Sepsis and MODS: A Comprehensive Guide PDF

**Sepsis** - One of the **most common types of circulatory shock** and the incidences of this disease continue to rise despite the technology. - Is a condition in which infectious microorganisms have entered the bloodstream (Ignativicius, 2020) - Systemic response to **infection**....

**Sepsis** - One of the **most common types of circulatory shock** and the incidences of this disease continue to rise despite the technology. - Is a condition in which infectious microorganisms have entered the bloodstream (Ignativicius, 2020) - Systemic response to **infection**. It is manifested by **two or more of the SIRS** (Systemic Inflammatory Response Syndrome) criteria as a consequence of documented or presumed infection. (Burns, 2019) - A severe, life-threatening condition that results from a dysregulation of the patient's response to an infection - Caused by a wide variety of microorganisms including: ----------------------------------------------------- - **Gram-negative** (Pseudomonas, E.coli, Klebsiella) - **Gram-positive bacteria** (Staphylococcus and Streptococcus) - Fungi ----- - **Viruses** - **Respiratory system**- most common site of infection producing severe sepsis and septic shock followed by genitourinary and gastrointestinal system - The predominant cause -- gram-positive bacteria ----------------------------------------------- +-----------------------------------+-----------------------------------+ | | - a sepsis syndrome accompanied | | | by a circulatory and | | | metabolic abnormalities that | | | can significantly increase | | | the mortality | | | | | | - associated with sepsis. It is | | | characterized by symptoms of | | | sepsis plus **hypotension** | | | and **hypoperfusion** despite | | | adequate fluid volume | | | replacement. | | | | | | | | | | | | - a sepsis plus sepsis induced | | | organ dysfunction or tissue | | | hypoperfusion wherein all | | | tissues involved would become | | | hypoxic and some organs are | | | experiencing cell death that | | | results in to the dysfunction | | | of organ | | | | | | | | | | | | - a constellation of | | | physiological and immune- | | | mediated reactions of the | | | body to an infection or | | | noninfectious insult | +-----------------------------------+-----------------------------------+ | | | +-----------------------------------+-----------------------------------+ -- -- - is the presence of altered organ function in acutely ill patients such that homeostasis cannot be maintained without intervention. - It usually involves two or more organ systems. - It calls for an **immediate intervention.** -- -- -- -- -- -- - **Inflammation** - **Thrombosis** - **Fibrinolysis/ hypofibrinolysis** - **Fibrinolysis**- present in early sepsis; cause the breakage of clot - **Hypofibrinolysis**- occur in late sepsis The following shows the process of how sepsis works its way inside of our body. ------------------------------------------------------------------------------- 1. Microorganisms invade the body tissues and in turn, patients exhibit an immune response. 2. The immune response provokes the activation of **biochemical [[cytokines]](https://nurseslabs.com/lymphatic-system-anatomy-physiology/)** and mediators associated with an inflammatory response. 3. Increased capillary permeability and vasodilation interrupt the body's ability to provide adequate perfusion, oxygen, and nutrients to the tissues and cells. 4. Proinflammatory and anti-inflammatory cytokines released during the inflammatory response and 5. The imbalance of the inflammatory response and the [[clotting]](https://nurseslabs.com/hemophilia-nursing-care-plans/) and fibrinolysis cascades are critical elements of the physiologic progression of sepsis in affected patients. Defining Characteristics of SIRS: --------------------------------- - Hypodynamic state -- because of vasodilation - Increased release of proinflammatory cytokine - Polling of the blood - Cellular hypoxia - Vascular damage - Formation of microthrombi Cause of the development of Multi Organ Dysfunction Syndrome is: ---------------------------------------------------------------- - Cell anoxia - Cell death - Failure of nonvital organs - Reduce function of the vital organs - Widespread DIC Sequence of events in patients with sepsis ------------------------------------------ - Patients with **immunosuppression** have greater chances of acquiring septic shock because they - **Extremes of age.** Elderly people and infants are more [[prone]](https://nurseslabs.com/patient-positioning/) to septic shock because of their **weak immune system**. - **Malnourishment**. Malnourishment can lower the body's defenses, making it susceptible to the invasion of pathogens. - **Chronic illness.** Patients with a longstanding illness are put at risk for sepsis because the body's immune system is already weakened by the existing pathogens. - **Invasive procedures.** Invasive procedures can introduce microorganisms inside the body that could lead to sepsis. +-----------------------------------------------------------------------+ | - - - **Gastrointestinal**: **Abdominal Infections** (e.g., | | intraabdominal abscess) | | | | - - **Implanted devices** (e.g., CVC, port-a-cath, urinary | | catheter, ET) | +-----------------------------------------------------------------------+ -- -- - The signs and symptoms that are associated with septic shock and sepsis include the following: - **Tachycardia**- Since the ability of the body to provide oxygen and nutrients is interrupted, the **heart compensates** by pumping faster. - **Hypotension** occurs because of **vasodilation**. - **Tachypnea**- To compensate for the decreased oxygen concentration, the patient tends to breathe faster, and also to eliminate more carbon dioxide from the body. - The inflammatory response is activated because of the invasion of pathogens. - **Decreased [[urine]](https://nurseslabs.com/urinary-system/) output.** The body conserves water to avoid undergoing **[[dehydration]](https://nurseslabs.com/cholera/)** because - **Changes in mentation**. As the body slowly becomes acidotic, the patient's mental status also deteriorates. - **Elevated lactate level.** The lactate level is elevated because there is maldistribution of [**[blood]**](https://nurseslabs.com/blood-anatomy-physiology/). Prevention ---------- - Strict infection control practices- **Effective aseptic techniques and interventions.** - Prevent central line infections. - Early debriding of wounds. - Equipment cleanliness. Complications ------------- - Severe sepsis - **Multiple organ dysfunction syndrome.** -- there is already the presence of altered function of either 1 or more of the organs in acutely ill patient requiring intervention to support the organs to achieve physiological functioning that is required to maintain the homeostasis of the body - Hypotension or hypoperfusion of organs - Lactic acidosis - Oliguria - Altered LOC - Coagulation disorder - Altered hepatic function 1. **Sepsis surveillance**: Identify patients with potential sepsis. - Quick SOFA (Sequential Organ Failure Assessment) criteria: ---------------------------------------------------------- - Alteration in mental status - Systolic blood pressure ≤ 100 mm Hg - Respiratory rate ≥ 22/min - The SIRS criteria also commonly still used to identify patients at risk of sepsis. 2. **Initial clinical evaluation** (should follow ABCDE approach) - IV access, vital signs, monitor - Initial labs - **Serum lactate:** Elevated lactate reflects hypoperfusion and is associated with worse outcomes. - **2 sets of blood cultures** (**aerobic and anaerobic**) before administering antibiotics (if possible) - Additional serum for further laboratory studies may be obtained at this time - If there is any concern for septic shock and/or respiratory failure or airway compromise: Provide immediate hemodynamic and respiratory support 3. Initial resuscitation and ongoing clinical reassessment ------------------------------------------------------- - **Provide hemodynamic support.** - **Fluid resuscitation**: Many patients may benefit from around 30 mL/kg of crystalloid fluids - If there is persistent hypotension; during or after fluid resuscitation, start **vasopressors (dopamine or levophed)** and titrate to maintain a MAP ≥ 65 mm Hg. - Start empiric broad-spectrum antibiotics - Continuous reassessment of the clinical response to resuscitation to guide the decision to escalate fluids or pressors 4. Supportive care --------------- - 2018 Surviving Sepsis Campaign recommendations for initial management - Hour-1 bundle for sepsis - **Five measures to start within the first hour of recognizing sepsis.** - **Blood cultures** - **Serum lactate** - **IV fluids** - **Vasopressors** - **Antibiotics** 5. **Respiratory support** - Address **hypoxemia** if present: Secure airway and start oxygen therapy as needed. - Consider mechanical ventilation - Maintain a high index of suspicion for ARDS to ensure early identification. - Shock and metabolic acidosis are both associated with a high risk of peri-intubation mortality. 6. Corticosteroids --------------- - E.g., **hydrocortisone** - Consider as adjuvant therapy if **hypotension is refractory** to the first vasopressor - Consider for patients with suspected adrenal insufficiency or patients taking long-term steroids +-----------------------------------------------------------------------+ | - **Initial resuscitation:** rapid crystalloid infusion of 30 mL/kg | | | | - **Indications**: sepsis and/or signs of hypoperfusion are | | present (e.g., hypotension, elevated lactate) | | | | - Start immediately (within the first hour of presentation) and | | complete within 3 hours. | | | | - There is no benefit of colloids over crystalloids for most | | patients. | | | | - **Additional fluids:** The decision to give additional fluids | | should be informed by fluid responsiveness | | | | - 6--10 L of IV fluids may be necessary during the first 24 hours. | +-----------------------------------------------------------------------+ +-----------------------------------------------------------------------+ | - Hemodynamic and perfusion status should be continually reassessed | | to determine whether additional fluids are indicated (i.e., | | whether the patient is fluid responsive or not) or hemodynamic | | support should be escalated (i.e., whether vasopressor support is | | needed). | | | | | | | | - **Monitor hemodynamic parameters** | | | | - **Vital signs:** e.g., mean arterial pressure (MAP), heart | | rate | +-----------------------------------------------------------------------+ - **Second-line:** if MAP persistently low - Add vasopressin - OR add continuous IV epinephrine infusion (off-label) - **Third-line:** consider as alternate vasopressors in select cases, or as an additional vasopressor for refractory tissue hypoperfusion. - **Dopamine**- to restore the MAP in patients who remains hypotensive after volume resuscitation - **Dobutamine**- administered to a maximum of 20mcg/kg/min -- counteract myocardial depression and maintain adequate cardiac output - **Corticosteroid** e.g Hydrocortisone - **Nutrition and electrolytes** - Improve the overall nutritional status and enhance the immune function and promote wound healing - Daily caloric intake of 20 to 30 kcal/kg of the usual body weight of the patient with sufficient protein of 1.2 to 2g/kg - Enteral nutrition- advised or preferred Electrolyte Replacement ----------------------- - Dependent on the electrolyte involved and the level of the electrolytes of the patients - Blood transfusion to consider as needed --------------------------------------- - Administration of platelet when having thrombocytopenia \< 5000 per mm3 - Bleeding and clotting factors are decreased- administered fresh frozen plasma or platelet concentrate - Administration of pack RBCs- hemoglobin is - VTE Prophylaxis --------------- - With the use of heparin therapy with fractionated heparin or low molecular weight heparin - Use of antiembolic stocking -- -- - Nurses must keep in mind that the risks of sepsis and the high mortality rate associated with sepsis, severe sepsis, and septic shock. +-----------------------------------------------------------------------+ | - Assessment is one of the | | [[nurse]](https://nurseslabs.com/registered-nurse/)'s | | primary responsibilities, and this must be done precisely and | | diligently. | | | | | | | | - **Signs and symptoms**. Assess if the patient has positive blood | | culture, currently receiving | | [[antibiotics]](https://nurseslabs.com/antibiotics/), | | had an examination or [[chest | | x-ray]](https://nurseslabs.com/chest-x-ray/), or has | | a suspected infected wound. | | | | - **Signs of acute organ dysfunction**. Assess for presence of | | hypotension, tachypnea, | +-----------------------------------------------------------------------+ +-----------------------------------------------------------------------+ | - Sepsis can affect a lot of body systems and even cause their | | failure, so diagnosis is an important part of the process to | | establish the presence of sepsis. | | | | | | | | - **Risk for [[deficient fluid | | volume]](https://nurseslabs.com/deficient-fluid-volum | | e/)** | | related to massive vasodilation. | | | | - **Risk for [[decreased cardiac | | output]](https://nurseslabs.com/decreased-cardiac-out | | put/)** | | related to decreased preload. | | | | - **Impaired [[gas | | exchange]](https://nurseslabs.com/impaired-gas-exchan | | ge/)** | | related to interference with oxygen delivery. | | | | - | +-----------------------------------------------------------------------+ -- -- - Is altered organ function in acutely ill patients requiring medical intervention to support continued organ function. - Results from progressive physiologic failure of two or more separate organ systems in an acutely ill patient such that homeostasis cannot be maintained without intervention. - MODS is the major cause of death in patients cared for in critical care units. - People at risk of MODS are those with a disturbance in homeostasis resulting from one or a combination of the following conditions: - Infection - Injury - Inflammation - Ischaemia - Immune response - Intoxication of substances - Iatrogenic factors. - The primary organ systems involved in MODS are the respiratory, renal, hepatic, haematological, cardiovascular, gastrointestinal and neurological systems -- -- -- -- - results from a well-defined insult in which organ dysfunction occurs early and is directly attributed to the insult itself. - Direct insults initially cause localized inflammatory responses. Primary MODS accounts for only a small percentage of MODS cases. - These cellular or microcirculatory insults may lead to a loss of critical organ function induced by failure of delivery of oxygen and substrates, coupled with the inability to remove end products of metabolism. -- -- - is a consequence of widespread sustained systemic inflammation that results in dysfunction of organs not involved in the initial insult. - Secondary MODS develops latently after an initial insult.86 The early impairment of organs normally involved in immunoregulatory function, such as the liver and the GI tract, intensifies the host response to the insult. - SIRS and sepsis are common initiating events in the development of Secondary MODS. - The **systemic inflammatory response (SIRS)** is an intense host response characterized by sustained generalized inflammation in organs remote from the initial insult. SIRS is widespread inflammation or clinical responses to inflammation that occur in patients suffering a variety of insults. -- -- Clinical Conditions ------------------- - Infection - Infection of vascular structures (heart and lungs) - Pancreatitis - Tissue ischemia or hypoxia - Multiple trauma with massive tissue injury - Hemorrhagic shock - Immune-mediated organ injury - Exogenous administration of tumor necrosis factor or other cytokines - Aspiration of gastric contents - Massive transfusion - Host defense abnormalities Clinical Manifestations (SIRS) ------------------------------ - Temperature \>38° C or \90 beats/min - Respiratory rate \>20 breaths/min or PaCO2 \12,000 cells/mm3 or \10% immature (band) forms - **SIRS** is a result of infection, the term ***sepsis*** is used. - **SIRS,** sepsis, severe sepsis, and septic shock represent a hierarchical continuum of the inflammatory response to infection - Organ dysfunction may begin in the lungs and progress to the liver, gut, and kidneys followed by cardiac and bone marrow dysfunction and neurologic and autonomic system impairment may occur and propagate the progression of organ failure. -- -- +-----------------------------------------------------------------------+ | - - is a highly metabolic fatty acid that is a precursor of many | | biologically active substances known as *eicosanoids* | | | | - Activation of the AA cascade by hypoxia, ischemia, endotoxin, | | catecholamines, and tissue injury produces metabolites from | | the cyclooxygenase and lipoxygenase pathways. | | | | - AA metabolites have profound effects on vasculature and cause | | vascular instability and maldistribution of blood flow. | | | | - - - - - are proteolytic (protein-digesting) enzymes | | released from neutrophils. Proteases damage endothelium and | | contribute to vascular permeability and organ dysfunction. | +=======================================================================+ | | +-----------------------------------------------------------------------+ | - - - | +-----------------------------------------------------------------------+ -- -- Gastrointestinal Dysfunction ---------------------------- - Abdominal distention and ascites - Intolerance to enteral feedings - Paralytic ileus - Upper or lower gastrointestinal bleeding - Diarrhea - Ischemic colitis - Mucosal ulceration - Decreased bowel sounds - Bacterial overgrowth in stool Hepatobiliary Dysfunction Liver ------------------------------- - Jaundice - Hepatomegaly - Increased serum bilirubin (hyperbilirubinemia) - Increased liver enzymes - Increased serum ammonia - Decreased serum albumin - Decreased serum transferrin Gallbladder ----------- - Right upper quadrant tenderness or pain - Abdominal distention - Unexplained fever - Decreased bowel sounds Pulmonary Dysfunction --------------------- - Tachypnea - Acute lung injury pattern of respiratory failure (dyspnea, patchy infiltrates, refractory hypoxemia, - Pulmonary hypertension Kidney Dysfunction ------------------ - Decreased glomerular filtration rate/creatinine clearance - Increased serum creatinine, blood urea nitrogen levels - Oliguria, anuria, or polyuria consistent with prerenal azotemia or acute kidney injury - Urinary indexes consistent with prerenal azotemia or acute kidney injury - Electrolyte imbalance Hyperdynamic ------------ - Decreased pulmonary capillary occlusion pressure - Decreased systemic vascular resistance - Decreased right atrial pressure - Decreased left ventricular stroke work index - Increased oxygen consumption - Increased cardiac output, cardiac index, heart rate Hypodynamic ----------- - Increased systemic vascular resistance - Increased right atrial pressure - Increased left ventricular stroke work index - Decreased oxygen delivery and consumption - Decreased cardiac output and cardiac index Central Nervous System ---------------------- - Lethargy - Altered level of consciousness - Fever - Hepatic encephalopathy Coagulation or Hematologic -------------------------- - Thrombocytopenia - Disseminated intravascular coagulation PROGNOSIS ========= - high mortality rate, clients may recover depending on the following factors: - Severity of illness or injury - Underlying organ reserve - Speed of instituting intervention or management - Adequacy of treatment - Number, severity of subsequent injuries or complications - If treatment is unsuccessful, death occurs between 21-28 days -- -- - The patient with MODS requires multidisciplinary collaboration in clinical management +-----------------------------------------------------------------------+ | 7. **Prevent and maintain surveillance for complications, | | particularly infection.** | | | | 8. | +-----------------------------------------------------------------------+ -- -- - Primary nursing interventions are aimed at supporting the patient and monitoring organ perfusion until primary organ insults are halted. +-----------------------------------------------------------------------+ | 1. 2. 3. 4. 5. | +-----------------------------------------------------------------------+ +-----------------------------------------------------------------------+ | 1. Assess for LOC, observe for respiratory depression and for | | increased ICP if necessary. | | | | 2. Observe for and report for: dyspnea, use of accessory muscle, | | discolored sputum, wheezes, crackles, rhonchi, poor capillary | | refill, decrease oxygen saturation, abnormal ABG. | | | | 3. Monitor for: HR, BP, CVP, decreased pulses, decreased urine | | output, dysrrhythmias, increased isoenzymes and increased | | troponins. | | | | 4. Assess for and report: decreased bowel sounds, abdominal | | distention, diarrhea, constipation or impaction, jaundice, | | ascites, increased ammonia level, decreased plasma proteins, | | decreased clotting factors, and increased liver enzymes. | | | | 5. Monitor and report for: changes in urine output, color, odor, | | monitor laboratory values of BUN, creatinine. | +-----------------------------------------------------------------------+