrinolysis, and proinflammatory cytokines disrupt the naturally occurring anti-inflammatory mediators antithrombin and activated protein-C.
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CLINICAL MANIFESTATIONS
Fever greater than 100.4° F or less than 96.8° F
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Malaise
Increased Pain
Inflammation
NURSING DIAGNOSES
Deficient Fluid Volume R/T compromised regulatory mechanisms
Short-term Goal: The patient will maintain a blood pressure between 120/80 and 130/90, a heart rate between 60-100, and body temperature between 97-99 degrees Fahrenheit throughout the nursing shift.
Long-term Goal: Prior to discharge, the patient will be able to verbalize three-five symptoms that indicate the need for provider consult due to fluid volume deficit.
Evaluation: We would consider this intervention effective if through close monitoring the patient's vitals remained within defined limits and consistently had urine output was 0.5-1ml/kg/hr.
Intervention: When ordered initiate fluid volume resuscitation measures for replacement of intravascular volume; monitor the client’s response to prescribed fluid therapy, especially noting vitals signs, urine output, blood lactate concentrations, and lung sounds.
ETIOLOGY
Drug Reactions
Ischemia - Myocardial Infarction
Autoimmune Disorders
Inflammation such as pancreatitis or vasculitis
Impaired Immunity
Infection
Seizures
Age - Greater than 65
Transfusion Reactions
Major surgeries, burns, or trauma
Community-acquired pneumonia
Diabetes and cancer
Septic Shock/Sepsis
TREATMENT
There is no specific drug of choice for the overall treatment of SIRS. Therefore, the drugs used within each stage target current symptoms and prophylaxis regimen for prevention of complications.
Broad spectrum antibiotics, such as Vancomycin, for suspected or confirmed infection
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Assess pain and give prescribed analgesics, such as Morphine
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IV fluids for hypotension and restoration of tissue perfusion early,and support kidneys
Vasopressors for hypotension not responsive to fluid administration
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Anticoagulants, such as enoxaparin for venous thromboembolism prophylaxis
Stool softeners such as docusate sodium (Colace)
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Kidney Failure: diuretics, antihypertensives if needed, iron and folic acid supplements
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Histamine-2 receptor antagonist, such as famotidine (Pepcid) and ranitidine hydrochloride (Zantac), for stress ulcer prophylaxis
Diet: NPO until condition stabilizes. Provide nutrition via the oral, enteral, or IV route
Activity: Bed rest until hemodynamically stable. Increase gradually as pt tolerates
Administer O2. Intubate/Ventilate if respiratory failure is present
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Surgical intervention based on initial cause, such as trauma or abscess
Auscultate both heart and lung sounds for changes
NSAIDs to decrease inflammatory response