Distributive shock is an immediate life-threatening state that involves diffuse vasodilation and resultant inadequate tissue perfusion and oxygenation despite normal or increased cardiac output. It creates a disassociation between oxygen supply and demand, ultimately producing cellular and organ dysfunction.
As compared to the other categories of shock, such as cardiogenic or hypovolemic shock, distributive shock is caused in most instances by the loss of vascular tone rather than a loss of cardiac function or blood volume. The leading cause is septic shock, although there are other causes as well, like anaphylactic, neurogenic, and endocrine shock (such as adrenal insufficiency).
Epidemiology
Occurrence in the United States
Over 750,000 U.S. people develop sepsis each year. Angus and colleagues estimated in their research that this number might reach 1 million cases yearly by 2010. From 1979 to 2000, there was a yearly increase of roughly 9% in sepsis cases.
Global Impact
Sepsis is a global leading cause of death, and it kills an estimated 1,400 individuals every day.
Age and Risk
The chance of dying of sepsis increases with age.
Anatomy
Pathophysiology
Vasodilation:
In distributive shock, the blood vessels (particularly arterioles) become over-dilated. This results in a reduction of systemic vascular resistance (SVR), which results in a fall in blood pressure and reduced blood supply to vital organs.
Endothelial Dysfunction:
In sepsis, inflammatory mediators (e.g., cytokines) harm the endothelial cells lining the blood vessels, and they lose their function to control blood vessel tone. This results in increased vasodilation and fluid leakage into the interstitial space.
Capillary Permeability:
In sepsis, the inflammatory process enhances capillary permeability, leading to the leakage of fluid and proteins from the blood into tissues. This decreases the effective circulating blood volume, exacerbating hypotension and tissue perfusion.
Increased Cardiac Output:
In certain situations (e.g., sepsis), the body tries to compensate for vasodilation by raising cardiac output. But this compensation is usually insufficient because the vasodilation cannot be reversed by cardiac output, and thus there is persistent hypotension.
Impaired Oxygen Delivery:
While cardiac output can be normal or increased, the tissues do not receive enough oxygen because the blood volume mismatch fails to accommodate effective distribution of that volume throughout the body. Therefore, cells experience hypoxia.
Etiology
Septic Shock: The most frequent cause, due to a severe infection that induces systemic inflammation and widespread vasodilation. This causes a reduction in vascular tone and blood pressure.
Neurogenic Shock: This happens when there is damage to the spinal cord or interruption in the sympathetic nervous system, with resultant vasodilation and reduced vascular tone, causing hypotension.
Anaphylactic Shock: An acute allergic reaction causes the release of histamine and other mediators that induce vasodilation, increased vascular permeability, and a drop in blood pressure.
Endocrine Shock (e.g., Adrenal Insufficiency): Insufficient cortisol, as seen in Addison’s disease, can impair the body’s ability to regulate blood vessel tone, leading to vasodilation and hypotension.
Toxic Shock Syndrome: Caused by bacterial toxins, most commonly from Staphylococcus aureus or Streptococcus pyogenes, these toxins cause widespread vasodilation and increased capillary permeability, leading to shock.
Genetics
Prognostic Factors
Underlying cause: The severity of the underlying condition (such as sepsis or anaphylaxis) greatly impacts prognosis. For example, sepsis has a higher mortality rate if not treated promptly, while anaphylaxis has a generally good prognosis if treated quickly.
Early treatment and detection: Early diagnosis and treatment, such as fluid resuscitation, vasopressor therapy, and addressing the cause, markedly enhances survival rates.
Age and health status: The prognosis is generally poorer in older individuals and in those with compromised immune systems in comparison to healthier, younger people.
Clinical History
Age Group:
Adults (18-65 years): This age group is usually affected by septic shock, anaphylactic shock, and neurogenic shock.
 Older Adults (65+ years): They have an increased risk for septic shock and anaphylactic shock because of the age-associated changes in immune function and comorbid conditions.
Children (under 18 years): Children may develop distributive shock mainly because of sepsis or profound anaphylaxis. Sepsis is a frequent cause in newborns and infants.
Neonates (0-30 days): Neonates are particularly vulnerable to sepsis as a cause of distributive shock because they have underdeveloped immune systems.
Physical Examination
Vital Signs
Skin assessment
Neurological examination
Cardiovascular examination
Other Signs
Distributive shock is defined by a sudden drop in blood pressure secondary to diffuse vasodilation and poor tissue perfusion. The acuity of presentation may be variable, but it tends to present quickly with evidence of hypotension, tachycardia, warm extremities (in some presentations such as septic shock), and change in mental status.
Severity and rapidity of symptoms vary depending on the causative condition, e.g., sepsis, anaphylaxis, or neurogenic shock, and can worsen rapidly without active intervention. The early detection and management are crucial to avoid organ failure.
Initial evaluation:
Prompt assessment of Airway, breathing, and circulation (ABCs).
Initiate intravenous access (two large-bore IVs or central access, if necessary).
Observe vital signs, including blood pressure, heart rate, oxygen saturation, and urine output.
Fluid resuscitation:
Initial treatment: Give crystalloids (normal saline or lactated Ringer’s solution) to reexpand circulating volume.
Fluid resuscitation is usually aggressive, aiming for adequate blood pressure and organ perfusion.
Observe for evidence of fluid overload, particularly in situations such as septic shock.
Address the underlying cause:
Septic shock: Administer broad-spectrum antibiotics as soon as possible, preferably within the first hour of suspected sepsis.
Anaphylactic shock: Immediate administration of epinephrine (first-line treatment), along with antihistamines, corticosteroids, and fluid resuscitation.
Neurogenic shock: Stabilize the spine if trauma is involved and consider vasopressors if needed to support blood pressure.
Vasopressors:
If blood pressure remains low despite adequate fluid resuscitation, start vasopressors. Norepinephrine is the first-choice agent for most cases of distributive shock.
For anaphylactic shock, epinephrine is the primary vasopressor.
In cases where norepinephrine is insufficient, consider adding dopamine or vasopressin.
Inotropic support:
If there is evidence of myocardial dysfunction or poor cardiac output, inotropes (e.g., dobutamine) may be used, especially in septic shock or cardiogenic shock.
Oxygen therapy and ventilation:
Provide supplemental oxygen to maintain oxygen saturation ≥ 90%.
If respiratory failure is present, consider invasive mechanical ventilation to improve oxygenation and support tissue perfusion.
Monitoring and reassessment:
Continuously monitor hemodynamics (blood pressure, heart rate, central venous pressure), urine output, and laboratory parameters (e.g., lactate levels, arterial blood gases).
Regular reassessment of response to therapy is crucial to guide further interventions.
Supportive care:
Maintain glucose control and provide other supportive measures, such as anticoagulation in septic shock to prevent DIC, or steroids if appropriate.
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
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Stem Cell Transplant
Targeted Therapy
Palliative Care
Effectiveness of antibiotics in treatment of distributive shock
Nafcillin
Nafcillin is usually the drug of choice for suspected infections due to penicillin G-resistant staphylococci or streptococci.
For severe infections, initiate parenteral therapy and change to oral therapy as the patient’s condition improves.
Because thrombophlebitis is a risk, particularly in elderly patients, use parenteral nafcillin briefly (1-2 days) and change to oral therapy when feasible.
Ceftazidime
Ceftazidime is a third-generation cephalosporin that has a wide range of gram-negative bacterial activity, although not as good activity against gram-positive bacteria.
Ceftazidime is specifically effective against resistant bacteria. It inhibits the growth of bacteria by binding with one or more penicillin-binding proteins.
Levofloxacin
Levofloxacin is used to treat infections caused by multidrug-resistant, gram-negative organisms.
Use of Corticosteroids in treatment of distributive shock
Hydrocortisone (Solu-Cortef, Cortef)
It is the corticosteroid of choice for the management of shock because of its mineralocorticoid and glucocorticoid effects. It can be given to hypotensive patients who are unresponsive to fluid resuscitation and vasopressors.
Use of Vasopressors in treatment of distributive shock
Norepinephrine (Levophed): This is typically the first-line vasopressor in most distributive shock types, including sepsis. It mainly acts by activating alpha-1 adrenergic receptors (causing vasoconstriction) and beta-1 receptors (enhancing contractility and heart rate).
Epinephrine (Adrenaline): It is used in cases of anaphylactic shock or when additional inotropic support is needed (e.g., in severe septic shock). It has both alpha- and beta-adrenergic effects, leading to vasoconstriction, increased heart rate, and improved myocardial contractility.
Dopamine: While used less frequently now, it can still be considered in some cases, especially for patients with bradycardia. At low doses, it stimulates dopamine receptors to increase renal blood flow, while higher doses activate beta-1 and alpha receptors to increase heart rate and blood pressure.
Phenylephrine: A pure alpha-1 agonist used when additional vasoconstriction is needed without affecting heart rate, often in cases of neurogenic shock or in patients where tachycardia is a concern.
Surgical Considerations for Distributive Shock
Surgery itself is not a primary treatment for distributive shock, but surgical intervention may be required depending on the underlying cause.
Common Surgical Scenarios Involving Distributive Shock
Septic Shock (Most Common Type of Distributive Shock)
Source Control Surgery: If sepsis is due to an abscess, infected prosthetic device, perforated organ (e.g., bowel perforation), or necrotic tissue, emergency surgery is required to remove the infectious source.
Examples of Surgery:
Laparotomy or laparoscopic drainage for intra-abdominal sepsis
Debridement for necrotizing soft tissue infections
Removal of infected catheters, hardware, or prosthetics
Surgical Stabilization: If caused by spinal trauma, early spinal decompression and fixation surgery (e.g., laminectomy, fusion) may help stabilize the spine and prevent further damage.
Anaphylactic Shock (Severe Allergic Reactions)
Surgery is rarely needed, but if airway obstruction occurs due to laryngeal edema, an emergency tracheostomy or cricothyroidotomy may be necessary.
Endocrine Shock (Adrenal Crisis, Myxedema Crisis)
No direct surgical intervention, but it may occur perioperatively in patients with undiagnosed adrenal insufficiency. Prompt administration of IV hydrocortisone and supportive care is essential.
Initial Assessment and Stabilization: Airway, Breathing, Circulation (ABCs): Ensure the airway is open, oxygenate, and establish IV access.
Monitoring: Continuous vital signs, including heart rate, blood pressure, and oxygen saturation.
Volume Resuscitation:
Administer IV fluids (e.g., crystalloids) to restore circulating blood volume and improve perfusion.
Vasopressor Support:
If hypotension persists despite fluid resuscitation, administer vasopressors (e.g., norepinephrine) to constrict blood vessels and increase blood pressure.
Targeted Therapy for Underlying Cause:
Infections: If sepsis is the cause, administer appropriate antibiotics.
Anaphylaxis: Administer epinephrine, antihistamines, and steroids.
Neurogenic Shock: Consider spinal precautions and potential steroid administration.
Reassessment and Adjustment:
Continuously reassess the patient’s response to treatment, adjusting fluid and medication as necessary to maintain adequate perfusion.
Distributive shock is an immediate life-threatening state that involves diffuse vasodilation and resultant inadequate tissue perfusion and oxygenation despite normal or increased cardiac output. It creates a disassociation between oxygen supply and demand, ultimately producing cellular and organ dysfunction.
As compared to the other categories of shock, such as cardiogenic or hypovolemic shock, distributive shock is caused in most instances by the loss of vascular tone rather than a loss of cardiac function or blood volume. The leading cause is septic shock, although there are other causes as well, like anaphylactic, neurogenic, and endocrine shock (such as adrenal insufficiency).
Occurrence in the United States
Over 750,000 U.S. people develop sepsis each year. Angus and colleagues estimated in their research that this number might reach 1 million cases yearly by 2010. From 1979 to 2000, there was a yearly increase of roughly 9% in sepsis cases.
Global Impact
Sepsis is a global leading cause of death, and it kills an estimated 1,400 individuals every day.
Age and Risk
The chance of dying of sepsis increases with age.
Vasodilation:
In distributive shock, the blood vessels (particularly arterioles) become over-dilated. This results in a reduction of systemic vascular resistance (SVR), which results in a fall in blood pressure and reduced blood supply to vital organs.
Endothelial Dysfunction:
In sepsis, inflammatory mediators (e.g., cytokines) harm the endothelial cells lining the blood vessels, and they lose their function to control blood vessel tone. This results in increased vasodilation and fluid leakage into the interstitial space.
Capillary Permeability:
In sepsis, the inflammatory process enhances capillary permeability, leading to the leakage of fluid and proteins from the blood into tissues. This decreases the effective circulating blood volume, exacerbating hypotension and tissue perfusion.
Increased Cardiac Output:
In certain situations (e.g., sepsis), the body tries to compensate for vasodilation by raising cardiac output. But this compensation is usually insufficient because the vasodilation cannot be reversed by cardiac output, and thus there is persistent hypotension.
Impaired Oxygen Delivery:
While cardiac output can be normal or increased, the tissues do not receive enough oxygen because the blood volume mismatch fails to accommodate effective distribution of that volume throughout the body. Therefore, cells experience hypoxia.
Septic Shock: The most frequent cause, due to a severe infection that induces systemic inflammation and widespread vasodilation. This causes a reduction in vascular tone and blood pressure.
Neurogenic Shock: This happens when there is damage to the spinal cord or interruption in the sympathetic nervous system, with resultant vasodilation and reduced vascular tone, causing hypotension.
Anaphylactic Shock: An acute allergic reaction causes the release of histamine and other mediators that induce vasodilation, increased vascular permeability, and a drop in blood pressure.
Endocrine Shock (e.g., Adrenal Insufficiency): Insufficient cortisol, as seen in Addison’s disease, can impair the body’s ability to regulate blood vessel tone, leading to vasodilation and hypotension.
Toxic Shock Syndrome: Caused by bacterial toxins, most commonly from Staphylococcus aureus or Streptococcus pyogenes, these toxins cause widespread vasodilation and increased capillary permeability, leading to shock.
Underlying cause: The severity of the underlying condition (such as sepsis or anaphylaxis) greatly impacts prognosis. For example, sepsis has a higher mortality rate if not treated promptly, while anaphylaxis has a generally good prognosis if treated quickly.
Early treatment and detection: Early diagnosis and treatment, such as fluid resuscitation, vasopressor therapy, and addressing the cause, markedly enhances survival rates.
Age and health status: The prognosis is generally poorer in older individuals and in those with compromised immune systems in comparison to healthier, younger people.
Age Group:
Adults (18-65 years): This age group is usually affected by septic shock, anaphylactic shock, and neurogenic shock.
 Older Adults (65+ years): They have an increased risk for septic shock and anaphylactic shock because of the age-associated changes in immune function and comorbid conditions.
Children (under 18 years): Children may develop distributive shock mainly because of sepsis or profound anaphylaxis. Sepsis is a frequent cause in newborns and infants.
Neonates (0-30 days): Neonates are particularly vulnerable to sepsis as a cause of distributive shock because they have underdeveloped immune systems.
Vital Signs
Skin assessment
Neurological examination
Cardiovascular examination
Other Signs
Distributive shock is defined by a sudden drop in blood pressure secondary to diffuse vasodilation and poor tissue perfusion. The acuity of presentation may be variable, but it tends to present quickly with evidence of hypotension, tachycardia, warm extremities (in some presentations such as septic shock), and change in mental status.
Severity and rapidity of symptoms vary depending on the causative condition, e.g., sepsis, anaphylaxis, or neurogenic shock, and can worsen rapidly without active intervention. The early detection and management are crucial to avoid organ failure.
Initial evaluation:
Prompt assessment of Airway, breathing, and circulation (ABCs).
Initiate intravenous access (two large-bore IVs or central access, if necessary).
Observe vital signs, including blood pressure, heart rate, oxygen saturation, and urine output.
Fluid resuscitation:
Initial treatment: Give crystalloids (normal saline or lactated Ringer’s solution) to reexpand circulating volume.
Fluid resuscitation is usually aggressive, aiming for adequate blood pressure and organ perfusion.
Observe for evidence of fluid overload, particularly in situations such as septic shock.
Address the underlying cause:
Septic shock: Administer broad-spectrum antibiotics as soon as possible, preferably within the first hour of suspected sepsis.
Anaphylactic shock: Immediate administration of epinephrine (first-line treatment), along with antihistamines, corticosteroids, and fluid resuscitation.
Neurogenic shock: Stabilize the spine if trauma is involved and consider vasopressors if needed to support blood pressure.
Vasopressors:
If blood pressure remains low despite adequate fluid resuscitation, start vasopressors. Norepinephrine is the first-choice agent for most cases of distributive shock.
For anaphylactic shock, epinephrine is the primary vasopressor.
In cases where norepinephrine is insufficient, consider adding dopamine or vasopressin.
Inotropic support:
If there is evidence of myocardial dysfunction or poor cardiac output, inotropes (e.g., dobutamine) may be used, especially in septic shock or cardiogenic shock.
Oxygen therapy and ventilation:
Provide supplemental oxygen to maintain oxygen saturation ≥ 90%.
If respiratory failure is present, consider invasive mechanical ventilation to improve oxygenation and support tissue perfusion.
Monitoring and reassessment:
Continuously monitor hemodynamics (blood pressure, heart rate, central venous pressure), urine output, and laboratory parameters (e.g., lactate levels, arterial blood gases).
Regular reassessment of response to therapy is crucial to guide further interventions.
Supportive care:
Maintain glucose control and provide other supportive measures, such as anticoagulation in septic shock to prevent DIC, or steroids if appropriate.
Emergency Medicine
Nafcillin
Nafcillin is usually the drug of choice for suspected infections due to penicillin G-resistant staphylococci or streptococci.
For severe infections, initiate parenteral therapy and change to oral therapy as the patient’s condition improves.
Because thrombophlebitis is a risk, particularly in elderly patients, use parenteral nafcillin briefly (1-2 days) and change to oral therapy when feasible.
Ceftazidime
Ceftazidime is a third-generation cephalosporin that has a wide range of gram-negative bacterial activity, although not as good activity against gram-positive bacteria.
Ceftazidime is specifically effective against resistant bacteria. It inhibits the growth of bacteria by binding with one or more penicillin-binding proteins.
Levofloxacin
Levofloxacin is used to treat infections caused by multidrug-resistant, gram-negative organisms.
Emergency Medicine
Hydrocortisone (Solu-Cortef, Cortef)
It is the corticosteroid of choice for the management of shock because of its mineralocorticoid and glucocorticoid effects. It can be given to hypotensive patients who are unresponsive to fluid resuscitation and vasopressors.
Emergency Medicine
Norepinephrine (Levophed): This is typically the first-line vasopressor in most distributive shock types, including sepsis. It mainly acts by activating alpha-1 adrenergic receptors (causing vasoconstriction) and beta-1 receptors (enhancing contractility and heart rate).
Epinephrine (Adrenaline): It is used in cases of anaphylactic shock or when additional inotropic support is needed (e.g., in severe septic shock). It has both alpha- and beta-adrenergic effects, leading to vasoconstriction, increased heart rate, and improved myocardial contractility.
Dopamine: While used less frequently now, it can still be considered in some cases, especially for patients with bradycardia. At low doses, it stimulates dopamine receptors to increase renal blood flow, while higher doses activate beta-1 and alpha receptors to increase heart rate and blood pressure.
Phenylephrine: A pure alpha-1 agonist used when additional vasoconstriction is needed without affecting heart rate, often in cases of neurogenic shock or in patients where tachycardia is a concern.
Dermatology, Cosmetic
Surgical Considerations for Distributive Shock
Surgery itself is not a primary treatment for distributive shock, but surgical intervention may be required depending on the underlying cause.
Common Surgical Scenarios Involving Distributive Shock
Septic Shock (Most Common Type of Distributive Shock)
Source Control Surgery: If sepsis is due to an abscess, infected prosthetic device, perforated organ (e.g., bowel perforation), or necrotic tissue, emergency surgery is required to remove the infectious source.
Examples of Surgery:
Laparotomy or laparoscopic drainage for intra-abdominal sepsis
Debridement for necrotizing soft tissue infections
Removal of infected catheters, hardware, or prosthetics
Surgical Stabilization: If caused by spinal trauma, early spinal decompression and fixation surgery (e.g., laminectomy, fusion) may help stabilize the spine and prevent further damage.
Anaphylactic Shock (Severe Allergic Reactions)
Surgery is rarely needed, but if airway obstruction occurs due to laryngeal edema, an emergency tracheostomy or cricothyroidotomy may be necessary.
Endocrine Shock (Adrenal Crisis, Myxedema Crisis)
No direct surgical intervention, but it may occur perioperatively in patients with undiagnosed adrenal insufficiency. Prompt administration of IV hydrocortisone and supportive care is essential.
Emergency Medicine
Initial Assessment and Stabilization: Airway, Breathing, Circulation (ABCs): Ensure the airway is open, oxygenate, and establish IV access.
Monitoring: Continuous vital signs, including heart rate, blood pressure, and oxygen saturation.
Volume Resuscitation:
Administer IV fluids (e.g., crystalloids) to restore circulating blood volume and improve perfusion.
Vasopressor Support:
If hypotension persists despite fluid resuscitation, administer vasopressors (e.g., norepinephrine) to constrict blood vessels and increase blood pressure.
Targeted Therapy for Underlying Cause:
Infections: If sepsis is the cause, administer appropriate antibiotics.
Anaphylaxis: Administer epinephrine, antihistamines, and steroids.
Neurogenic Shock: Consider spinal precautions and potential steroid administration.
Reassessment and Adjustment:
Continuously reassess the patient’s response to treatment, adjusting fluid and medication as necessary to maintain adequate perfusion.
Distributive shock is an immediate life-threatening state that involves diffuse vasodilation and resultant inadequate tissue perfusion and oxygenation despite normal or increased cardiac output. It creates a disassociation between oxygen supply and demand, ultimately producing cellular and organ dysfunction.
As compared to the other categories of shock, such as cardiogenic or hypovolemic shock, distributive shock is caused in most instances by the loss of vascular tone rather than a loss of cardiac function or blood volume. The leading cause is septic shock, although there are other causes as well, like anaphylactic, neurogenic, and endocrine shock (such as adrenal insufficiency).
Occurrence in the United States
Over 750,000 U.S. people develop sepsis each year. Angus and colleagues estimated in their research that this number might reach 1 million cases yearly by 2010. From 1979 to 2000, there was a yearly increase of roughly 9% in sepsis cases.
Global Impact
Sepsis is a global leading cause of death, and it kills an estimated 1,400 individuals every day.
Age and Risk
The chance of dying of sepsis increases with age.
Vasodilation:
In distributive shock, the blood vessels (particularly arterioles) become over-dilated. This results in a reduction of systemic vascular resistance (SVR), which results in a fall in blood pressure and reduced blood supply to vital organs.
Endothelial Dysfunction:
In sepsis, inflammatory mediators (e.g., cytokines) harm the endothelial cells lining the blood vessels, and they lose their function to control blood vessel tone. This results in increased vasodilation and fluid leakage into the interstitial space.
Capillary Permeability:
In sepsis, the inflammatory process enhances capillary permeability, leading to the leakage of fluid and proteins from the blood into tissues. This decreases the effective circulating blood volume, exacerbating hypotension and tissue perfusion.
Increased Cardiac Output:
In certain situations (e.g., sepsis), the body tries to compensate for vasodilation by raising cardiac output. But this compensation is usually insufficient because the vasodilation cannot be reversed by cardiac output, and thus there is persistent hypotension.
Impaired Oxygen Delivery:
While cardiac output can be normal or increased, the tissues do not receive enough oxygen because the blood volume mismatch fails to accommodate effective distribution of that volume throughout the body. Therefore, cells experience hypoxia.
Septic Shock: The most frequent cause, due to a severe infection that induces systemic inflammation and widespread vasodilation. This causes a reduction in vascular tone and blood pressure.
Neurogenic Shock: This happens when there is damage to the spinal cord or interruption in the sympathetic nervous system, with resultant vasodilation and reduced vascular tone, causing hypotension.
Anaphylactic Shock: An acute allergic reaction causes the release of histamine and other mediators that induce vasodilation, increased vascular permeability, and a drop in blood pressure.
Endocrine Shock (e.g., Adrenal Insufficiency): Insufficient cortisol, as seen in Addison’s disease, can impair the body’s ability to regulate blood vessel tone, leading to vasodilation and hypotension.
Toxic Shock Syndrome: Caused by bacterial toxins, most commonly from Staphylococcus aureus or Streptococcus pyogenes, these toxins cause widespread vasodilation and increased capillary permeability, leading to shock.
Underlying cause: The severity of the underlying condition (such as sepsis or anaphylaxis) greatly impacts prognosis. For example, sepsis has a higher mortality rate if not treated promptly, while anaphylaxis has a generally good prognosis if treated quickly.
Early treatment and detection: Early diagnosis and treatment, such as fluid resuscitation, vasopressor therapy, and addressing the cause, markedly enhances survival rates.
Age and health status: The prognosis is generally poorer in older individuals and in those with compromised immune systems in comparison to healthier, younger people.
Age Group:
Adults (18-65 years): This age group is usually affected by septic shock, anaphylactic shock, and neurogenic shock.
 Older Adults (65+ years): They have an increased risk for septic shock and anaphylactic shock because of the age-associated changes in immune function and comorbid conditions.
Children (under 18 years): Children may develop distributive shock mainly because of sepsis or profound anaphylaxis. Sepsis is a frequent cause in newborns and infants.
Neonates (0-30 days): Neonates are particularly vulnerable to sepsis as a cause of distributive shock because they have underdeveloped immune systems.
Vital Signs
Skin assessment
Neurological examination
Cardiovascular examination
Other Signs
Distributive shock is defined by a sudden drop in blood pressure secondary to diffuse vasodilation and poor tissue perfusion. The acuity of presentation may be variable, but it tends to present quickly with evidence of hypotension, tachycardia, warm extremities (in some presentations such as septic shock), and change in mental status.
Severity and rapidity of symptoms vary depending on the causative condition, e.g., sepsis, anaphylaxis, or neurogenic shock, and can worsen rapidly without active intervention. The early detection and management are crucial to avoid organ failure.
Initial evaluation:
Prompt assessment of Airway, breathing, and circulation (ABCs).
Initiate intravenous access (two large-bore IVs or central access, if necessary).
Observe vital signs, including blood pressure, heart rate, oxygen saturation, and urine output.
Fluid resuscitation:
Initial treatment: Give crystalloids (normal saline or lactated Ringer’s solution) to reexpand circulating volume.
Fluid resuscitation is usually aggressive, aiming for adequate blood pressure and organ perfusion.
Observe for evidence of fluid overload, particularly in situations such as septic shock.
Address the underlying cause:
Septic shock: Administer broad-spectrum antibiotics as soon as possible, preferably within the first hour of suspected sepsis.
Anaphylactic shock: Immediate administration of epinephrine (first-line treatment), along with antihistamines, corticosteroids, and fluid resuscitation.
Neurogenic shock: Stabilize the spine if trauma is involved and consider vasopressors if needed to support blood pressure.
Vasopressors:
If blood pressure remains low despite adequate fluid resuscitation, start vasopressors. Norepinephrine is the first-choice agent for most cases of distributive shock.
For anaphylactic shock, epinephrine is the primary vasopressor.
In cases where norepinephrine is insufficient, consider adding dopamine or vasopressin.
Inotropic support:
If there is evidence of myocardial dysfunction or poor cardiac output, inotropes (e.g., dobutamine) may be used, especially in septic shock or cardiogenic shock.
Oxygen therapy and ventilation:
Provide supplemental oxygen to maintain oxygen saturation ≥ 90%.
If respiratory failure is present, consider invasive mechanical ventilation to improve oxygenation and support tissue perfusion.
Monitoring and reassessment:
Continuously monitor hemodynamics (blood pressure, heart rate, central venous pressure), urine output, and laboratory parameters (e.g., lactate levels, arterial blood gases).
Regular reassessment of response to therapy is crucial to guide further interventions.
Supportive care:
Maintain glucose control and provide other supportive measures, such as anticoagulation in septic shock to prevent DIC, or steroids if appropriate.
Emergency Medicine
Emergency Medicine
Nafcillin
Nafcillin is usually the drug of choice for suspected infections due to penicillin G-resistant staphylococci or streptococci.
For severe infections, initiate parenteral therapy and change to oral therapy as the patient’s condition improves.
Because thrombophlebitis is a risk, particularly in elderly patients, use parenteral nafcillin briefly (1-2 days) and change to oral therapy when feasible.
Ceftazidime
Ceftazidime is a third-generation cephalosporin that has a wide range of gram-negative bacterial activity, although not as good activity against gram-positive bacteria.
Ceftazidime is specifically effective against resistant bacteria. It inhibits the growth of bacteria by binding with one or more penicillin-binding proteins.
Levofloxacin
Levofloxacin is used to treat infections caused by multidrug-resistant, gram-negative organisms.
Emergency Medicine
Hydrocortisone (Solu-Cortef, Cortef)
It is the corticosteroid of choice for the management of shock because of its mineralocorticoid and glucocorticoid effects. It can be given to hypotensive patients who are unresponsive to fluid resuscitation and vasopressors.
Emergency Medicine
Norepinephrine (Levophed): This is typically the first-line vasopressor in most distributive shock types, including sepsis. It mainly acts by activating alpha-1 adrenergic receptors (causing vasoconstriction) and beta-1 receptors (enhancing contractility and heart rate).
Epinephrine (Adrenaline): It is used in cases of anaphylactic shock or when additional inotropic support is needed (e.g., in severe septic shock). It has both alpha- and beta-adrenergic effects, leading to vasoconstriction, increased heart rate, and improved myocardial contractility.
Dopamine: While used less frequently now, it can still be considered in some cases, especially for patients with bradycardia. At low doses, it stimulates dopamine receptors to increase renal blood flow, while higher doses activate beta-1 and alpha receptors to increase heart rate and blood pressure.
Phenylephrine: A pure alpha-1 agonist used when additional vasoconstriction is needed without affecting heart rate, often in cases of neurogenic shock or in patients where tachycardia is a concern.
Dermatology, Cosmetic
Surgical Considerations for Distributive Shock
Surgery itself is not a primary treatment for distributive shock, but surgical intervention may be required depending on the underlying cause.
Common Surgical Scenarios Involving Distributive Shock
Septic Shock (Most Common Type of Distributive Shock)
Source Control Surgery: If sepsis is due to an abscess, infected prosthetic device, perforated organ (e.g., bowel perforation), or necrotic tissue, emergency surgery is required to remove the infectious source.
Examples of Surgery:
Laparotomy or laparoscopic drainage for intra-abdominal sepsis
Debridement for necrotizing soft tissue infections
Removal of infected catheters, hardware, or prosthetics
Surgical Stabilization: If caused by spinal trauma, early spinal decompression and fixation surgery (e.g., laminectomy, fusion) may help stabilize the spine and prevent further damage.
Anaphylactic Shock (Severe Allergic Reactions)
Surgery is rarely needed, but if airway obstruction occurs due to laryngeal edema, an emergency tracheostomy or cricothyroidotomy may be necessary.
Endocrine Shock (Adrenal Crisis, Myxedema Crisis)
No direct surgical intervention, but it may occur perioperatively in patients with undiagnosed adrenal insufficiency. Prompt administration of IV hydrocortisone and supportive care is essential.
Emergency Medicine
Initial Assessment and Stabilization: Airway, Breathing, Circulation (ABCs): Ensure the airway is open, oxygenate, and establish IV access.
Monitoring: Continuous vital signs, including heart rate, blood pressure, and oxygen saturation.
Volume Resuscitation:
Administer IV fluids (e.g., crystalloids) to restore circulating blood volume and improve perfusion.
Vasopressor Support:
If hypotension persists despite fluid resuscitation, administer vasopressors (e.g., norepinephrine) to constrict blood vessels and increase blood pressure.
Targeted Therapy for Underlying Cause:
Infections: If sepsis is the cause, administer appropriate antibiotics.
Anaphylaxis: Administer epinephrine, antihistamines, and steroids.
Neurogenic Shock: Consider spinal precautions and potential steroid administration.
Reassessment and Adjustment:
Continuously reassess the patient’s response to treatment, adjusting fluid and medication as necessary to maintain adequate perfusion.
Both our subscription plans include Free CME/CPD AMA PRA Category 1 credits.
Digital Certificate PDF
On course completion, you will receive a full-sized presentation quality digital certificate.
medtigo Simulation
A dynamic medical simulation platform designed to train healthcare professionals and students to effectively run code situations through an immersive hands-on experience in a live, interactive 3D environment.
medtigo Points
medtigo points is our unique point redemption system created to award users for interacting on our site. These points can be redeemed for special discounts on the medtigo marketplace as well as towards the membership cost itself.
Community Forum post/reply = 5 points
*Redemption of points can occur only through the medtigo marketplace, courses, or simulation system. Money will not be credited to your bank account. 10 points = $1.
All Your Certificates in One Place
When you have your licenses, certificates and CMEs in one place, it's easier to track your career growth. You can easily share these with hospitals as well, using your medtigo app.
