Multisystem Study Guide for the CCRN

Shock and Sepsis

Two important conditions to know in critical care nursing are shock and sepsis. While these two diagnoses often occur together or because of each other, they can also occur independently. Sepsis is the result of harmful microorganisms in the blood. Shock is associated with a drop in blood pressure due to serious events such as sepsis, blood loss, neurogenic injury, and other illnesses. Both will be reviewed in the next section of this guide.

Sepsis Continuum

Sepsis is the body’s extreme reaction to an infection. Many infectious conditions can lead to sepsis; however, sepsis occurs on a continuum starting from less-severe bacteremia all the way to septic shock. Sepsis should be identified and treated as early as possible to prevent complications. It may develop over the course of several days or within several hours and can range in severity.

The difference between bacteremia and septicemia is that in bacteremia, there is just the presence of bacteria in the blood without systemic infection. When the bacteria in the blood cause systemic infection, it then develops into septicemia. Septicemia generally occurs due to bacterial infection but can also be viral or fungal. The infection may need to be treated with antibiotics or antifungal medications while other bodily responses are managed, including blood pressure, fever, and pain.

Systemic inflammatory response syndrome (SIRS)—SIRS is the multiorgan inflammation that can occur due to systemic infection. It may also happen in the event of burns, trauma, adrenal insufficiency, drug overdose, and pulmonary embolism. To be diagnosed with SIRS, a patient must have at least two of the four following symptoms: rectal temperature greater than \(38\) or less than \(36\) degrees Celsius, \(\text{PaCO}_2\) less than \(32\, \text{mmHg}\) or tachypnea, tachycardia, and/or leukocytosis represented by a number greater than \(12\text{,}000\,\text{WBC per}\, \text{mm}^3\) or leukopenia less than \(4\text{,}000 \,\text{WBC per mm}^3\).

Sepsis—Sepsis develops when patients have an identified or suspected infection with presence of SIRS.

Severe sepsis—Patients with severe sepsis have SIRS and all the symptoms of sepsis described above, as well as signs of end-organ dysfunction. This includes changes in mental status, hypoxemia, elevated plasma lactate, or decreased urinary output (<5 mL/kg/hr for >1 hr).

Septic shock—Sepsis can develop into septic shock when infection and symptoms progress to refractory hypotension despite treatment of sepsis. Patients with septic shock will show significant signs of organ damage and often experience abnormal lab values, including electrolyte imbalances, increased WBC count, and lactic acidosis.

Sepsis is initially managed by obtaining blood cultures to identify the underlying pathogen, starting broad-spectrum antibiotics until the blood cultures result, rapid IV-fluid resuscitation at 30 mL/kg, trending serum lactate levels, and starting vasopressors if shock is present.

Shock States

Shock occurs when there is a significant decrease in tissue perfusion due to inadequate blood flow or impaired oxygen delivery. This state is triggered by an underlying event such as blood loss, infection, or allergic reaction. Insufficient tissue perfusion decreases oxygen flow to the cells, ultimately leading to tissue injury. The hallmark symptoms of shock include hypotension, tachycardia, decreased urinary output, and altered mental status. Hyperglycemia may also occur in shock as part of the body’s stress response. Lactate levels rise in shock as poor perfusion forces cells into anaerobic metabolism. The buildup of lactate is the main cause of metabolic acidosis in shock.

Several types of shock exist, but all share similar physiological responses. The primary types of shock are distributive, obstructive, cardiogenic, and hypovolemic. Cardiogenic shock is covered in the cardiovascular guide, and the remaining three types will be discussed here.

Distributive Shock

Septic shock is one of the most common causes of distributive shock. Other types include anaphylactic shock and neurogenic shock. These types of shock occur because there is an inadequate effective circulating volume due to widespread vasodilation and increased permeability from infectious, neurogenic, or allergic bodily responses. Patients with distributive shock often have adequate blood volume but may experience decreased cardiac and vascular function due to the shock response. A distinguishing feature of distributive shock is that skin may initially be warm due to vasodilation but becomes cool and clammy as perfusion worsens.

Patients who experience distributive shock will need to be stabilized and have any underlying causes treated. Oxygen therapy and intubation may be required. Fluid resuscitation, as well as vasoconstrictive and/or inotropic medications, may be used to help restore blood volume and correct hypotension.

Septic Shock

Septic shock develops due to the toxins released by bacteria and cytokines in response to infection within the body. As the shock progresses, damage can occur to other organs, including acute kidney injury, liver dysfunction, acute respiratory distress syndrome (ARDS), and myocardial depression.

Those at highest risk for septic shock are newborns, patients older than 50 years, and immunocompromised patients. Common laboratory work collected when septic shock is considered include CBC, lactate, electrolyte panel, liver function tests, blood glucose, ABG, urinalysis, DIC panel, and BUN. Patients should also have blood and urine cultures performed, as well as radiologic imaging, to identify the source of infection, which is the underlying cause of septic shock and the key defining feature compared to the other types.

Treatment includes early broad-spectrum antibiotics, rapid fluid resuscitation, and supportive care, with vasopressors initiated if hypotension persists. For more information on the management sepsis, refer to the section above.

Anaphylactic Shock

Patients with severe allergies may experience anaphylaxis which is a severe, systemic hypersensitivity reaction that occurs rapidly. Symptoms include angioedema, urticaria, flushing, wheezing, laryngospasm or bronchospasm; and gastrointestinal symptoms like nausea, vomiting, and diarrhea. This reaction can become severe enough to cause significant vasodilation and airway compromise, leading to anaphylactic shock.

Patients experiencing anaphylactic shock will need to have a secured, patent airway with \(100\%\) oxygen administration. Administration of epinephrine should be performed to help block the progressive allergic reaction. Albuterol may also be used for bronchospasm. Diphenhydramine and methylprednisolone are used as an adjunctive treatment after epinephrine is given. Vital signs should be monitored closely. Patients may require IV fluid resuscitation to treat hypotension.

Neurogenic Shock

Neurogenic shock occurs when there is a loss of sympathetic tone, most commonly from a spinal cord injury at or above T6. It may also follow trauma, neurologic disease, drugs, or anesthesia.

This disruption of sympathetic pathways causes vasodilation, leading to low blood pressure and reduced perfusion. A unique feature of neurogenic shock is bradycardia as opposed to other shock types that present with tachycardia. Additionally, patients often have impaired thermoregulation due to disruption of hypothalamic control. This may result in a neurogenic fever or temperature instability. Treatment of neurogenic shock includes supportive care, fluid resuscitation, vasopressors (specifically norepinephrine) and inotropic agents. Patients with persistent and symptomatic bradycardia may be given atropine. Patients with neurogenic shock may need placement of a pulmonary artery catheter to monitor fluid overload.

Obstructive Shock

Obstructive shock results from a physical obstruction to blood flow that prevents adequate cardiac output despite normal circulating volume. Common causes include pulmonary embolism, cardiac tamponade, and tension pneumothorax. This obstruction leads to decreased venous return, reduced stroke volume, and ultimately impaired tissue perfusion.

The distinguishing feature is the presence of signs related to the underlying cause of obstruction. In pulmonary embolism, patients may exhibit sudden dyspnea, chest pain, tachycardia, and hypoxemia.Cardiac tamponade may present with jugular venous distention and muffled heart sounds. In tension pneumothorax, findings may include unilateral absent breath sounds, tracheal deviation away from the affected side, and respiratory distress.

Treatment focuses on rapid identification and removal of the obstruction. Interventions such as thrombolysis, periocardiocentesis, or chest decompression may be needed depending on the cause, as well as hemodynamic support and oxygen therapy. Unlike in other types of shock, IV fluids are used cautiously in small boluses as a temporary measure to support cardiac output until definitive treatment can be performed.

Hypovolemic Shock

Hypovolemic shock results from insufficient vascular volume. Insufficient volume levels can be a result of external fluid loss (bleeding, diarrhea, vomiting, etc.) or internal fluid shift. It can be related to vasodilation, decreased osmotic pressure, or increased capillary permeability.

Hypovolemic shock is typically divided into hemorrhagic shock (blood loss) and non-hemorrhagic shock (any fluid loss unrelated to bleeding). There are several classes of hypovolemic shock signifying the severity of the fluid loss.

• Class I is diagnosed when fluid loss is less than 750 mL or less than 15% of the total circulating volume.

• In Class II, fluid loss ranges from 750 to 1000 mL or 15 to 30% of total circulating volume.

• Class III progresses to 1500 to 2000 mL or 30 to 40% of loss.

• Class IV is identified as greater than 2000 mL or greater than 40% of fluid loss.

A patient with extensive fluid loss will experience cardiac involvement due to lowered circulating fluid volume. It can be expected that patients will have a decrease in ventricular filling and preload, leading to decreased stroke volume and cardiac output.The body initially compensates with tachycardia, which helps maintain cardiac output. In severe or prolonged hypoperfusion, patients are at increased risk of dysrhythmias, myocardial ischemia, and eventual progression to cardiac arrest if untreated. Vasoconstriction develops, which decreases tissue perfusion and can cause cellular injury.

Symptoms of hypovolemic shock include cold and clammy skin, pallor, anxiety, cyanosis, hypotension, increased respirations, and weakened pulse. Treatment of hypovolemic shock includes treating underlying causes. The priority treatment is to replace fluid loss with blood, crystalloids fluids, or colloids depending on the primary fluid deficit. The other treatments are to use oxygen support and to use vasopressors or dopamine as needed for fluid-resistant hypotension.

Other Multisystem Issues

Critically ill patients are often plagued by several conditions that complicate their hospital stay. These can affect several bodily systems and be difficult to manage. Understanding the conditions discussed previously and how they can affect the body as a whole is a critical part of intensive care nursing.

Toxin/Drug Exposure

Several ingested or inhaled medications and illicit drugs can cause severe reactions in patients. These reactions may be caused by an allergy, adverse side effects, medication overdose, or exposure to toxic chemicals. The severity of the reaction depends on the offending medication or drug and the length of exposure. Patients with severe reactions may develop metabolic acidosis due to tissue hypoperfusion and lactic acidosis. Patients are also at risk for shock, organ damage/failure, and death if the toxicity is not treated.

Symptoms

Clinical presentation varies by the substance. Patients with allergic reactions to a toxin or drug may exhibit urticaria, pruritus, generalized trunk pain, facial flushing, edema, difficulty breathing, and wheezing. Patients with specific drug exposure may have different effects. Patients with stimulant exposure such as amphetamine, cocaine, ephedrine, and pseudoephedrine may experience diaphoresis, hypertension, pupil dilation, and tachycardia. This is otherwise known as the beta- and alpha-adrenergic response. Toxic ingestions or inhalations from substances like illicit drugs, alcohol, acetaminophen, salicylates, household cleaners, and benzodiazepines can cause a wide range of symptoms depending on the organ system affected.

Diagnosis and Treatment

Diagnosis focuses on obtaining a thorough patient history, laboratory evaluation, toxicology screen, and allergy testing. Treatment of this condition is focused on eliminating any continued exposure to the offending substances. Antidotes to medications may be used when available. Naloxone (Narcan®) may be used in the event of an opiate overdose. N-acetylcysteine works to inactivate acetaminophen. Calcium channel blockers can be reversed with calcium chloride, and beta-blockers can be reversed with glucagon. Sodium bicarbonate can be used to negate tricyclic antidepressants. Deferoxamine does the same for iron. Activated charcoal (1 g/kg within one hour of ingestion) may also be used to absorb toxins from ingested substances and can be repeated every four to six hours if needed. Injected epinephrine and/or diphenhydramine (Benadryl®) should be used for patients with allergic reactions. In some cases, dialysis may be needed to clear toxins from the bloodstream while supporting kidney healing and function.

Anoxic Injury

While hypoxia and asphyxiation events are covered in our respiratory study guide, anoxia refers to a complete lack of oxygen delivery to the tissues, leading to widespread, multisystem injury. The most common cause is cardiac arrest because once the heart stops, there is no blood flow to deliver oxygen to any organ. Other causes of anoxia include severe hypotension and/or blood loss, stroke, airway obstruction, carbon monoxide poisoning, and drug overdose or any other kind of respiratory failure. Because the brain and heart utilize a significant amount of the body’s oxygen, patients often present with altered mental status, seizures, arrhythmias, or progression to cardiac arrest. Patients may also demonstrate clinical indicators of poor oxygenation and gas exchange, such as pallor, cyanosis, apnea, and decreased or unobtainable SpO2 readings. Diagnosis is clinical and may rely on laboratory and imaging studies. Lactate is typically elevated and ABGs show severe acidosis. Management focuses on immediate restoration of oxygenation and/or perfusion through airway support, ventilation, and hemodynamic stabilization, followed by treatment of the underlying cause.

Anoxia impacts all organ systems, but after immediate stabilization, the primary concern becomes neurologic recovery. The brain is extremely sensitive to oxygen deprivation, and even brief periods of anoxia can lead to irreversible injury. This is referred to as an anoxic brain injury, which can result in long-term or permanent deficits depending on the duration and severity of oxygen deprivation. Patients may experience cognitive impairment, memory loss, motor dysfunction, seizures, or a vegetative state in severe cases.

Rhabdomyolysis

Rhabdomyolysis occurs when damaged skeletal muscles release toxins into the bloodstream. Skeletal muscle damage can occur due to trauma, infection, sepsis, immobilization, ischemia, myopathy, extreme physical activity, and medications including SSRIs, lithium, antihistamines, and statins. Alcohol and drug abuse, especially cocaine, and toxins from animal or mushroom poisoning can also cause this condition.

Early recognition of rhabdomyolysis is critical to preventing long-term complications and renal failure. It may become life-threatening. Signs and symptoms of rhabdomyolysis include muscle pain, weakness, fever, tachycardia, electrolyte imbalance, lethargy, hypotension, and metabolic acidosis. Presence of myoglobin in the urine may cause the urine to turn dark reddish-brown.

Diagnosis of rhabdomyolysis can be confirmed with creatine kinase (CK) levels above 1000 u/L, which is five times greater than the normal level. Other labs that may be drawn include metabolic panel, urinalysis, and arterial blood gases.

Treatment of rhabdomyolysis focuses on the clearing of toxins from the body and reduction of risk for renal failure. Patients will require increased fluid administration to help flush the toxins. If experiencing metabolic acidosis, interventions should be initiated to normalize blood gas levels. Electrolyte imbalances should be corrected and in some cases, patients may be given mannitol or dopamine as it is thought to increase renal perfusion to assist in filtration and function. If rhabdomyolysis progresses to renal failure, dialysis may be indicated.

Multiple Organ Dysfunction Syndrome (MODS)

Multiple organ dysfunction syndrome (MODS) is a term used to describe when two or more organ systems are failing. It usually develops in conjunction or as a result of sepsis, but it can be caused by any significant infection or injury such as trauma or burns. Patients with MODS are at high risk for sepsis-related death. When MODS occurs, the patient may experience decreases in any organ system including pulmonary, cardiac, liver, and kidney function. The kidneys may suffer acute tubular necrosis or cortical necrosis as a result of the inflammation and infection associated with the patient’s condition. Patients may need interventions implemented for acute respiratory distress syndrome (ARDS). Patients are also at acute risk for coagulation disorders such as thrombocytopenia and disseminated intravascular coagulation (DIC).

Treatment of MODS revolves around treatment of the underlying infection and/or inflammation. Patients will also need correction of any electrolyte and blood gas imbalances. While patients are receiving antibiotics or antifungal medications, they may also need supportive therapies such as fluid resuscitation, vasopressor medications, supportive or mechanical ventilation, extracorporeal membrane oxygenation (ECMO), and dialysis.

Multisystem Trauma

In the event of a multisystem trauma, nurses must prioritize patient care to treat the most critical needs first. Proper management of a trauma greatly increases the patient’s chance for survival. By the time trauma patients present to the hospital setting, several interventions are likely to have been implemented. Common prehospital interventions include frequent neurologic assessments, neck/spine immobilization, management of bleeding, and shock prevention.

Upon arriving at the hospital, trauma patients will need a quick, but thorough, assessment and critical interventions. Generally, hospitals have a designated trauma area with a team consisting of physicians, nurses, respiratory therapists, and other staff trained in these types of patient scenarios. The trauma team can determine which injuries/conditions are the most life-threatening. They will first ensure the patient has a secure and patent airway and place one if the patient has an airway compromise.

Secondly, the trauma team will assess the patient’s cardiovascular and hemodynamic status to determine the need for fluid resuscitation or blood product. If large volumes of IV fluids or blood products are required, they are typically warmed prior to administration to help prevent hypothermia because hypothermia can impair blood clotting and worsen outcomes for trauma patients. In cases of severe hemorrhage, a massive transfusion protocol (MTP) may be activated to ensure rapid, coordinated resuscitation. An MTP is a structured, hospital-wide protocol that delivers blood products in predefined ratios (commonly packed red blood cells, plasma, and platelets) to restore circulating volume quickly. Furthermore, some hospitals utilize a rapid infuser device that can administer blood products and fluids in a matter of minutes. For facilities that do not carry these devices, pressure bags are commonly used to speed up infusion delivery in major trauma cases. During the acute phase of trauma evaluation, patients will also undergo several tests, including EKG, several laboratory levels, and radiologic imaging.

Trauma patients should be monitored closely for several complications that may develop in the acute phase of injury. The complications may be directly related to the traumatic event or be secondary to the treatments of the event. A list of potential complications is printed below:

• acute respiratory distress syndrome (ARDS)
• renal failure
• infection
• compartment syndrome
• sepsis
• dysrhythmias
• disseminated intravascular coagulopathy