Answer the questions in both scenarios in your own words. Answer these questions as if you were talking to a peer, unless otherwise indicated.
Shock Case Studies
K.L., a 25-yr-old Korean American, was not wearing his seat belt when he was the driver involved in a motor vehicle crash. The windshield was broken and K.L. was found 10 ft from his car. He was face down, conscious, and moaning. His wife and daughter were found in the car with their seat belts on. They sustained minor injuries and were very frightened and upset. All passengers were taken to the emergency department (ED). The following information pertains to K.L.
States, “I can’t breathe”
Cries out when abdomen is palpated
Cardiovascular: BP 80/56 mm Hg; apical pulse 138 but no palpable radial or pedal pulses; carotid pulse present but weak
Respiratory: respiratory rate 35 breaths/minute; labored breathing with shallow respirations; asymmetric chestwall movement; absence of breath sounds on left side
Trachea deviated slightly to the right
Abdomen: slightly distended and left upper quadrant painful on palpation
Musculoskeletal: open compound fracture of the lower left leg
Chest x-ray: Hemothorax and six rib fractures on left side
Interprofessional Care in the ED
Intraosseous access in right proximal tibia placed prehospital
Left chest tube placed, draining bright red blood
Fluid resuscitation started with crystalloids
High-flow O2via non-rebreather mask
Emergency Surgical Procedures
Repair of torn intercostal artery
Repair of compound fracture
What types of shock is K.L. experiencing? What clinical manifestations did he display that support your answer?
What were the causes of K.L.’s shock states? What are other causes of these types of shock?
Priority Decision: What are the priority nursing responsibilities for K.L.?
Priority Decision: What ongoing nursing assessment parameters are essential for this patient?
What are his potential complications?
Patient-Centered Care: K.L.’s parents arrive. English is their second language. They are very anxious and asking about their son. What can you do to provide culturally competent family-centered care?
Priority Decision: Based on the assessment data presented, what are the priority nursing diagnoses?
Teamwork and Collaboration: Identify the tasks that could be delegated to unlicensed assistive personnel (UAP).
Evidence-Based Practice: You are orienting a new graduate RN. He asks you why crystalloids are used instead of colloids for fluid resuscitation. What is your response?
Examine therapeutic nursing interventions associated end-of-life decision-making.
The following is information that will assist you in answering the question associated with scenario #2
Septic shock is
“A life-threatening organ dysfunction caused by a dysregulated host response to infection” (McCance & Huether, 2019, p. 1550).
The infectious process starts with an infectious agent entering the bloodstream and causing bacteremia either directly from the site of infection or indirectly by releasing toxic substances into the bloodstream. Some of the most common causes of septic shock are gram-negative or gram-positive bacteria, viruses, and fungi. The most common sites of infection are the lungs, bloodstream, intravascular catheters, intra-abdominal, urinary tract, and surgical wounds (McCance & Huether, 2019).
In normal physiology, when a pathogen invades the body, the body will react with local and systemic responses.
Our first line of defense is the body’s natural physical, mechanical, and biochemical barriers such as the epithelial cells and surfaces of the skin. These defenses prevent microorganisms from getting into tissues and also have the ability to remove infectious microorganisms. The surfaces of the skin and mucous membranes of the body also contain normal microbiomes (“normal flora”) that also protects the body by releasing chemicals to prevent pathogens from being colonized (McCance & Huether, 2019).
The body’s second line of defense is the inflammatory response. Inflammation causes a vascular response that makes vessel walls become leaky and more permeable and makes white blood cells adhere to vessel walls and migrate out into the tissues. Symptoms usually produced by inflammation are the heat, redness, edema and pain. The goal of inflammation is to prevent and limit infection and interact with components of the adaptive immune system as well as prepare the body for healing (McCance & Huether, 2019).
There are three important plasma protein systems involved to provide an active barrier against invading pathogens in the inflammatory response.
One is a complement system which destroys pathogens directly and work with other components of the immune responses by three pathways: (1) classic, (2) lectin and (3) alternative. The main functions of these are to induce rapid mast cell degranulation, attract white blood cells to pathogens, and “tag” pathogens for destruction (McCance & Huether, 2019).
Second is the clotting or coagulation system which forms blood clots that include a meshwork of protein strands at the injured or inflamed site to stop bleeding, trap pathogens to prevent the spread of infection, and provide a framework for repair and healing (McCance & Huether, 2019).
The last important inflammatory response is from the kinin system which activates and assists inflammatory cells by the release of mainly bradykinin which causes dilation of blood vessels, pain, smooth muscle contraction, increase vascular permeability and leukocyte chemotaxis (McCance & Huether, 2019).
There are also many biochemical mediators of the innate immune system that secrete cytokines responsible for activating other cells such as interleukins, chemokines, interferons, and other molecules. These chemicals are important to the vascular changes that occur during the inflammatory process (McCance & Huether, 2019).
Along with the cellular mediators are the cellular components such as platelets, phagocytes (neutrophils, eosinophils, monocytes, macrophages, and dendritic cells), natural killer cells, and lymphocytes. The components respond to the site of the injury together to limit the tissue injury, kill pathogens, remove the debris, and prepare for healing and tissue repair (McCance & Huether, 2019).
Septic shock begins when the pathogen enters the bloodstream. This stimulates the release toxic substances called the triggering molecules, which triggers the body to activate the proinflammatory responses and release proinflammatory cells such as leukocytes, macrophages, monocytes and platelets as well as proinflammatory mediators such as cytokines (interleukins, tumor necrosis factor alpha and other mediators). Cytokines along with the vasoactive peptides cause vasodilation causing hypotension, relative hypovolemia, and decreased in oxygen delivery to the tissues. The release of proinflammatory cytokines also activate plasma protein systems of the complement, coagulation and kinin systems (McCance & Huether, 2019).
Dysfunction of epithelial cells cause further capillary leaking and microvascular thrombus, tissue hypoxia and apoptosis. Due to tissue hypoxia, the body will start breaking down carbohydrates to make ATP or energy for the body. As more anaerobic cells are being used for energy, the more lactic acid is produced. Without correction, the accumulation will lead to metabolic acidosis causing further damage to the tissues (McCance & Huether, 2019).
As the responses of proinflammatory and anti-inflammatory mediators intensify the body experiences persistent low arterial pressure, low tissue perfusion, low systemic vascular resistance which will profoundly affect the circulatory, cellular, and metabolic systems. These responses will lead to multiple organ dysfunction syndrome (MODS) due to dysfunction of the kidneys, liver, intestines, lungs, and brain as a result of tissue hypoxia and lack of tissue perfusion (McCance & Huether, 2019).
Septic shock is measured by the SOFA score and assessing different systems in relation to the severity of the organ failure. The quick SOFA criteria include a respiratory rate equal or greater than 22 per minutes, altered mentation and systolic blood pressure less than 100 mmHg. The standard SOFA scoring includes respiration, coagulation of platelets, bilirubin level of the liver, mean arterial pressure, Glasgow coma scale score, creatinine level, and urine output.
Clinical manifestations of septic shock usually include fever, chills, sweating, warm progressing to cool skin, respiratory distress, altered mentation, decreased urine output, hypotension, elevated liver enzymes, and decreased platelet counts (McCance & Huether, 2019).
Mr. S. S. is a 56-year-old, white male with a right diabetic foot ulcer. He was at his podiatrist’s office for a wound check and was referred to the emergency department (ED) due to increasing purulent drainage and necrotic tissue in the wound. Mr. S.S. noticed the drainage getting worse over the last week and has experienced fevers up to 102 degrees F for two days. He also complains of diaphoresis, fatigue, abdominal pain, and general malaise. He states he just does not feel like himself.
Past Medical History:
Allergic to Penicillin and shellfish
Uncontrolled Type 2 Diabetes Mellitus
Hypertension [baseline 140/90]
Cholecystectomy, age 32 years
Left Above the Knee Amputation (AKA), age 54 years
Pertinent Family History:
Mother- Hyperlipidemia, Hypertension, CABG x2 vessels
Father- Prostate Cancer, age 63 years
Pertinent Social History:
Active Smoker (2 packs/day)
History of Alcoholism
Previous history of homelessness
In the ED, assessment reveals moderate foul odor, purulent drainage from right foot ulcer, and capillary refill of four seconds on upper and lower extremities. Patient is alert and oriented but short-term memory appears to be impaired and the patient is asking abnormal questions. Two peripheral IVs and an indwelling foley catheter are placed, a 1000mL bolus of IVF is initiated, wound and blood cultures are obtained, and the patient is started on broad spectrum antibiotics. An x-ray of his right foot demonstrates soft tissue inflammation and concern for osteomyelitis, so an MRI was completed of his foot. The patient is transferred to MICU for further management.
Temperature: 101.6 degrees F
Heart Rate: 117 bpm
Respiration Rate: 24 breaths/min
Blood Pressure: 92/45 mm Hg (MAP 61)
Blood glucose: 315 mg/dL
SpO2: 91% on 2L NC
Lactate: 6.0 mmol/L
C-reactive Protein: 11mg/L
Creatinine: 1.4 mg/dL
Medical Intensive Care Unit
Upon admission to MICU, Mr. S.S. is lethargic and flushed. Further assessment demonstrates bounding pulses and right lower extremity edema. His heart rate increased and blood pressure dropped despite the liter bolus. The patient is started on vasopressors to maintain his blood pressure and intubated to protect his airway.
Temperature: 101.4 degrees
Heart Rate: 154 bpm
Respiration Rate: 30 breaths/min
Blood Pressure: 72/34 (MAP 47)
SpO2: 86% on 2L NC
All of the options below are the most common causes of septic shock except for:
Which of the following criteria would you expect to see from a patient with septic shock?
Elevated lactate level
30 ml/hr of urine output
Respiration of 18 rate per minute
Patient is alert and oriented
Which of the following are measurable components of the quick SOFA? Select all that apply.
Systolic blood pressure
The patient wants to know more about sepsis asking if he or any of his family members would be at higher risk for sepsis. You tell the patient that most vulnerable patients for this problem would be: (Select all that apply)
Children younger than one
Patients who have received recommended vaccinations
Adults 65 years old and older
People with weakened immune systems
People with chronic diseases
People have been traveled outside of the United States
Discuss why septic shock is one of the leading causes of death in the intensive care units.
Examine therapeutic nursing interventions associated end-of-life decision-making.