Shock – StatPearls – NCBI Bookshelf

Continuing Education Activity

Shock is a life-threatening manifestation of circulatory failure. Circulatory shock leads to cellular and tissue hypoxia resulting in cellular death and dysfunction of vital organs. Effects of shock are reversible in the early stages and a delay in diagnosis and/or timely initiation of treatment can lead to irreversible changes including multiorgan failure (MOF) and death. This activity reviews the evaluation and management of shock, and explains the role of the interprofessional team in evaluating and treating patients with this condition.

Objectives:

• Identify the etiology and epidemiology of shock and describe the types of shock.

• Outline the evaluation of a patient potentially in shock.

• Summarize the treatment and management options available for shock.

• Review the importance of improving care coordination among the interprofessional team to improve outcomes for patients in shock.

Access free multiple choice questions on this topic.

Introduction

Shock is a life-threatening manifestation of circulatory failure.  Circulatory shock leads to cellular and tissue hypoxia resulting in cellular death and dysfunction of vital organs. Effects of shock are reversible in the early stages, and a delay in diagnosis and/or timely initiation of treatment can lead to irreversible changes, including multiorgan failure (MOF) and death.

Etiology

Shock is characterized by decreased oxygen delivery and/or increased oxygen consumption or inadequate oxygen utilization leading to cellular and tissue hypoxia. It is a life-threatening condition of circulatory failure and most commonly manifested as hypotension (systolic blood pressure less than 90 mm Hg or MAP less than 65 mmHg). Shock is the final manifestation of a complex list of etiologies and could be fatal without timely management. There are mainly four broad categories of shock: distributive, hypovolemic, cardiogenic, and obstructive. [1] The wide range of etiologies can contribute to each of these categories and are manifested by the final outcome of shock. Undifferentiated shock means that the diagnosis of shock has been made; however, the underlying etiology has not been uncovered.

1. Distributive Shock

Characterized by peripheral vasodilatation. 

Types of distributive shock include:

Septic Shock

Sepsis is defined as life-threatening organ dysfunction resulting from dysregulated host response to infection.[2] Septic shock is a subset of sepsis with severe circulatory, cellular, and metabolic abnormalities resulting in tissue hypoperfusion manifested as hypotension which requires vasopressor therapy and elevated lactate levels (more than 2 mmol/L)

The most common pathogens associated with sepsis and septic shock in the United States are gram-positive bacteria, including streptococcal pneumonia and Enterococcus.

Systemic Inflammatory Response Syndrome

Systemic inflammatory response syndrome (SIRS) is a clinical syndrome of the vigorous inflammatory response caused by either infectious or noninfectious causes. Infectious causes include pathogens such as gram-positive (most common) and gram-negative bacteria, fungi, viral infections (e.g., respiratory viruses), parasitic (e.g., malaria), rickettsial infections. Noninfectious causes of SIRS include but are not limited to pancreatitis, burns, fat embolism, air embolism, and amniotic fluid embolism

Anaphylactic Shock

Anaphylactic shock is a clinical syndrome of severe hypersensitivity reaction mediated by immunoglobulin E (Ig-E), resulting in cardiovascular collapse and respiratory distress due to bronchospasm. The immediate hypersensitivity reactions can occur within seconds to minutes after the presentation of the inciting antigen. Common allergens include drugs (e.g., antibiotics, NSAIDs), food, insect stings, and latex.

Neurogenic Shock

Neurogenic shock can occur in the setting of trauma to the spinal cord or the brain. The underlying mechanism is the disruption of the autonomic pathway resulting in decreased vascular resistance and changes in vagal tone.

Endocrine Shock

Due to underlying endocrine etiologies such as adrenal failure (Addisonian crisis) and myxedema.

2. Hypovolemic Shock

Hypovolemic shock is characterized by decreased intravascular volume and increased systemic venous assistance (compensatory the mechanism to maintain perfusion in the early stages of shock). In the later stages of shock due to progressive volume depletion, cardiac output also decreases and manifest as hypotension. Hypovolemic shock divides into two broad subtypes: hemorrhagic and non-hemorrhagic.

Common causes of hemorrhagic hypovolemic shock include

• Gastrointestinal bleed (both upper and lower gastrointestinal bleed (e.g., variceal bleed, portal hypertensive gastropathy bleed, peptic ulcer, diverticulosis) trauma

• Vascular etiologies (e.g., aortoenteric fistula, ruptured abdominal aortic aneurysm, tumor eroding into a major blood vessel)

• Spontaneous bleeding in the setting of anticoagulant use (in the setting of supratherapeutic INR from drug interactions)

Common causes of non-hemorrhagic hypovolemic shock include:

• GI losses – the setting of vomiting, diarrhea, NG suction, or drains.

• Renal losses – medication-induced diuresis, endocrine disorders such as hypoaldosteronism.

• Skin losses/insensible losses – burns, Stevens-Johnson syndrome, Toxic epidermal necrolysis, heatstroke, pyrexia.

• Third-space loss – in the setting of pancreatitis, cirrhosis, intestinal obstruction, trauma.

3. Cardiogenic Shock

Due to intracardiac causes leading to decreased cardiac output and systemic hypoperfusion. Different subtypes of etiologies contributing to cardiogenic shock include:

• Cardiomyopathies – include acute myocardial infarction affecting more than 40% of the left ventricle, acute myocardial infarction in the setting of multi-vessel coronary artery disease, right ventricular myocardial infarction, fulminant dilated cardiomyopathy, cardiac arrest (due to myocardial stunning), myocarditis.

• Arrhythmias – both tachy- and bradyarrhythmias

• Mechanical – severe aortic insufficiency, severe mitral insufficiency, rupture of papillary muscles, or chordae tendinae trauma rupture of ventricular free wall aneurysm.

4. Obstructive Shock

Mostly due to extracardiac causes leading to a decrease in the left ventricular cardiac output

• Pulmonary vascular – due to impaired blood flow from the right heart to the left heart. Examples include hemodynamically significant pulmonary embolism, severe pulmonary hypertension.[3]

• Mechanical – impaired filling of right heart or due to decreased venous return to the right heart due to extrinsic compression. Examples include tension pneumothorax, pericardial tamponade, restrictive cardiomyopathy, constrictive pericarditis.

Epidemiology

Distributive shock is the most common type of shock, followed by hypovolemic and cardiogenic shock. Obstructive shock is relatively less common. The most common type of distributive shock is septic shock and has a mortality rate between 40 to 50%.

Pathophysiology

Hypoxia at the cellular level causes a series of physiologic and biochemical changes, resulting in acidosis and a decrease in regional blood flow, which further worsens the tissue hypoxia. [4] In hypovolemic, obstructive, and cardiogenic shock, there is a decrease in cardiac output and decreased oxygen transport. In distributive shock, there is decreased peripheral vascular resistance and abnormal oxygen extraction. Excitement is a spectrum of physiologic changes, ranging from early stages, which are reversible to the final stages, which are irreversible with multiorgan failure and death. Generally, shock has the following three stages:

1. Pre-shock or compensated shock – As the name suggests, this stage is characterized by compensatory mechanisms to counter the decrease in tissue perfusion, including tachycardia, peripheral vasoconstriction, and changes in systemic blood pressure

2. Shock – During this stage, most of the classic signs and symptoms of shock appear due to early organ dysfunction, resulting from the progression of the pre-shock stage as the compensatory mechanisms become insufficient.

3. End-organ dysfunction – This is the final stage, leading to irreversible organ dysfunction, multiorgan failure, and death

History and Physical

A focused history should be obtained from the patient (if feasible) and/or patient’s relatives. Also, a review of the patient’s outpatient medical records (information regarding risk factors, medications, and trend of baseline vital signs including blood pressure), as well as hospital medical records, could give valuable clues regarding the patient’s risk for shock and potential etiology. Clinical features and symptoms can vary according to the type and stage of shock. The most common clinical features/labs which are suggestive of shock include hypotension, tachycardia, tachypnea, obtundation or abnormal mental status, cold, clammy extremities, mottled skin, oliguria, metabolic acidosis, and hyperlactatemia.[5][6] Also, features pertaining to the underlying cause of the shock can be present.

Patients with hypovolemic shock can have general features as mentioned above as well as evidence of orthostatic hypotension, pallor, flattened jugular venous pulsations, may have sequelae of chronic liver disease (in case of variceal bleeding).

Patients with septic shock may present with symptoms suggestive of the source of infection (example-skin manifestations of primary infection such as erysipelas, cellulitis, necrotizing soft-tissue infections), and cutaneous manifestations of infective endocarditis.

Patients with anaphylactic shock can have hypotension, flushing, urticaria, tachypnea, hoarseness of voice, oral and facial edema, hives, wheeze, inspiratory stridor, and history of exposure to common allergens such as medications or food items the patient is allergic to or insect stings.

Tension pneumothorax should be suspected in a patient with undifferentiated shock who has tachypnea, unilateral pleuritic chest pain, absent or diminished breath sounds, tracheal deviation to the normal side, distended neck veins and also has pertinent risk factors for tension pneumothorax such as recent trauma, mechanical ventilation, underlying cystic lung disease).

In a patient with undifferentiated shock, diagnostic clues to pericardial tamponade as the etiology include dyspnea, the Beck triad (elevated jugular venous pressure, muffled heart sounds, hypotension), pulses paradoxus, and known risk factors such as trauma, the recent history of pericardial effusion, and thoracic procedures.  

Cardiogenic shock should be considered as the etiology if the patient with undifferentiated shock had chest pain suggestive of cardiac origin, narrow pulse pressure, elevated jugular venous pulsations or lung crackles, and significant arrhythmias on telemetry or EKG.

Evaluation

Resuscitation should not delay while investigating the etiology of undifferentiated shock. Physicians should have a high clinical suspicion for the presence of shock, and an attempt to stratify the severity of the shock should also take place to assess the need for emergent or early interventions. Evaluation of undifferentiated shock should begin with a thorough history and physical examination.

Besides telemetry monitoring, a 12-lead electrocardiogram should be obtained. ECGs might show evidence of acute coronary syndrome, arrhythmias, or provide diagnostic clues suggestive of pericardial effusion or pulmonary embolism.

Laboratory tests in a patient with undifferentiated shock should include a CBC and differential, renal and liver function tests, serum lactate level, cardiac biomarkers, D-dimer level, coagulation profile, type and screen for a possible blood transfusion if appropriate (if concern for hemorrhagic shock), blood and urine cultures, and blood gas analysis. Initial imaging studies recommended in patients with undifferentiated shock and hypotension include chest x-rays to look for the source of infection such as pneumonia, complications of shock such as ARDS, clinical findings supporting the diagnosis of pulmonary edema in cardiogenic shock, widened mediastinum in aortic dissection. CT scans can also assist in unmasking the etiology of shock in appropriate clinical scenarios. Point of care ultrasonography or focused cardiac ultrasound is also a useful bedside diagnostic tool.[7]

Treatment / Management

The initial approach to management is the stabilization of the airway and breathing with oxygen and oral mechanical ventilation when needed. Peripheral IV or intraosseous infusion (IO) access should be obtained. Central venous access may be required in the setting of shock if there is difficulty securing peripheral venous access, or the patient needs prolonged vasopressor therapy or large-volume resuscitation. Immediate treatment with intravenous (IV) fluid should be initiated, followed by vasopressor therapy, if needed, to maintain tissue perfusion. Depending on the underlying etiology of shock, specific therapies might also be needed.

Septic shock – initial aggressive fluid resuscitation with IV isotonic crystalloids 30 mL/kg within 3 hrs with additional fluid based on frequent reassessment, empiric antibiotic therapy within one hr. [8] For patients with septic shock requiring vasopressors, target a mean arterial pressure (MAP) of 65 mmHg. The first choice of a vasopressor is norepinephrine, with the addition of vasopressin if refractory.[9]

Anaphylactic shock – aggressive IV fluid resuscitation with 4 to 6 L of IV crystalloids. Stop the offending agent, intramuscular epinephrine, antihistamines, corticosteroids, nebulized albuterol.

In adrenal crisis – judicious fluid resuscitation, IV dexamethasone.

Hypovolemic shock – obtain two large-bore IVs or central line. Place the patient in the Trendelenburg position. Aggressive IV fluid resuscitation with 2 to 4 L of isotonic crystalloids. PRBC transfusion if ongoing bleed.  Appropriate medical or interventional strategies to treat the underlying etiology. Continue with isotonic crystalloids and use vasopressors if needed

Obstructive shock – the judicious use of IV crystalloids. If shock persists, early initiation of vasopressors-norepinephrine is the first choice and add vasopressin if refractory. Continue IV fluids but monitor very closely. 

If acute massive pulmonary embolism -thrombolysis. Judicious use of IV fluids has a paradoxical worsening of hypotension; it may develop due to severe right ventricular dilatation and septal bowing compromising left ventricle filling. 

If tension pneumothorax – needle thoracotomy followed by tube thoracotomy. If cardiac tamponade-pericardiocentesis, significant clinical improvement is possible, even with minimal fluid removal).

Cardiogenic shock – if unstable tachyarrhythmia or bradyarrhythmias, initiate ACLS protocol and cardioversion. Judicious use of IV fluids in the absence of pulmonary edema. Consider inotropes (dobutamine is the most commonly used agent) or intra-aortic balloon pump (IABP), if refractory shock, and vasopressor (norepinephrine) with inotropes.

If STEMI – consider thrombolysis or coronary revascularization procedures and or IABP.

Differential Diagnosis

Uncovering the etiology of undifferentiated shock is very important. In a patient presenting with undifferentiated shock, the differential diagnosis includes a wide variety of etiologies that falls under the four major categories of shock, as outlined above. Also, sometimes patients can have a combination of shock syndromes. Another differential is “pharmacological shock,” which results from vasodilatation or myocardial depression from medications (e.g., benzodiazepines, beta-blockers, calcium channel blockers, opiates, anticholinergics, and sildenafil).

Prognosis

Sepsis and septic shock, in general, are associated with long-term morbidity and mortality, with many of the survivors requiring placement into long-term acute care facilities or post-acute care centers. [10][11] Septic shock has a mortality rate between 40% and 50%. Cardiogenic shock has a mortality rate ranging from 50% to 75%, an improvement over prior mortality rates. Hypovolemic and obstructive shock generally have much lower mortality and respond better to timely treatment. 

Pearls and Other Issues

• Shock is a clinical manifestation of circulatory failure and is associated with high morbidity and mortality.

• There are broadly four types of shock: distributive, cardiogenic, hypovolemic, and obstructive.

• An accurate diagnosis requires a good understanding of underlying pathophysiology, clinical, biochemical, and hemodynamic manifestations of the different types of shock.

• Serum lactate level is a useful risk stratification tool in managing undifferentiated shock.

• Timely diagnosis and initiation of appropriate therapy are of paramount importance as it can prevent progression to the reversible shock, multiorgan failure, and death.

• Treatment includes hemodynamic stabilization and correction of underlying etiology of shock.

Enhancing Healthcare Team Outcomes

The management of patients with shock calls for a collaborative, interprofessional approach. Clinicians must react promptly to the emergency and determine the precise cause of shock. Nursing will be on hand to assist at every step of the way, assisting with measures such as intubation and administering medications. Pharmacists must rapidly prepare and deliver the needed drugs and yet still verify that dosing and interactions do not present a problem. Depending on the etiology, various specialists may also be called in on the case. Each area will need to act and react as the situation dictates. WIth interprofessional cooperation, these patients will stand a better chance of recovery from shock with minimal deleterious effects. [Level 5]

Review Questions

• Access free multiple choice questions on this topic.

• Comment on this article.

References

1.

Vincent JL, De Backer D. Circulatory shock. N Engl J Med. 2014 Feb 06;370(6):583. [PubMed: 24499231]

2.

Angus DC, van der Poll T. Severe sepsis and septic shock. N Engl J Med. 2013 Aug 29;369(9):840-51. [PubMed: 23984731]

3.

Smulders YM. Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction. Cardiovasc Res. 2000 Oct;48(1):23-33. [PubMed: 11033105]

4.

Barber AE, Shires GT. Cell damage after shock. New Horiz. 1996 May;4(2):161-7. [PubMed: 8774792]

5.

Seymour CW, Liu VX, Iwashyna TJ, Brunkhorst FM, Rea TD, Scherag A, Rubenfeld G, Kahn JM, Shankar-Hari M, Singer M, Deutschman CS, Escobar GJ, Angus DC. Assessment of Clinical Criteria for Sepsis: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23;315(8):762-74. [PMC free article: PMC5433435] [PubMed: 26903335]

6.

Kraut JA, Madias NE. Lactic acidosis. N Engl J Med. 2015 Mar 12;372(11):1078-9. [PubMed: 25760366]

7.

Shokoohi H, Boniface KS, Pourmand A, Liu YT, Davison DL, Hawkins KD, Buhumaid RE, Salimian M, Yadav K. Bedside Ultrasound Reduces Diagnostic Uncertainty and Guides Resuscitation in Patients With Undifferentiated Hypotension. Crit Care Med. 2015 Dec;43(12):2562-9. [PubMed: 26575653]

8.

Howell MD, Davis AM. Management of Sepsis and Septic Shock. JAMA. 2017 Feb 28;317(8):847-848. [PubMed: 28114603]

9.

Hylands M, Moller MH, Asfar P, Toma A, Frenette AJ, Beaudoin N, Belley-Côté É, D’Aragon F, Laake JH, Siemieniuk RA, Charbonney E, Lauzier F, Kwong J, Rochwerg B, Vandvik PO, Guyatt G, Lamontagne F. A systematic review of vasopressor blood pressure targets in critically ill adults with hypotension. Can J Anaesth. 2017 Jul;64(7):703-715. [PubMed: 28497426]

10.

Shankar-Hari M, Phillips GS, Levy ML, Seymour CW, Liu VX, Deutschman CS, Angus DC, Rubenfeld GD, Singer M., Sepsis Definitions Task Force. Developing a New Definition and Assessing New Clinical Criteria for Septic Shock: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23;315(8):775-87. [PMC free article: PMC4910392] [PubMed: 26903336]

11.

Cecconi M, Evans L, Levy M, Rhodes A. Sepsis and septic shock. Lancet. 2018 Jul 07;392(10141):75-87. [PubMed: 29937192]

Disclosure: Hayas Haseer Koya declares no relevant financial relationships with ineligible companies.

Disclosure: Manju Paul declares no relevant financial relationships with ineligible companies.

Shock – StatPearls – NCBI Bookshelf

Continuing Education Activity

Shock is a life-threatening manifestation of circulatory failure. Circulatory shock leads to cellular and tissue hypoxia resulting in cellular death and dysfunction of vital organs. Effects of shock are reversible in the early stages and a delay in diagnosis and/or timely initiation of treatment can lead to irreversible changes including multiorgan failure (MOF) and death. This activity reviews the evaluation and management of shock, and explains the role of the interprofessional team in evaluating and treating patients with this condition.

Objectives:

• Identify the etiology and epidemiology of shock and describe the types of shock.

• Outline the evaluation of a patient potentially in shock.

• Summarize the treatment and management options available for shock.

• Review the importance of improving care coordination among the interprofessional team to improve outcomes for patients in shock.

Access free multiple choice questions on this topic.

Introduction

Shock is a life-threatening manifestation of circulatory failure.   Circulatory shock leads to cellular and tissue hypoxia resulting in cellular death and dysfunction of vital organs. Effects of shock are reversible in the early stages, and a delay in diagnosis and/or timely initiation of treatment can lead to irreversible changes, including multiorgan failure (MOF) and death.

Etiology

Shock is characterized by decreased oxygen delivery and/or increased oxygen consumption or inadequate oxygen utilization leading to cellular and tissue hypoxia. It is a life-threatening condition of circulatory failure and most commonly manifested as hypotension (systolic blood pressure less than 90 mm Hg or MAP less than 65 mmHg). Shock is the final manifestation of a complex list of etiologies and could be fatal without timely management. There are mainly four broad categories of shock: distributive, hypovolemic, cardiogenic, and obstructive.[1] The wide range of etiologies can contribute to each of these categories and are manifested by the final outcome of shock. Undifferentiated shock means that the diagnosis of shock has been made; however, the underlying etiology has not been uncovered.

1. Distributive Shock

Characterized by peripheral vasodilatation. 

Types of distributive shock include:

Septic Shock

Sepsis is defined as life-threatening organ dysfunction resulting from dysregulated host response to infection.[2] Septic shock is a subset of sepsis with severe circulatory, cellular, and metabolic abnormalities resulting in tissue hypoperfusion manifested as hypotension which requires vasopressor therapy and elevated lactate levels (more than 2 mmol/L)

The most common pathogens associated with sepsis and septic shock in the United States are gram-positive bacteria, including streptococcal pneumonia and Enterococcus.

Systemic Inflammatory Response Syndrome

Systemic inflammatory response syndrome (SIRS) is a clinical syndrome of the vigorous inflammatory response caused by either infectious or noninfectious causes. Infectious causes include pathogens such as gram-positive (most common) and gram-negative bacteria, fungi, viral infections (e.g., respiratory viruses), parasitic (e.g., malaria), rickettsial infections. Noninfectious causes of SIRS include but are not limited to pancreatitis, burns, fat embolism, air embolism, and amniotic fluid embolism

Anaphylactic Shock

Anaphylactic shock is a clinical syndrome of severe hypersensitivity reaction mediated by immunoglobulin E (Ig-E), resulting in cardiovascular collapse and respiratory distress due to bronchospasm. The immediate hypersensitivity reactions can occur within seconds to minutes after the presentation of the inciting antigen. Common allergens include drugs (e.g., antibiotics, NSAIDs), food, insect stings, and latex.

Neurogenic Shock

Neurogenic shock can occur in the setting of trauma to the spinal cord or the brain. The underlying mechanism is the disruption of the autonomic pathway resulting in decreased vascular resistance and changes in vagal tone.

Endocrine Shock

Due to underlying endocrine etiologies such as adrenal failure (Addisonian crisis) and myxedema.

2. Hypovolemic Shock

Hypovolemic shock is characterized by decreased intravascular volume and increased systemic venous assistance (compensatory the mechanism to maintain perfusion in the early stages of shock). In the later stages of shock due to progressive volume depletion, cardiac output also decreases and manifest as hypotension. Hypovolemic shock divides into two broad subtypes: hemorrhagic and non-hemorrhagic.

Common causes of hemorrhagic hypovolemic shock include

• Gastrointestinal bleed (both upper and lower gastrointestinal bleed (e.g., variceal bleed, portal hypertensive gastropathy bleed, peptic ulcer, diverticulosis) trauma

• Vascular etiologies (e.g., aortoenteric fistula, ruptured abdominal aortic aneurysm, tumor eroding into a major blood vessel)

• Spontaneous bleeding in the setting of anticoagulant use (in the setting of supratherapeutic INR from drug interactions)

Common causes of non-hemorrhagic hypovolemic shock include:

• GI losses – the setting of vomiting, diarrhea, NG suction, or drains.

• Renal losses – medication-induced diuresis, endocrine disorders such as hypoaldosteronism.

• Skin losses/insensible losses – burns, Stevens-Johnson syndrome, Toxic epidermal necrolysis, heatstroke, pyrexia.

• Third-space loss – in the setting of pancreatitis, cirrhosis, intestinal obstruction, trauma.

3. Cardiogenic Shock

Due to intracardiac causes leading to decreased cardiac output and systemic hypoperfusion. Different subtypes of etiologies contributing to cardiogenic shock include:

• Cardiomyopathies – include acute myocardial infarction affecting more than 40% of the left ventricle, acute myocardial infarction in the setting of multi-vessel coronary artery disease, right ventricular myocardial infarction, fulminant dilated cardiomyopathy, cardiac arrest (due to myocardial stunning), myocarditis.

• Arrhythmias – both tachy- and bradyarrhythmias

• Mechanical – severe aortic insufficiency, severe mitral insufficiency, rupture of papillary muscles, or chordae tendinae trauma rupture of ventricular free wall aneurysm.

4. Obstructive Shock

Mostly due to extracardiac causes leading to a decrease in the left ventricular cardiac output

• Pulmonary vascular – due to impaired blood flow from the right heart to the left heart. Examples include hemodynamically significant pulmonary embolism, severe pulmonary hypertension.[3]

• Mechanical – impaired filling of right heart or due to decreased venous return to the right heart due to extrinsic compression. Examples include tension pneumothorax, pericardial tamponade, restrictive cardiomyopathy, constrictive pericarditis.

Epidemiology

Distributive shock is the most common type of shock, followed by hypovolemic and cardiogenic shock. Obstructive shock is relatively less common. The most common type of distributive shock is septic shock and has a mortality rate between 40 to 50%.

Pathophysiology

Hypoxia at the cellular level causes a series of physiologic and biochemical changes, resulting in acidosis and a decrease in regional blood flow, which further worsens the tissue hypoxia. [4] In hypovolemic, obstructive, and cardiogenic shock, there is a decrease in cardiac output and decreased oxygen transport. In distributive shock, there is decreased peripheral vascular resistance and abnormal oxygen extraction. Excitement is a spectrum of physiologic changes, ranging from early stages, which are reversible to the final stages, which are irreversible with multiorgan failure and death. Generally, shock has the following three stages:

1. Pre-shock or compensated shock – As the name suggests, this stage is characterized by compensatory mechanisms to counter the decrease in tissue perfusion, including tachycardia, peripheral vasoconstriction, and changes in systemic blood pressure

2. Shock – During this stage, most of the classic signs and symptoms of shock appear due to early organ dysfunction, resulting from the progression of the pre-shock stage as the compensatory mechanisms become insufficient.

3. End-organ dysfunction – This is the final stage, leading to irreversible organ dysfunction, multiorgan failure, and death

History and Physical

A focused history should be obtained from the patient (if feasible) and/or patient’s relatives. Also, a review of the patient’s outpatient medical records (information regarding risk factors, medications, and trend of baseline vital signs including blood pressure), as well as hospital medical records, could give valuable clues regarding the patient’s risk for shock and potential etiology. Clinical features and symptoms can vary according to the type and stage of shock. The most common clinical features/labs which are suggestive of shock include hypotension, tachycardia, tachypnea, obtundation or abnormal mental status, cold, clammy extremities, mottled skin, oliguria, metabolic acidosis, and hyperlactatemia.[5][6] Also, features pertaining to the underlying cause of the shock can be present.

Patients with hypovolemic shock can have general features as mentioned above as well as evidence of orthostatic hypotension, pallor, flattened jugular venous pulsations, may have sequelae of chronic liver disease (in case of variceal bleeding).

Patients with septic shock may present with symptoms suggestive of the source of infection (example-skin manifestations of primary infection such as erysipelas, cellulitis, necrotizing soft-tissue infections), and cutaneous manifestations of infective endocarditis.

Patients with anaphylactic shock can have hypotension, flushing, urticaria, tachypnea, hoarseness of voice, oral and facial edema, hives, wheeze, inspiratory stridor, and history of exposure to common allergens such as medications or food items the patient is allergic to or insect stings.

Tension pneumothorax should be suspected in a patient with undifferentiated shock who has tachypnea, unilateral pleuritic chest pain, absent or diminished breath sounds, tracheal deviation to the normal side, distended neck veins and also has pertinent risk factors for tension pneumothorax such as recent trauma, mechanical ventilation, underlying cystic lung disease).

In a patient with undifferentiated shock, diagnostic clues to pericardial tamponade as the etiology include dyspnea, the Beck triad (elevated jugular venous pressure, muffled heart sounds, hypotension), pulses paradoxus, and known risk factors such as trauma, the recent history of pericardial effusion, and thoracic procedures.  

Cardiogenic shock should be considered as the etiology if the patient with undifferentiated shock had chest pain suggestive of cardiac origin, narrow pulse pressure, elevated jugular venous pulsations or lung crackles, and significant arrhythmias on telemetry or EKG.

Evaluation

Resuscitation should not delay while investigating the etiology of undifferentiated shock. Physicians should have a high clinical suspicion for the presence of shock, and an attempt to stratify the severity of the shock should also take place to assess the need for emergent or early interventions. Evaluation of undifferentiated shock should begin with a thorough history and physical examination.

Besides telemetry monitoring, a 12-lead electrocardiogram should be obtained. ECGs might show evidence of acute coronary syndrome, arrhythmias, or provide diagnostic clues suggestive of pericardial effusion or pulmonary embolism.

Laboratory tests in a patient with undifferentiated shock should include a CBC and differential, renal and liver function tests, serum lactate level, cardiac biomarkers, D-dimer level, coagulation profile, type and screen for a possible blood transfusion if appropriate (if concern for hemorrhagic shock), blood and urine cultures, and blood gas analysis. Initial imaging studies recommended in patients with undifferentiated shock and hypotension include chest x-rays to look for the source of infection such as pneumonia, complications of shock such as ARDS, clinical findings supporting the diagnosis of pulmonary edema in cardiogenic shock, widened mediastinum in aortic dissection. CT scans can also assist in unmasking the etiology of shock in appropriate clinical scenarios. Point of care ultrasonography or focused cardiac ultrasound is also a useful bedside diagnostic tool.[7]

Treatment / Management

The initial approach to management is the stabilization of the airway and breathing with oxygen and oral mechanical ventilation when needed. Peripheral IV or intraosseous infusion (IO) access should be obtained. Central venous access may be required in the setting of shock if there is difficulty securing peripheral venous access, or the patient needs prolonged vasopressor therapy or large-volume resuscitation. Immediate treatment with intravenous (IV) fluid should be initiated, followed by vasopressor therapy, if needed, to maintain tissue perfusion. Depending on the underlying etiology of shock, specific therapies might also be needed.

Septic shock – initial aggressive fluid resuscitation with IV isotonic crystalloids 30 mL/kg within 3 hrs with additional fluid based on frequent reassessment, empiric antibiotic therapy within one hr. [8] For patients with septic shock requiring vasopressors, target a mean arterial pressure (MAP) of 65 mmHg. The first choice of a vasopressor is norepinephrine, with the addition of vasopressin if refractory.[9]

Anaphylactic shock – aggressive IV fluid resuscitation with 4 to 6 L of IV crystalloids. Stop the offending agent, intramuscular epinephrine, antihistamines, corticosteroids, nebulized albuterol.

In adrenal crisis – judicious fluid resuscitation, IV dexamethasone.

Hypovolemic shock – obtain two large-bore IVs or central line. Place the patient in the Trendelenburg position. Aggressive IV fluid resuscitation with 2 to 4 L of isotonic crystalloids. PRBC transfusion if ongoing bleed.  Appropriate medical or interventional strategies to treat the underlying etiology. Continue with isotonic crystalloids and use vasopressors if needed

Obstructive shock – the judicious use of IV crystalloids. If shock persists, early initiation of vasopressors-norepinephrine is the first choice and add vasopressin if refractory. Continue IV fluids but monitor very closely. 

If acute massive pulmonary embolism -thrombolysis. Judicious use of IV fluids has a paradoxical worsening of hypotension; it may develop due to severe right ventricular dilatation and septal bowing compromising left ventricle filling. 

If tension pneumothorax – needle thoracotomy followed by tube thoracotomy. If cardiac tamponade-pericardiocentesis, significant clinical improvement is possible, even with minimal fluid removal).

Cardiogenic shock – if unstable tachyarrhythmia or bradyarrhythmias, initiate ACLS protocol and cardioversion. Judicious use of IV fluids in the absence of pulmonary edema. Consider inotropes (dobutamine is the most commonly used agent) or intra-aortic balloon pump (IABP), if refractory shock, and vasopressor (norepinephrine) with inotropes.

If STEMI – consider thrombolysis or coronary revascularization procedures and or IABP.

Differential Diagnosis

Uncovering the etiology of undifferentiated shock is very important. In a patient presenting with undifferentiated shock, the differential diagnosis includes a wide variety of etiologies that falls under the four major categories of shock, as outlined above. Also, sometimes patients can have a combination of shock syndromes. Another differential is “pharmacological shock,” which results from vasodilatation or myocardial depression from medications (e.g., benzodiazepines, beta-blockers, calcium channel blockers, opiates, anticholinergics, and sildenafil).

Prognosis

Sepsis and septic shock, in general, are associated with long-term morbidity and mortality, with many of the survivors requiring placement into long-term acute care facilities or post-acute care centers. [10][11] Septic shock has a mortality rate between 40% and 50%. Cardiogenic shock has a mortality rate ranging from 50% to 75%, an improvement over prior mortality rates. Hypovolemic and obstructive shock generally have much lower mortality and respond better to timely treatment. 

Pearls and Other Issues

• Shock is a clinical manifestation of circulatory failure and is associated with high morbidity and mortality.

• There are broadly four types of shock: distributive, cardiogenic, hypovolemic, and obstructive.

• An accurate diagnosis requires a good understanding of underlying pathophysiology, clinical, biochemical, and hemodynamic manifestations of the different types of shock.

• Serum lactate level is a useful risk stratification tool in managing undifferentiated shock.

• Timely diagnosis and initiation of appropriate therapy are of paramount importance as it can prevent progression to the reversible shock, multiorgan failure, and death.

• Treatment includes hemodynamic stabilization and correction of underlying etiology of shock.

Enhancing Healthcare Team Outcomes

The management of patients with shock calls for a collaborative, interprofessional approach. Clinicians must react promptly to the emergency and determine the precise cause of shock. Nursing will be on hand to assist at every step of the way, assisting with measures such as intubation and administering medications. Pharmacists must rapidly prepare and deliver the needed drugs and yet still verify that dosing and interactions do not present a problem. Depending on the etiology, various specialists may also be called in on the case. Each area will need to act and react as the situation dictates. WIth interprofessional cooperation, these patients will stand a better chance of recovery from shock with minimal deleterious effects. [Level 5]

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References

1.

Vincent JL, De Backer D. Circulatory shock. N Engl J Med. 2014 Feb 06;370(6):583. [PubMed: 24499231]

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Angus DC, van der Poll T. Severe sepsis and septic shock. N Engl J Med. 2013 Aug 29;369(9):840-51. [PubMed: 23984731]

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Smulders YM. Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction. Cardiovasc Res. 2000 Oct;48(1):23-33. [PubMed: 11033105]

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Barber AE, Shires GT. Cell damage after shock. New Horiz. 1996 May;4(2):161-7. [PubMed: 8774792]

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Seymour CW, Liu VX, Iwashyna TJ, Brunkhorst FM, Rea TD, Scherag A, Rubenfeld G, Kahn JM, Shankar-Hari M, Singer M, Deutschman CS, Escobar GJ, Angus DC. Assessment of Clinical Criteria for Sepsis: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23;315(8):762-74. [PMC free article: PMC5433435] [PubMed: 26903335]

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Kraut JA, Madias NE. Lactic acidosis. N Engl J Med. 2015 Mar 12;372(11):1078-9. [PubMed: 25760366]

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Shokoohi H, Boniface KS, Pourmand A, Liu YT, Davison DL, Hawkins KD, Buhumaid RE, Salimian M, Yadav K. Bedside Ultrasound Reduces Diagnostic Uncertainty and Guides Resuscitation in Patients With Undifferentiated Hypotension. Crit Care Med. 2015 Dec;43(12):2562-9. [PubMed: 26575653]

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Howell MD, Davis AM. Management of Sepsis and Septic Shock. JAMA. 2017 Feb 28;317(8):847-848. [PubMed: 28114603]

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Hylands M, Moller MH, Asfar P, Toma A, Frenette AJ, Beaudoin N, Belley-Côté É, D’Aragon F, Laake JH, Siemieniuk RA, Charbonney E, Lauzier F, Kwong J, Rochwerg B, Vandvik PO, Guyatt G, Lamontagne F. A systematic review of vasopressor blood pressure targets in critically ill adults with hypotension. Can J Anaesth. 2017 Jul;64(7):703-715. [PubMed: 28497426]

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Shankar-Hari M, Phillips GS, Levy ML, Seymour CW, Liu VX, Deutschman CS, Angus DC, Rubenfeld GD, Singer M., Sepsis Definitions Task Force. Developing a New Definition and Assessing New Clinical Criteria for Septic Shock: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23;315(8):775-87. [PMC free article: PMC4910392] [PubMed: 26903336]

11.

Cecconi M, Evans L, Levy M, Rhodes A. Sepsis and septic shock. Lancet. 2018 Jul 07;392(10141):75-87. [PubMed: 29937192]

Disclosure: Hayas Haseer Koya declares no relevant financial relationships with ineligible companies.

Disclosure: Manju Paul declares no relevant financial relationships with ineligible companies.

Hemorrhagic shock – an article from the Vascular Innovation Center

Hemorrhagic shock (HS) is a critical condition of the body associated with acute blood loss, resulting in a crisis of macro- and microcirculation, a syndrome of multiple organ and polysystemic insufficiency. From a pathophysiological point of view, this is a microcirculation crisis, its inability to provide adequate tissue metabolism, satisfy the tissue need for oxygen, energy products, and remove toxic metabolic products.

The body of a healthy person can restore blood loss up to 20% of BCC (approximately 1000 ml) due to autohemodilution and redistribution of blood in the vascular bed. With blood loss of more than 20-25%, these mechanisms can eliminate the BCC deficiency. With massive blood loss, persistent vasoconstriction remains the leading “protective” reaction of the body, in connection with which normal or close to normal blood pressure is maintained, blood supply to the brain and heart is carried out (centralization of blood circulation), but due to weakening of blood flow in the muscles of internal organs, including kidneys, lungs, liver.

Long-term stable vasoconstriction, as a protective reaction of the body, at first maintains blood pressure within certain limits for some time, later, with the progression of shock and in the absence of adequate therapy, it contributes to the consistent development of severe microcirculation disorders, the formation of “shock” organs and the development of acute renal failure and other pathological conditions.

The severity and speed of disorders in HS depends on the duration of arterial hypotension, the ascending state of organs and systems. With ascending hypovolemia, short-term hypoxia during childbirth leads to shock, as it is a trigger for impaired hemostasis.

Hemorrhagic shock clinic

Hemorrhagic shock is manifested by weakness, dizziness, nausea, dry mouth, darkening of the eyes, with increased blood loss – loss of consciousness. In connection with the compensatory redistribution of blood, its amount decreases in the muscles, the skin is manifested by pallor of the skin with a gray tint; the limbs are cold, wet. A decrease in renal blood flow is manifested by a decrease in diuresis, subsequently with impaired microcirculation in the kidneys, with the development of ischemia, hypoxia, and tubular necrosis. With an increase in blood loss, symptoms of respiratory failure increase: shortness of breath, respiratory rhythm disturbance, agitation, peripheral cyanosis.

Four degrees of severity of hemorrhagic shock are distinguished:

• I degree of severity is noted with a BCC deficit of 15%. The general condition is satisfactory, the skin is pale, slight tachycardia (up to 80-90 beats / min), blood pressure within 100 mm Hg, hemoglobin 90g / l, central venous pressure is normal.
• II degree severity – BCC deficiency up to 30%. General condition of moderate severity, complaints of weakness, dizziness, darkening of the eyes, nausea, skin is pale, cold. Blood pressure 80-90 mm Hg, central venous pressure below 60 mm wg, tachycardia up to 100-120 beats/min, reduced diuresis, hemoglobin 80 g/l and below.
• III degree severity occurs with a BCC deficiency of 30-40%. The general condition is severe. There is a sharp lethargy, dizziness, pale skin, acrocyanosis, blood pressure below 60-70 mm Hg, CVP drops (20-30 mm water column and below). There is hypothermia, frequent pulse (130-140 beats / min), oliguria.
• IV degree severity is observed with a BCC deficiency of more than 40%. The condition is very serious, consciousness is absent. Arterial pressure and central venous pressure are not determined, the pulse is noted only on the carotid arteries. Breathing is superficial, rapid, with an abnormal rhythm, mobile excitation, hyporeflexia, anuria are noted.

Treatment of hemorrhagic shock

• Fast and reliable bleeding control.
• Replenishment of BCC and maintaining macro-, microcirculation and adequate tissue perfusion using controlled hemodilution, blood transfusion, rheocorrectors, glucocorticoids, etc.;
• Artificial ventilation of the lungs in the mode of moderate hyperventilation with positive end-expiratory pressure (prevention of “shock lungs”)
• Treatment of disseminated intravascular coagulation, disorders of the acid-base state, protein and water-electrolyte metabolism, correction of metabolic acidosis;
• Anesthesia, medical anesthesia, antihypoxic protection of the brain;
• Maintain adequate urine output at 50-60 ml/hour;
• Maintaining the activity of the heart, liver;

Elimination of the cause of bleeding is the main point in the treatment of hemorrhagic shock. The choice of method to stop bleeding depends on its cause. In the treatment of great importance is the speed of compensation for blood loss and timely surgical treatment. At the II degree of severity, hemorrhagic shock is an absolute indication for the operational stop of bleeding.

Infusion therapy for hemorrhagic shock should be carried out in 2-3 veins: with blood pressure in the range of 40-50 mm Hg. the volumetric infusion rate should be 300 ml/min at a blood pressure of 70-80 mm Hg. – 150-200 ml / min with stabilization of blood pressure up to 100-110 mm Hg. infusion is carried out drip under the control of blood pressure and hourly diuresis.

The ratio of colloids and crystalloids should be 2:1. Infusion therapy includes: rheopolyglucin, volecam, erythromass, native or fresh frozen plasma (5-6 vials), albumin, Ringer-Locke solution, glucose, panangin, prednisolone, corglicon, for the correction of metabolic acidosis – 4% sodium bicarbonate solution, trisamine . In hypotensive syndrome – the introduction of dopamine or dopamine. The volume of infusion should exceed the estimated blood loss by 60-80%, at the same time, blood transfusion is carried out in the amount of not more than 75% of blood loss with its simultaneous replacement, then delayed blood transfusion in smaller doses.

To eliminate vasospasm after eliminating bleeding and eliminating BCC deficiency, ganglionic blockers are used with drugs that improve the rheological properties of blood (rheopolyglucin, trental, complamin, chimes). It is necessary to use high doses of glucocorticoids (30-50mg/kg of hydrocortisone or 10-30mg/kg of prednisone), diuretics, mechanical ventilation.

For the treatment of DIC in HS, fresh frozen plasma is used, protease inhibitors – contrical (trasilol) 60-80000 OD each, Gordox 500-600000 OD each. Dicynon, etamzilat, androxon reduce capillary fragility, enhance the functional activity of platelets. Cardiac glycosides, immunocorrectors, vitamins are used, according to indications – antibacterial therapy, anabolics (nerobol, retabolil), Essentiale.

Mortality in hemorrhagic shock depends on the time of elimination of bleeding, the volume of blood loss and intensive care measures. It currently accounts for about 15% of all cases.

Rehabilitation therapy and therapeutic exercises are of great importance after intensive therapy.

Septic shock. What is septic shock?

IMPORTANT
The information in this section should not be used for self-diagnosis or self-treatment. In case of pain or other exacerbation of the disease, only the attending physician should prescribe diagnostic tests. For diagnosis and proper treatment, you should contact your doctor.

Septic shock is a serious pathological condition that occurs when a massive intake of bacterial endotoxins into the blood. Accompanied by tissue hypoperfusion, a critical decrease in blood pressure and symptoms of multiple organ failure. The diagnosis is made on the basis of the general clinical picture, which combines signs of damage to the lungs, cardiovascular system (CVS), liver and kidneys, and centralization of blood circulation. Treatment: massive antibiotic therapy, infusion of colloid and crystalloid solutions, maintenance of CCC activity by introducing vasopressors, correction of respiratory disorders by mechanical ventilation.

ICD-10

R57.2

• Causes
• Pathogenesis
• Classification
• Symptoms of septic shock
• Complications
• Diagnostics
• Treatment of septic shock
• Prognosis and prevention
• Prices for treatment

General

Septic shock (SS) is also called infectious-toxic shock (ITS). As an independent nosological unit, pathology was first described in the 19th century, however, a full-fledged study with the development of specific anti-shock measures began no more than 25 years ago. It can occur with any infectious process. Most often occurs in patients of surgical departments, with meningococcal septicemia, typhoid fever, salmonellosis and plague. It is common in countries where the largest number of bacterial and parasitic diseases is diagnosed (Africa, Afghanistan, Indonesia). More than 500,000 people around the world die each year from TSS.

Septic shock

Causes

In the vast majority of cases, pathology develops against the background of weakened immune responses. It occurs in patients suffering from chronic severe diseases, as well as in the elderly. Due to physiological characteristics, sepsis is more often diagnosed in men. The list of the most common diseases in which TTS events can occur includes:

• Foci of purulent infection. Signs of a systemic inflammatory reaction and associated disorders in the functioning of internal organs are noted in the presence of volumetric abscesses or phlegmon of soft tissues. The risk of a generalized toxic response increases with a long course of the disease, the absence of adequate antibiotic therapy, and the patient’s age over 60 years.
• Prolonged stay in the ICU. Hospitalization in the intensive care unit is always associated with the risk of sepsis and infectious shock. This is due to constant contact with microflora resistant to antibacterial drugs, weakening of the body’s defenses as a result of a serious illness, the presence of multiple gates of infection: catheters, gastric tubes, drainage tubes.
• Wounds. Violations of the integrity of the skin, including those that occurred during surgery, significantly increase the risk of infection with a highly contagious flora. TSS begins in patients with contaminated wounds who have not received timely care. Tissue trauma during surgery becomes the cause of a generalized infection only if the rules of asepsis and antisepsis are not followed. In most cases, septic shock occurs in patients who have undergone manipulations on the stomach and pancreas. Another common cause is diffuse peritonitis.
• Taking immunosuppressants. Immune depressant drugs (mercaptopurine, krizanol) are used to suppress the rejection reaction after organ transplantation. To a lesser extent, the level of self-protection decreases with the use of chemotherapeutic agents – cytostatics intended for the treatment of oncological diseases (doxorubicin, fluorouracil).
• AIDS. HIV infection in the AIDS stage leads to the development of atypical sepsis, provoked not by a bacterial culture, but by a fungus of the genus Candida. Clinical manifestations of the disease are characterized by a low degree of severity. The lack of an adequate immune response allows the pathogenic flora to multiply freely.

The causative agent of sepsis is gram-positive (streptococci, staphylococci, enterococci) and gram-negative (Enterobacter cloacae, Clostridium pneumoniae) bacteria. In many cases, cultures are insensitive to antibiotics, making it difficult to treat patients. Septic shock of viral origin is currently controversial among specialists. Some representatives of the scientific world argue that viruses are unable to cause pathology, others that an extracellular life form can provoke a systemic inflammatory response, which is the pathogenetic basis of TSS.

Pathogenesis

The symptoms are based on the uncontrolled spread of inflammatory mediators from the pathological focus. In this case, activation of macrophages, lymphocytes and neutrophils occurs. A systemic inflammatory response syndrome occurs. Against this background, peripheral vascular tone decreases, the volume of circulating blood decreases due to increased vascular permeability and fluid stagnation in the microvasculature. Further changes are due to a sharp decrease in perfusion. Insufficient blood supply causes hypoxia, ischemia of internal organs and disruption of their function. The most sensitive is the brain. In addition, the functional activity of the lungs, kidneys and liver worsens.

In addition to SVR, endogenous intoxication plays an important role in the formation of septic shock. In connection with a decrease in the efficiency of excretory systems, products of normal metabolism accumulate in the blood: creatinine, urea, lactate, guanine and pyruvate. In internal environments, the concentration of intermediate results of lipid oxidation (skatol, aldehydes, ketones) and bacterial endotoxins increases. All this causes severe changes in homeostasis, acid-base balance disorders, disturbances in the functioning of receptor systems.

Classification

The state of shock is classified according to pathogenetic and clinical principles. Pathogenetically, the disease can be “warm” and “cold”. Warm shock is characterized by an increase in cardiac output against the background of a decrease in overall vascular tone, endogenous hypercatecholaminemia, and dilation of intradermal vessels. The phenomena of organ failure are expressed moderately. The cold variety is manifested by a decrease in cardiac output, a sharp decrease in tissue perfusion, centralization of blood circulation, and severe MOF. According to the clinical course, septic shock is divided into the following varieties:

• Compensated. Consciousness is clear, safe, the patient is inhibited, but fully contactable. Arterial pressure is slightly reduced, the level of SBP is not less than 90 mm Hg. Tachycardia is detected (PS <100 bpm). Subjectively, the patient feels weakness, dizziness, headache and decreased muscle tone.
• Subcompensated. The skin is pale, the heart sounds are deaf, the heart rate reaches 140 beats per minute. SBP <90 mm. rt. Art., Respiration is rapid, shortness of breath up to 25 movements / min. Consciousness is confused, the patient answers questions with a delay, poorly understands what is happening around, where he is. Speech is quiet, slow, unintelligible.
• Decompensated. Marked depression of consciousness. The patient answers in monosyllables, in a whisper, often after 2-3 attempts. Motor activity is practically absent, the reaction to pain is weak. The skin is cyanotic, covered with sticky cold sweat. The heart sounds are deaf, the pulse on the peripheral arteries is not determined or is sharply weakened. Heart rate up to 180 beats / min, respiratory rate 25-30, shallow breathing. BP below 70/40, anuria.
• Terminal (irreversible). Consciousness is absent, the skin is marbled or gray, covered with bluish spots. Pathological breathing according to the type of Biot or Kussmaul, the respiratory rate decreases to 8-10 times / minute, sometimes breathing stops completely. SBP less than 50 mm Hg. pillar. There is no urination. The pulse is hardly palpable even on the central vessels.

Symptoms of septic shock

One of the defining signs of TSS is arterial hypotension. It is not possible to restore the level of blood pressure even with an adequate infusion volume (20-40 ml / kg). To maintain hemodynamics, it is necessary to use pressor amines (dopamine). Acute oliguria is noted, diuresis does not exceed 0.5 ml/kg/h. Body temperature reaches febrile values ​​- 38-39 ° C, it is poorly reduced with the help of antipyretics. To prevent convulsions caused by hyperthermia, it is necessary to use physical methods of cooling.

90% of cases of SS are accompanied by respiratory failure of varying severity. Patients with decompensated and terminal course of the disease need hardware respiratory support. The liver and spleen are enlarged, compacted, their function is impaired. There may be intestinal atony, flatulence, stools mixed with mucus, blood and pus. In the later stages, symptoms of disseminated intravascular coagulation occur: petechial rash, internal and external bleeding.

Complications

Septic shock leads to a number of severe complications. The most common of these is multiple organ failure, in which the function of two or more systems is impaired. First of all, the central nervous system, lungs, kidneys and heart suffer. Somewhat less common damage to the liver, intestines and spleen. Mortality among patients with MOF reaches 60%. Some of them die 3-5 days after being removed from a critical state. This is due to organic changes in internal structures.

Another common consequence of TSS is bleeding. With the formation of intracerebral hematomas, the patient develops a clinic of acute hemorrhagic stroke. The accumulation of extravasate in other organs can lead to their compression. A decrease in blood volume in the vascular bed potentiates a more significant decrease in blood pressure. DIC against the background of infectious-toxic shock causes the death of the patient in 40-45% of cases. Secondary organ damage, provoked by microthromboses that occur at the initial stage of coagulopathy formation, is observed in almost 100% of patients.

Diagnostics

The diagnosis is established by an anesthesiologist-resuscitator. The assumption is based on clinical data, however, it is possible to accurately determine the existing condition only if there are results of hardware and laboratory studies. If septic shock is suspected, all tests are done in an emergency mode, “according to cito”. Resuscitation activities should begin without waiting for the end of the support services. A comprehensive examination necessary to determine and confirm TTS includes:

• Examination and physical examination. Implemented directly by the attending physician. The specialist detects the characteristic clinical signs of a shock state. For this, tonometry, a visual assessment of the color of the skin, features of respiratory movements, counting the pulse and respiratory rate, auscultation of the heart and lungs are performed. If complications are suspected, an assessment of the neurological status is necessary for symptoms of cerebral hemorrhage.
• Hardware research. Has an auxiliary value. The patient is shown to control the condition using an anesthetic monitor. The screen of the device displays information about the value of blood pressure, heart rate, degree of blood oxygen saturation (with lung failure SpO2<90%) and coronary rhythm. Against the background of respiratory disorders and toxic damage to the myocardium, tachycardia, arrhythmia and blockade of intracardiac conduction may occur.
• Laboratory research. Allows you to identify existing violations of homeostasis, failures in the work of internal organs. In patients with shock of septic origin, elevated levels of creatinine (> 0.177 mmol / l), bilirubin (> 34.2 μmol / l), lactate (> 2 mmol / l) are found. Thrombocytopenia (<100 × 10⁹/l) indicates a violation of coagulation. With progressive anemia, erythrocytes are 1.5-2.5 million per 1 mm3, hemoglobin is below 90 g/l. venous blood pH <7.3 (metabolic acidosis).

Treatment of septic shock

Patients are given intensive care. Treatment is carried out in intensive care units using the methods of hardware and drug support. The attending physician is a resuscitator. Consultation with an infectious disease specialist, cardiologist, gastroenterologist and other specialists may be required. It is required to transfer the patient to artificial lung ventilation, round-the-clock supervision of nursing staff, parenteral feeding. Mixtures and products intended for introduction into the stomach are not used. All methods of exposure are conditionally divided into pathogenetic and symptomatic:

• Pathogenetic treatment. If sepsis is suspected, the patient is prescribed antibiotics. The scheme should include 2-3 drugs of various groups with a wide spectrum of action. The selection of the drug at the initial stage is carried out empirically, in accordance with the expected sensitivity of the pathogen. At the same time, blood is taken for sterility and susceptibility to antibiotics. The result of the analysis is prepared within 10 days. If by this time it was not possible to select an effective drug regimen, the study data should be used.
• Symptomatic treatment. It is selected taking into account the existing clinical picture. Usually patients receive massive infusion therapy, glucocorticosteroids, inotropic agents, antiplatelet agents or hemostatics (depending on the state of the blood coagulation system). In severe cases of the disease, blood products are used: fresh frozen plasma, albumin, immunoglobulins. If the patient is conscious, the introduction of analgesic and sedative drugs is indicated.

Prognosis and prevention

Septic shock has a poor prognosis for life. With a subcompensated course, about 40% of patients die. Decompensated and terminal varieties end in the death of 60% of patients. In the absence of timely medical care, mortality reaches 95-100%. Some patients die a few days after the elimination of the pathological condition. Prevention of TSS consists in the timely relief of foci of infection, the competent selection of antibiotic therapy in surgical patients, compliance with antiseptic requirements in departments involved in invasive manipulations, and the maintenance of an adequate immune status in representatives of the HIV-infected stratum of the population.

Sources

1. Resuscitation and intensive care// Zhdanov G.G., Zilber A.P. – 2007.
2. Tactics of managing patients with sepsis and septic shock in a multidisciplinary hospital / Sapicheva Yu.Yu., Likhvantsev VV. – 2015.