# 2 Shock, haemorrhage and transfusion

# After haemorrhage control

After haemorrhage control

- Once haemorrhage is controlled, patients should be defini - tively resuscitated, warmed and have coagulopathy corrected. Attention should be paid to fluid responsiveness and the end - points of  resuscitation to ensure that patients are fully resusci - tated and to reduce the incidence and severity of organ failure ( Figure 2.2 and Shock resuscitation ). - After haemorrhage control

- Once haemorrhage is controlled, patients should be defini - tively resuscitated, warmed and have coagulopathy corrected. Attention should be paid to fluid responsiveness and the end - points of  resuscitation to ensure that patients are fully resusci - tated and to reduce the incidence and severity of organ failure ( Figure 2.2 and Shock resuscitation ). - After haemorrhage control

- Once haemorrhage is controlled, patients should be defini - tively resuscitated, warmed and have coagulopathy corrected. Attention should be paid to fluid responsiveness and the end - points of  resuscitation to ensure that patients are fully resusci - tated and to reduce the incidence and severity of organ failure ( Figure 2.2 and Shock resuscitation ). -

# Blood and blood products

Blood and blood products

Blood is collected from donors who have been previously screened before donating to exclude any donor whose blood may have the potential to harm the patient or to prevent possible harm that donating a unit of  blood may have for the donor. In the UK, up to 450 /uni00A0 mL of  blood is drawn, a maximum of  three times each year. Each unit is tested for evidence of - hepatitis B, hepatitis C, human immunodeficiency virus - (HIV)-1, HIV-2 and syphilis. Donations are leukodepleted as a precaution against variant Creutzfeldt–Jakob disease (this may also reduce the immunogenicity of  the transfusion). as the presence of  irregular red cell antibodies. The blood is then processed into subcomponents. Whole blood Whole blood is now rarely available in civilian practice because it has been seen as an ine ffi cient use of  the limited resource. However, whole blood transfusion has significant advantages over packed cells as it is coagulation factor rich and, if  fresh, more metabolically active than stored blood. Packed red cells Packed red blood cells are spun-down and concentrated packs of  red blood cells. Each unit is approximately 330 /uni00A0 mL and has a haematocrit of  50–70%. Packed cells are stored in a SAG-M (saline–adenine–glucose–mannitol) solution to increase shelf life to 5 weeks at 2–6°C. (Older storage regimes included storage in CPD [citrate–phosphate–dextrose] solutions, which have a shelf  life of  2–3 weeks.) Fresh-frozen plasma Fresh-frozen plasma (FFP) is rich in coagulation factors and is removed from fresh blood and stored at − 40°C to − 50°C with a 2-year shelf  life. It is the first-line therapy in the treatment of  coagulopathic haemorrhage (see Management of coag ulopathy ). Rhesus D-positive FFP may be given to a rhesus D-negative woman, although it is possible for seroconversion to occur with large volumes owing to the presence of  red cell fragments and Rh-D immunisa tion should be considered. Cryoprecipitate Cryoprecipitate is a supernatant precipitate of  FFP and is rich in fibrinogen, factor VIII and factor XIII. It is stored at − 30°C with a 2-year shelf  life. It is given in low-fibrinogen states or factor VIII deficiency . Platelets Platelets are supplied as a pooled platelet concentrate and 9 contain about 250 /uni00A0×/uni00A0 10 /litre. Platelets are stored on a special agitator at 20–24°C and have a shelf  life of  only 5 days. Plate let transfusions are given to patients with thrombocytopenia or with platelet dysfunction who are bleeding or undergoing surgery . Patients are increasingly presenting on antiplatelet therapy such as aspirin or clopidogrel for reduction of  cardiovascu lar risk. Aspirin therapy rarely poses a problem b ut control of haemorrhage on the more potent platelet inhibitors can be extremely di ffi cult. Patients on clopidogrel who are actively bleeding and undergoing major surgery may require almost continuous infusion of  platelets during the course of  the proce dure. Arginine vasopressin or its analogues (DDA VP) have also been used in this patient group, although with limited success. Prothrombin complex concentrates Prothrombin complex concentrates are highly purified concen trates prepared from pooled plasma. They contain factors II, IX and X. Factor VII may be included or produced separately . It is indicated for the emergency reversal of  anticoagulant (warfarin) therapy in uncontrolled haemorrhage. It is possible for patients undergoing elective surgery to pre-donate their own blood up to 3 weeks before surgery for re-transfusion during the operation. Similarly , during surgery blood can be collected in a cell saver, which washes and collects red blood cells that can then be returned to the patient. Blood and blood products

Blood is collected from donors who have been previously screened before donating to exclude any donor whose blood may have the potential to harm the patient or to prevent possible harm that donating a unit of  blood may have for the donor. In the UK, up to 450 /uni00A0 mL of  blood is drawn, a maximum of  three times each year. Each unit is tested for evidence of - hepatitis B, hepatitis C, human immunodeficiency virus - (HIV)-1, HIV-2 and syphilis. Donations are leukodepleted as a precaution against variant Creutzfeldt–Jakob disease (this may also reduce the immunogenicity of  the transfusion). as the presence of  irregular red cell antibodies. The blood is then processed into subcomponents. Whole blood Whole blood is now rarely available in civilian practice because it has been seen as an ine ffi cient use of  the limited resource. However, whole blood transfusion has significant advantages over packed cells as it is coagulation factor rich and, if  fresh, more metabolically active than stored blood. Packed red cells Packed red blood cells are spun-down and concentrated packs of  red blood cells. Each unit is approximately 330 /uni00A0 mL and has a haematocrit of  50–70%. Packed cells are stored in a SAG-M (saline–adenine–glucose–mannitol) solution to increase shelf life to 5 weeks at 2–6°C. (Older storage regimes included storage in CPD [citrate–phosphate–dextrose] solutions, which have a shelf  life of  2–3 weeks.) Fresh-frozen plasma Fresh-frozen plasma (FFP) is rich in coagulation factors and is removed from fresh blood and stored at − 40°C to − 50°C with a 2-year shelf  life. It is the first-line therapy in the treatment of  coagulopathic haemorrhage (see Management of coag ulopathy ). Rhesus D-positive FFP may be given to a rhesus D-negative woman, although it is possible for seroconversion to occur with large volumes owing to the presence of  red cell fragments and Rh-D immunisa tion should be considered. Cryoprecipitate Cryoprecipitate is a supernatant precipitate of  FFP and is rich in fibrinogen, factor VIII and factor XIII. It is stored at − 30°C with a 2-year shelf  life. It is given in low-fibrinogen states or factor VIII deficiency . Platelets Platelets are supplied as a pooled platelet concentrate and 9 contain about 250 /uni00A0×/uni00A0 10 /litre. Platelets are stored on a special agitator at 20–24°C and have a shelf  life of  only 5 days. Plate let transfusions are given to patients with thrombocytopenia or with platelet dysfunction who are bleeding or undergoing surgery . Patients are increasingly presenting on antiplatelet therapy such as aspirin or clopidogrel for reduction of  cardiovascu lar risk. Aspirin therapy rarely poses a problem b ut control of haemorrhage on the more potent platelet inhibitors can be extremely di ffi cult. Patients on clopidogrel who are actively bleeding and undergoing major surgery may require almost continuous infusion of  platelets during the course of  the proce dure. Arginine vasopressin or its analogues (DDA VP) have also been used in this patient group, although with limited success. Prothrombin complex concentrates Prothrombin complex concentrates are highly purified concen trates prepared from pooled plasma. They contain factors II, IX and X. Factor VII may be included or produced separately . It is indicated for the emergency reversal of  anticoagulant (warfarin) therapy in uncontrolled haemorrhage. It is possible for patients undergoing elective surgery to pre-donate their own blood up to 3 weeks before surgery for re-transfusion during the operation. Similarly , during surgery blood can be collected in a cell saver, which washes and collects red blood cells that can then be returned to the patient. Blood and blood products

Blood is collected from donors who have been previously screened before donating to exclude any donor whose blood may have the potential to harm the patient or to prevent possible harm that donating a unit of  blood may have for the donor. In the UK, up to 450 /uni00A0 mL of  blood is drawn, a maximum of  three times each year. Each unit is tested for evidence of - hepatitis B, hepatitis C, human immunodeficiency virus - (HIV)-1, HIV-2 and syphilis. Donations are leukodepleted as a precaution against variant Creutzfeldt–Jakob disease (this may also reduce the immunogenicity of  the transfusion). as the presence of  irregular red cell antibodies. The blood is then processed into subcomponents. Whole blood Whole blood is now rarely available in civilian practice because it has been seen as an ine ffi cient use of  the limited resource. However, whole blood transfusion has significant advantages over packed cells as it is coagulation factor rich and, if  fresh, more metabolically active than stored blood. Packed red cells Packed red blood cells are spun-down and concentrated packs of  red blood cells. Each unit is approximately 330 /uni00A0 mL and has a haematocrit of  50–70%. Packed cells are stored in a SAG-M (saline–adenine–glucose–mannitol) solution to increase shelf life to 5 weeks at 2–6°C. (Older storage regimes included storage in CPD [citrate–phosphate–dextrose] solutions, which have a shelf  life of  2–3 weeks.) Fresh-frozen plasma Fresh-frozen plasma (FFP) is rich in coagulation factors and is removed from fresh blood and stored at − 40°C to − 50°C with a 2-year shelf  life. It is the first-line therapy in the treatment of  coagulopathic haemorrhage (see Management of coag ulopathy ). Rhesus D-positive FFP may be given to a rhesus D-negative woman, although it is possible for seroconversion to occur with large volumes owing to the presence of  red cell fragments and Rh-D immunisa tion should be considered. Cryoprecipitate Cryoprecipitate is a supernatant precipitate of  FFP and is rich in fibrinogen, factor VIII and factor XIII. It is stored at − 30°C with a 2-year shelf  life. It is given in low-fibrinogen states or factor VIII deficiency . Platelets Platelets are supplied as a pooled platelet concentrate and 9 contain about 250 /uni00A0×/uni00A0 10 /litre. Platelets are stored on a special agitator at 20–24°C and have a shelf  life of  only 5 days. Plate let transfusions are given to patients with thrombocytopenia or with platelet dysfunction who are bleeding or undergoing surgery . Patients are increasingly presenting on antiplatelet therapy such as aspirin or clopidogrel for reduction of  cardiovascu lar risk. Aspirin therapy rarely poses a problem b ut control of haemorrhage on the more potent platelet inhibitors can be extremely di ffi cult. Patients on clopidogrel who are actively bleeding and undergoing major surgery may require almost continuous infusion of  platelets during the course of  the proce dure. Arginine vasopressin or its analogues (DDA VP) have also been used in this patient group, although with limited success. Prothrombin complex concentrates Prothrombin complex concentrates are highly purified concen trates prepared from pooled plasma. They contain factors II, IX and X. Factor VII may be included or produced separately . It is indicated for the emergency reversal of  anticoagulant (warfarin) therapy in uncontrolled haemorrhage. It is possible for patients undergoing elective surgery to pre-donate their own blood up to 3 weeks before surgery for re-transfusion during the operation. Similarly , during surgery blood can be collected in a cell saver, which washes and collects red blood cells that can then be returned to the patient.

# Blood groups and cross-matching

Blood groups and cross-matching

Human red cells have on their cell surface many di ff erent - antigens. Two groups of  antigens are of  major importance in surgical practice /uni00A0 – /uni00A0 the ABO and rhesus systems. ABO system These proteins are strongly antigenic and are associated with - naturally occurring antibodies in the serum. The system consists of  three allelic genes /uni00A0 – /uni00A0 A, B and O /uni00A0 – /uni00A0 which control synthesis of  enzymes that add carbohydrate residues to cell surface glycoproteins. A and B genes add specific residues while the O gene is an amorph and does not transform the glycoprotein. The system allows for six possible genotypes although there are only four phenotypes. Naturally occurring antibodies are found in the serum of  those lacking the corresponding antigen ( Table 2.7 ). Blood group O is the universal donor type as it contains no antigens to provoke a reaction. Conversely , group AB individ uals are ‘universal recipients’ and can receive an y ABO blood type because they have no circulating antibodies. Rhesus system The rhesus D (Rh(D)) antigen is strongly antigenic and is present in approximately 85% of  the population in the UK. Antibodies to the D antigen are not naturally present in the serum of the remaining 15% of  individuals, but their formation may be stimulated by the transfusion of  Rh-positive red cells or they may be acquired during delivery of  a Rh(D)-positive baby . Acquired antibodies are capable, during pregnancy , of crossing the placenta and, if present in a Rh(D)-negative mother, may cause sever e haemolytic anaemia and even death (hydrops fetalis) in a Rh(D)-positive fetus in utero. The other minor blood group antigens may be associated with naturally occurring antibodies, or may stimulate the formation of  anti bodies on relatively rare occasions. 

Phenotype
Genotype
Antigens
O
OO
O
A
AA or AO
A
B
BB or BO
B
AB
AB
AB

Blood groups and cross-matching

Human red cells have on their cell surface many di ff erent - antigens. Two groups of  antigens are of  major importance in surgical practice /uni00A0 – /uni00A0 the ABO and rhesus systems. ABO system These proteins are strongly antigenic and are associated with - naturally occurring antibodies in the serum. The system consists of  three allelic genes /uni00A0 – /uni00A0 A, B and O /uni00A0 – /uni00A0 which control synthesis of  enzymes that add carbohydrate residues to cell surface glycoproteins. A and B genes add specific residues while the O gene is an amorph and does not transform the glycoprotein. The system allows for six possible genotypes although there are only four phenotypes. Naturally occurring antibodies are found in the serum of  those lacking the corresponding antigen ( Table 2.7 ). Blood group O is the universal donor type as it contains no antigens to provoke a reaction. Conversely , group AB individ uals are ‘universal recipients’ and can receive an y ABO blood type because they have no circulating antibodies. Rhesus system The rhesus D (Rh(D)) antigen is strongly antigenic and is present in approximately 85% of  the population in the UK. Antibodies to the D antigen are not naturally present in the serum of the remaining 15% of  individuals, but their formation may be stimulated by the transfusion of  Rh-positive red cells or they may be acquired during delivery of  a Rh(D)-positive baby . Acquired antibodies are capable, during pregnancy , of crossing the placenta and, if present in a Rh(D)-negative mother, may cause sever e haemolytic anaemia and even death (hydrops fetalis) in a Rh(D)-positive fetus in utero. The other minor blood group antigens may be associated with naturally occurring antibodies, or may stimulate the formation of  anti bodies on relatively rare occasions. 

Phenotype
Genotype
Antigens
O
OO
O
A
AA or AO
A
B
BB or BO
B
AB
AB
AB

Blood groups and cross-matching

Human red cells have on their cell surface many di ff erent - antigens. Two groups of  antigens are of  major importance in surgical practice /uni00A0 – /uni00A0 the ABO and rhesus systems. ABO system These proteins are strongly antigenic and are associated with - naturally occurring antibodies in the serum. The system consists of  three allelic genes /uni00A0 – /uni00A0 A, B and O /uni00A0 – /uni00A0 which control synthesis of  enzymes that add carbohydrate residues to cell surface glycoproteins. A and B genes add specific residues while the O gene is an amorph and does not transform the glycoprotein. The system allows for six possible genotypes although there are only four phenotypes. Naturally occurring antibodies are found in the serum of  those lacking the corresponding antigen ( Table 2.7 ). Blood group O is the universal donor type as it contains no antigens to provoke a reaction. Conversely , group AB individ uals are ‘universal recipients’ and can receive an y ABO blood type because they have no circulating antibodies. Rhesus system The rhesus D (Rh(D)) antigen is strongly antigenic and is present in approximately 85% of  the population in the UK. Antibodies to the D antigen are not naturally present in the serum of the remaining 15% of  individuals, but their formation may be stimulated by the transfusion of  Rh-positive red cells or they may be acquired during delivery of  a Rh(D)-positive baby . Acquired antibodies are capable, during pregnancy , of crossing the placenta and, if present in a Rh(D)-negative mother, may cause sever e haemolytic anaemia and even death (hydrops fetalis) in a Rh(D)-positive fetus in utero. The other minor blood group antigens may be associated with naturally occurring antibodies, or may stimulate the formation of  anti bodies on relatively rare occasions. 

Phenotype
Genotype
Antigens
O
OO
O
A
AA or AO
A
B
BB or BO
B
AB
AB
AB

# Blood substitutes

Blood substitutes

Blood substitutes are an attractive alternative to the costly process of  donating, checking, storing and administering blood, especially given the immunogenic and potential infec tious complications associated with transfusion. There are several oxygen-carrying blood substitutes under investigation in experimental animal or early clinical trials. Blood substitutes are either biomimetic or abiotic. Biomimetic the blood and are haemoglobin based. Abiotic substitutes ar e synthetic oxygen carriers and are currently primarily per- fluorocarbon based. Haemoglobin is seen as the ob vious candidate for devel - oping an e ff ective blood substitute, and one free haemoglobin - solution is available in some countries where blood compo - nents are not readily available. Various other engineered molecules are under clinical trials and are based on human, bovine or recombinant technologies. Second-generation per - fluorocarbon emulsions are also showing potential in clinical trials. Blood substitutes

Blood substitutes are an attractive alternative to the costly process of  donating, checking, storing and administering blood, especially given the immunogenic and potential infec tious complications associated with transfusion. There are several oxygen-carrying blood substitutes under investigation in experimental animal or early clinical trials. Blood substitutes are either biomimetic or abiotic. Biomimetic the blood and are haemoglobin based. Abiotic substitutes ar e synthetic oxygen carriers and are currently primarily per- fluorocarbon based. Haemoglobin is seen as the ob vious candidate for devel - oping an e ff ective blood substitute, and one free haemoglobin - solution is available in some countries where blood compo - nents are not readily available. Various other engineered molecules are under clinical trials and are based on human, bovine or recombinant technologies. Second-generation per - fluorocarbon emulsions are also showing potential in clinical trials. Blood substitutes

Blood substitutes are an attractive alternative to the costly process of  donating, checking, storing and administering blood, especially given the immunogenic and potential infec tious complications associated with transfusion. There are several oxygen-carrying blood substitutes under investigation in experimental animal or early clinical trials. Blood substitutes are either biomimetic or abiotic. Biomimetic the blood and are haemoglobin based. Abiotic substitutes ar e synthetic oxygen carriers and are currently primarily per- fluorocarbon based. Haemoglobin is seen as the ob vious candidate for devel - oping an e ff ective blood substitute, and one free haemoglobin - solution is available in some countries where blood compo - nents are not readily available. Various other engineered molecules are under clinical trials and are based on human, bovine or recombinant technologies. Second-generation per - fluorocarbon emulsions are also showing potential in clinical trials.

# Classification of shock

Classification of shock

There are numerous ways to classify shock, but the most common and most clinically applicable is one based on the initiating mechanism. All states are characterised by systemic tissue hypoperfusion, and di ff erent states may coexist within the same patient. Summary box 2.1 Classification of shock /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF Haemorrhagic and hypovolaemic shock Hypovolaemic shock is due to a reduced circulating volume. Hypovolaemia may be due to haemorrhagic or non- haemorrhagic causes. Non-haemorrhagic causes include poor fluid intake (dehydration), excessive fluid loss due to vomiting, diarrhoea, urinary loss (e.g. diabetes), evaporation or ‘third-spacing’, where fluid is lost into the gastrointestinal tract and interstitial spaces, as for example in bowel obstruction or pancreatitis. Hypovolaemia is the most common form of  shock, and to some degree is a component of  all other forms of  shock. Absolute or relative hypovolaemia must be excluded or treated in the management of the shocked state, regardless of  cause. Cardiogenic shock Cardiogenic shock is due to primary failure of  the heart to pump blood to the tissues. Causes of  cardiogenic shock include myocardial infarction, cardiac dysrhythmias, valvular heart disease, blunt myocardial injury and cardiomyopathy . Cardiac insu ffi ciency may also be due to myocardial depression caused by endogenous factors (e.g. bacterial and humoral agents agents or drug abuse. Evidence of  venous hypertension with pulmonary or systemic oedema may coexist with the classical signs of  shock. - Obstructive shock In obstructive shock there is a reduction in preload owing to mechanical obstruction of  cardiac filling. Common causes of  obstructive shock include cardiac tamponade, tension pneumothorax, massive pulmonary embolus or air embolus. In each case, there is reduced filling of  the left and/or right sides of  the heart, leading to low cardiac output. Distributive shock Distributive shock describes the pattern of  cardiovascular responses characterising a variety of  conditions, including septic shock, anaphylaxis and spinal cord injury . Inadequate organ perfusion is accompanied by vascular dilatation with hypotension, low systemic vascular resistance, inadequate afterload and a resulting abnormally high cardiac output. In anaphylaxis, vasodilatation is due to histamine release, while in high spinal cord injury there is failure of  sympathetic outflow and adequate vascular tone (neurogenic shock). The cause in sepsis is less clear but is related to the release of bac - terial products (endotoxin) and the activation of  cellular and humoral components of  the immune system. There is mal- distribution of  blood flow at a microvascular level, with arte - riovenous shunting and dysfunction of  cellular utilisation of oxygen. In the later phases of septic shock there is hypovolaemia from fluid loss into interstitial spaces and there may be con - comitant my ocardial depression, complicating the clinical pic - ture ( Table 2.1 ). Endocrine shock Endocrine shock may present as a combination of hypovolae- mic, cardiogenic or distributive shock. Causes of  endocrine shock include hypo- and hyperthyroidism and adrenal insuf - ficiency . Hypothyroidism causes a shock state similar to that of  neurogenic shock due to disordered vascular and cardiac responsiveness to circulating catecholamines. Cardiac output falls as a result of  low inotropy and bradycardia. There may also be an associated cardiomyopathy . Thyrotoxicosis may cause a high-output cardiac failure. Adrenal insu ffi ciency leads to shock due to hypovolae- mia and a poor response to circulating and exogenous 

Haemorrhagic/hypovolaemic shock
Cardiogenic shock
Obstructive shock
Distributive shock
Endocrine shock
TABLE 2.1
Cardiovascular and metabolic characteristics of shock.
Hypovolaemic
Cardiac output
Low
Systemic vascular resistance High
Venous pressure
Low
Mixed venous saturation Low
Base de
/f_i
cit
High
Cardiogenic
Obstructive
Distributive
Low
Low
High
High
High
Low
High
High
Low
Low
Low
High
High
High
High

existing Addison’s disease or be a relative insu ffi ciency due to a pathological disease state, such as systemic sepsis. Classification of shock

There are numerous ways to classify shock, but the most common and most clinically applicable is one based on the initiating mechanism. All states are characterised by systemic tissue hypoperfusion, and di ff erent states may coexist within the same patient. Summary box 2.1 Classification of shock /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF Haemorrhagic and hypovolaemic shock Hypovolaemic shock is due to a reduced circulating volume. Hypovolaemia may be due to haemorrhagic or non- haemorrhagic causes. Non-haemorrhagic causes include poor fluid intake (dehydration), excessive fluid loss due to vomiting, diarrhoea, urinary loss (e.g. diabetes), evaporation or ‘third-spacing’, where fluid is lost into the gastrointestinal tract and interstitial spaces, as for example in bowel obstruction or pancreatitis. Hypovolaemia is the most common form of  shock, and to some degree is a component of  all other forms of  shock. Absolute or relative hypovolaemia must be excluded or treated in the management of the shocked state, regardless of  cause. Cardiogenic shock Cardiogenic shock is due to primary failure of  the heart to pump blood to the tissues. Causes of  cardiogenic shock include myocardial infarction, cardiac dysrhythmias, valvular heart disease, blunt myocardial injury and cardiomyopathy . Cardiac insu ffi ciency may also be due to myocardial depression caused by endogenous factors (e.g. bacterial and humoral agents agents or drug abuse. Evidence of  venous hypertension with pulmonary or systemic oedema may coexist with the classical signs of  shock. - Obstructive shock In obstructive shock there is a reduction in preload owing to mechanical obstruction of  cardiac filling. Common causes of  obstructive shock include cardiac tamponade, tension pneumothorax, massive pulmonary embolus or air embolus. In each case, there is reduced filling of  the left and/or right sides of  the heart, leading to low cardiac output. Distributive shock Distributive shock describes the pattern of  cardiovascular responses characterising a variety of  conditions, including septic shock, anaphylaxis and spinal cord injury . Inadequate organ perfusion is accompanied by vascular dilatation with hypotension, low systemic vascular resistance, inadequate afterload and a resulting abnormally high cardiac output. In anaphylaxis, vasodilatation is due to histamine release, while in high spinal cord injury there is failure of  sympathetic outflow and adequate vascular tone (neurogenic shock). The cause in sepsis is less clear but is related to the release of bac - terial products (endotoxin) and the activation of  cellular and humoral components of  the immune system. There is mal- distribution of  blood flow at a microvascular level, with arte - riovenous shunting and dysfunction of  cellular utilisation of oxygen. In the later phases of septic shock there is hypovolaemia from fluid loss into interstitial spaces and there may be con - comitant my ocardial depression, complicating the clinical pic - ture ( Table 2.1 ). Endocrine shock Endocrine shock may present as a combination of hypovolae- mic, cardiogenic or distributive shock. Causes of  endocrine shock include hypo- and hyperthyroidism and adrenal insuf - ficiency . Hypothyroidism causes a shock state similar to that of  neurogenic shock due to disordered vascular and cardiac responsiveness to circulating catecholamines. Cardiac output falls as a result of  low inotropy and bradycardia. There may also be an associated cardiomyopathy . Thyrotoxicosis may cause a high-output cardiac failure. Adrenal insu ffi ciency leads to shock due to hypovolae- mia and a poor response to circulating and exogenous 

Haemorrhagic/hypovolaemic shock
Cardiogenic shock
Obstructive shock
Distributive shock
Endocrine shock
TABLE 2.1
Cardiovascular and metabolic characteristics of shock.
Hypovolaemic
Cardiac output
Low
Systemic vascular resistance High
Venous pressure
Low
Mixed venous saturation Low
Base de
/f_i
cit
High
Cardiogenic
Obstructive
Distributive
Low
Low
High
High
High
Low
High
High
Low
Low
Low
High
High
High
High

existing Addison’s disease or be a relative insu ffi ciency due to a pathological disease state, such as systemic sepsis. Classification of shock

There are numerous ways to classify shock, but the most common and most clinically applicable is one based on the initiating mechanism. All states are characterised by systemic tissue hypoperfusion, and di ff erent states may coexist within the same patient. Summary box 2.1 Classification of shock /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF Haemorrhagic and hypovolaemic shock Hypovolaemic shock is due to a reduced circulating volume. Hypovolaemia may be due to haemorrhagic or non- haemorrhagic causes. Non-haemorrhagic causes include poor fluid intake (dehydration), excessive fluid loss due to vomiting, diarrhoea, urinary loss (e.g. diabetes), evaporation or ‘third-spacing’, where fluid is lost into the gastrointestinal tract and interstitial spaces, as for example in bowel obstruction or pancreatitis. Hypovolaemia is the most common form of  shock, and to some degree is a component of  all other forms of  shock. Absolute or relative hypovolaemia must be excluded or treated in the management of the shocked state, regardless of  cause. Cardiogenic shock Cardiogenic shock is due to primary failure of  the heart to pump blood to the tissues. Causes of  cardiogenic shock include myocardial infarction, cardiac dysrhythmias, valvular heart disease, blunt myocardial injury and cardiomyopathy . Cardiac insu ffi ciency may also be due to myocardial depression caused by endogenous factors (e.g. bacterial and humoral agents agents or drug abuse. Evidence of  venous hypertension with pulmonary or systemic oedema may coexist with the classical signs of  shock. - Obstructive shock In obstructive shock there is a reduction in preload owing to mechanical obstruction of  cardiac filling. Common causes of  obstructive shock include cardiac tamponade, tension pneumothorax, massive pulmonary embolus or air embolus. In each case, there is reduced filling of  the left and/or right sides of  the heart, leading to low cardiac output. Distributive shock Distributive shock describes the pattern of  cardiovascular responses characterising a variety of  conditions, including septic shock, anaphylaxis and spinal cord injury . Inadequate organ perfusion is accompanied by vascular dilatation with hypotension, low systemic vascular resistance, inadequate afterload and a resulting abnormally high cardiac output. In anaphylaxis, vasodilatation is due to histamine release, while in high spinal cord injury there is failure of  sympathetic outflow and adequate vascular tone (neurogenic shock). The cause in sepsis is less clear but is related to the release of bac - terial products (endotoxin) and the activation of  cellular and humoral components of  the immune system. There is mal- distribution of  blood flow at a microvascular level, with arte - riovenous shunting and dysfunction of  cellular utilisation of oxygen. In the later phases of septic shock there is hypovolaemia from fluid loss into interstitial spaces and there may be con - comitant my ocardial depression, complicating the clinical pic - ture ( Table 2.1 ). Endocrine shock Endocrine shock may present as a combination of hypovolae- mic, cardiogenic or distributive shock. Causes of  endocrine shock include hypo- and hyperthyroidism and adrenal insuf - ficiency . Hypothyroidism causes a shock state similar to that of  neurogenic shock due to disordered vascular and cardiac responsiveness to circulating catecholamines. Cardiac output falls as a result of  low inotropy and bradycardia. There may also be an associated cardiomyopathy . Thyrotoxicosis may cause a high-output cardiac failure. Adrenal insu ffi ciency leads to shock due to hypovolae- mia and a poor response to circulating and exogenous 

Haemorrhagic/hypovolaemic shock
Cardiogenic shock
Obstructive shock
Distributive shock
Endocrine shock
TABLE 2.1
Cardiovascular and metabolic characteristics of shock.
Hypovolaemic
Cardiac output
Low
Systemic vascular resistance High
Venous pressure
Low
Mixed venous saturation Low
Base de
/f_i
cit
High
Cardiogenic
Obstructive
Distributive
Low
Low
High
High
High
Low
High
High
Low
Low
Low
High
High
High
High

existing Addison’s disease or be a relative insu ffi ciency due to a pathological disease state, such as systemic sepsis.

# Clinical consequences of shock

Clinical consequences of shock

Unresuscitatable shock Patients who are in profound shock for a prolonged period of time become ‘unresuscitatable’. Cell death follows from cellu lar ischaemia and the ability of  the body to compensate is lost. In the heart there is myocardial cell death from poor coronary perfusion and myocardial depression from severe acidaemia and hyperkalaemia. This leads to poor cardiac output and limited response to fluids or inotropic therapy . Peripherally there may also be loss of  the ability to maintain systemic vascu lar resistance and further hypotension ensues. The peripheries no longer respond appropriately to vasopressor agents. Once patients enter this stage of  systemic ischaemic injury , death is inevitable. Ischaemia–reperfusion and the systemic inflammatory response syndrome (SIRS) During the period of  systemic hypoperfusion, cellular and organ damage progresses owing to the direct e ff ects of  tissue hypoxia and local activation of  inflammation. Further injury occurs once normal circulation is restored to these tissues. The acid and potassium load that has built up can lead to direct myocardial depression, vascular dilatation and further hypotension. Molecules released from the interior of  cells are released into the circulation. These are sensed by and activate leukocytes. These, together with cellular and humoral elements activated by the hypoxia (complement, neutrophils, micro vascular thrombi), overwhelm the local anti-inflammatory response and are flushed back into the systemic circulation, where they cause injury to distant organs such as the lungs and the kidneys. This leads to acute lung injury , acute renal injury , cerebral oedema, multiple organ failure and death. Reperfu sion injury can currently only be attenuated by reducing the extent and duration of  tissue hypoperfusion. Multiple organ failure As techniques of  resuscitation have improved, more and more patients are surviving shock. Where intervention is timely and the period of  shock is limited, patients may make a rapid, uncomplicated recovery . However, the result of  prolonged systemic ischaemia and reperfusion injury is end-organ damage and multiple organ failure. Multiple organ failure is defined as two or more failed organ systems. There is no specific treatment for multiple organ fail ure. Management is support of  organ systems, with v entilation, cardiovascular support and haemofiltration/dialysis until there is recovery of  organ function. Multiple organ failure currently carries a mortality of  60%; thus, prevention is vital by early aggressive identification and reversal of  shock. Thomas Addison , 1799–1860, physician, Guy’s Hospital, London, UK, described the e ff ects of  disease of  the suprarenal capsules in 1849. Effects of organ failure /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF - 

Cardiac: Cardiovascular failure
Lung: Acute respiratory distress syndrome
Kidney: Acute renal insuf
/f_i
ciency
Liver: Liver failure and coagulopathy
Brain: Cerebral swelling and dysfunction

Clinical consequences of shock

Unresuscitatable shock Patients who are in profound shock for a prolonged period of time become ‘unresuscitatable’. Cell death follows from cellu lar ischaemia and the ability of  the body to compensate is lost. In the heart there is myocardial cell death from poor coronary perfusion and myocardial depression from severe acidaemia and hyperkalaemia. This leads to poor cardiac output and limited response to fluids or inotropic therapy . Peripherally there may also be loss of  the ability to maintain systemic vascu lar resistance and further hypotension ensues. The peripheries no longer respond appropriately to vasopressor agents. Once patients enter this stage of  systemic ischaemic injury , death is inevitable. Ischaemia–reperfusion and the systemic inflammatory response syndrome (SIRS) During the period of  systemic hypoperfusion, cellular and organ damage progresses owing to the direct e ff ects of  tissue hypoxia and local activation of  inflammation. Further injury occurs once normal circulation is restored to these tissues. The acid and potassium load that has built up can lead to direct myocardial depression, vascular dilatation and further hypotension. Molecules released from the interior of  cells are released into the circulation. These are sensed by and activate leukocytes. These, together with cellular and humoral elements activated by the hypoxia (complement, neutrophils, micro vascular thrombi), overwhelm the local anti-inflammatory response and are flushed back into the systemic circulation, where they cause injury to distant organs such as the lungs and the kidneys. This leads to acute lung injury , acute renal injury , cerebral oedema, multiple organ failure and death. Reperfu sion injury can currently only be attenuated by reducing the extent and duration of  tissue hypoperfusion. Multiple organ failure As techniques of  resuscitation have improved, more and more patients are surviving shock. Where intervention is timely and the period of  shock is limited, patients may make a rapid, uncomplicated recovery . However, the result of  prolonged systemic ischaemia and reperfusion injury is end-organ damage and multiple organ failure. Multiple organ failure is defined as two or more failed organ systems. There is no specific treatment for multiple organ fail ure. Management is support of  organ systems, with v entilation, cardiovascular support and haemofiltration/dialysis until there is recovery of  organ function. Multiple organ failure currently carries a mortality of  60%; thus, prevention is vital by early aggressive identification and reversal of  shock. Thomas Addison , 1799–1860, physician, Guy’s Hospital, London, UK, described the e ff ects of  disease of  the suprarenal capsules in 1849. Effects of organ failure /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF - 

Cardiac: Cardiovascular failure
Lung: Acute respiratory distress syndrome
Kidney: Acute renal insuf
/f_i
ciency
Liver: Liver failure and coagulopathy
Brain: Cerebral swelling and dysfunction

Clinical consequences of shock

Unresuscitatable shock Patients who are in profound shock for a prolonged period of time become ‘unresuscitatable’. Cell death follows from cellu lar ischaemia and the ability of  the body to compensate is lost. In the heart there is myocardial cell death from poor coronary perfusion and myocardial depression from severe acidaemia and hyperkalaemia. This leads to poor cardiac output and limited response to fluids or inotropic therapy . Peripherally there may also be loss of  the ability to maintain systemic vascu lar resistance and further hypotension ensues. The peripheries no longer respond appropriately to vasopressor agents. Once patients enter this stage of  systemic ischaemic injury , death is inevitable. Ischaemia–reperfusion and the systemic inflammatory response syndrome (SIRS) During the period of  systemic hypoperfusion, cellular and organ damage progresses owing to the direct e ff ects of  tissue hypoxia and local activation of  inflammation. Further injury occurs once normal circulation is restored to these tissues. The acid and potassium load that has built up can lead to direct myocardial depression, vascular dilatation and further hypotension. Molecules released from the interior of  cells are released into the circulation. These are sensed by and activate leukocytes. These, together with cellular and humoral elements activated by the hypoxia (complement, neutrophils, micro vascular thrombi), overwhelm the local anti-inflammatory response and are flushed back into the systemic circulation, where they cause injury to distant organs such as the lungs and the kidneys. This leads to acute lung injury , acute renal injury , cerebral oedema, multiple organ failure and death. Reperfu sion injury can currently only be attenuated by reducing the extent and duration of  tissue hypoperfusion. Multiple organ failure As techniques of  resuscitation have improved, more and more patients are surviving shock. Where intervention is timely and the period of  shock is limited, patients may make a rapid, uncomplicated recovery . However, the result of  prolonged systemic ischaemia and reperfusion injury is end-organ damage and multiple organ failure. Multiple organ failure is defined as two or more failed organ systems. There is no specific treatment for multiple organ fail ure. Management is support of  organ systems, with v entilation, cardiovascular support and haemofiltration/dialysis until there is recovery of  organ function. Multiple organ failure currently carries a mortality of  60%; thus, prevention is vital by early aggressive identification and reversal of  shock. Thomas Addison , 1799–1860, physician, Guy’s Hospital, London, UK, described the e ff ects of  disease of  the suprarenal capsules in 1849. Effects of organ failure /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF - 

Cardiac: Cardiovascular failure
Lung: Acute respiratory distress syndrome
Kidney: Acute renal insuf
/f_i
ciency
Liver: Liver failure and coagulopathy
Brain: Cerebral swelling and dysfunction

# Complications of blood transfusion

Complications of blood transfusion

Complications from blood transfusion can be categorised as those arising from a single transfusion and those related to massive transfusion. - Complications from a single transfusion Complications from a single transfusion include: /uni25CF incompatibility haemolytic transfusion reaction; /uni25CF febrile transfusion reaction; /uni25CF allergic reaction; /uni25CF infection: - /uni25CF bacterial infection (usually due to faulty storage); - /uni25CF hepatitis; /uni25CF HIV; /uni25CF malaria; /uni25CF air embolism; /uni25CF thrombophlebitis; /uni25CF transfusion-related acute lung injury (usually from FFP). Complications from massive transfusion Complications from massive transfusion include: /uni25CF coagulopathy; /uni25CF hypocalcaemia; /uni25CF hyperkalaemia; /uni25CF hypokalaemia; /uni25CF hypothermia. In addition, patients who receive repeated transfusions over long periods of  time (e.g. patients with thalassaemia) may develop iron overload. (Each transfused unit of  red blood cells contains appr oximately 250 /uni00A0 mg of  elemental iron.) Correction of  coagulopathy is not necessary if  there is no active bleeding and haemorrhage is not anticipated (not due for surgery). However, coagulopathy will occur during major haemorrhage and should be anticipated and managed actively . Prevention of  dilutional coagulopathy is central to the dam age control resuscitation of  patients who are actively bleeding. This is the prime reason for delivering balanced transfusion regimes that deliv er a resuscitation which approximates that of whole blood. In most practice this means delivering matched units of  red blood cells, plasma and platelets in a 1:1:1 ratio. Crystalloids and colloids should be avoided if  at all possible. The balanced transfusion approach will not correct an established coagulopathy . Most bleeding patients are hyper fibrinolytic, and should be empirically given tranexamic acid, an antifibrinolytic agent, as quickly as possible. Low fibrinogen levels are v ery common, and fibrinogen is vital to clot formation and stabilisation. Cryoprecipitate can be given empirically or guided by laboratory or point-of-care tests of  clotting (e.g. thr omboelastometry). Similarly platelet con centrates are given for low platelet counts or observed platelet dysfunction. Clotting function should be assayed frequently during haemorrhage and acted upon until bleeding has been controlled. Complications of blood transfusion

Complications from blood transfusion can be categorised as those arising from a single transfusion and those related to massive transfusion. - Complications from a single transfusion Complications from a single transfusion include: /uni25CF incompatibility haemolytic transfusion reaction; /uni25CF febrile transfusion reaction; /uni25CF allergic reaction; /uni25CF infection: - /uni25CF bacterial infection (usually due to faulty storage); - /uni25CF hepatitis; /uni25CF HIV; /uni25CF malaria; /uni25CF air embolism; /uni25CF thrombophlebitis; /uni25CF transfusion-related acute lung injury (usually from FFP). Complications from massive transfusion Complications from massive transfusion include: /uni25CF coagulopathy; /uni25CF hypocalcaemia; /uni25CF hyperkalaemia; /uni25CF hypokalaemia; /uni25CF hypothermia. In addition, patients who receive repeated transfusions over long periods of  time (e.g. patients with thalassaemia) may develop iron overload. (Each transfused unit of  red blood cells contains appr oximately 250 /uni00A0 mg of  elemental iron.) Correction of  coagulopathy is not necessary if  there is no active bleeding and haemorrhage is not anticipated (not due for surgery). However, coagulopathy will occur during major haemorrhage and should be anticipated and managed actively . Prevention of  dilutional coagulopathy is central to the dam age control resuscitation of  patients who are actively bleeding. This is the prime reason for delivering balanced transfusion regimes that deliv er a resuscitation which approximates that of whole blood. In most practice this means delivering matched units of  red blood cells, plasma and platelets in a 1:1:1 ratio. Crystalloids and colloids should be avoided if  at all possible. The balanced transfusion approach will not correct an established coagulopathy . Most bleeding patients are hyper fibrinolytic, and should be empirically given tranexamic acid, an antifibrinolytic agent, as quickly as possible. Low fibrinogen levels are v ery common, and fibrinogen is vital to clot formation and stabilisation. Cryoprecipitate can be given empirically or guided by laboratory or point-of-care tests of  clotting (e.g. thr omboelastometry). Similarly platelet con centrates are given for low platelet counts or observed platelet dysfunction. Clotting function should be assayed frequently during haemorrhage and acted upon until bleeding has been controlled. Complications of blood transfusion

Complications from blood transfusion can be categorised as those arising from a single transfusion and those related to massive transfusion. - Complications from a single transfusion Complications from a single transfusion include: /uni25CF incompatibility haemolytic transfusion reaction; /uni25CF febrile transfusion reaction; /uni25CF allergic reaction; /uni25CF infection: - /uni25CF bacterial infection (usually due to faulty storage); - /uni25CF hepatitis; /uni25CF HIV; /uni25CF malaria; /uni25CF air embolism; /uni25CF thrombophlebitis; /uni25CF transfusion-related acute lung injury (usually from FFP). Complications from massive transfusion Complications from massive transfusion include: /uni25CF coagulopathy; /uni25CF hypocalcaemia; /uni25CF hyperkalaemia; /uni25CF hypokalaemia; /uni25CF hypothermia. In addition, patients who receive repeated transfusions over long periods of  time (e.g. patients with thalassaemia) may develop iron overload. (Each transfused unit of  red blood cells contains appr oximately 250 /uni00A0 mg of  elemental iron.) Correction of  coagulopathy is not necessary if  there is no active bleeding and haemorrhage is not anticipated (not due for surgery). However, coagulopathy will occur during major haemorrhage and should be anticipated and managed actively . Prevention of  dilutional coagulopathy is central to the dam age control resuscitation of  patients who are actively bleeding. This is the prime reason for delivering balanced transfusion regimes that deliv er a resuscitation which approximates that of whole blood. In most practice this means delivering matched units of  red blood cells, plasma and platelets in a 1:1:1 ratio. Crystalloids and colloids should be avoided if  at all possible. The balanced transfusion approach will not correct an established coagulopathy . Most bleeding patients are hyper fibrinolytic, and should be empirically given tranexamic acid, an antifibrinolytic agent, as quickly as possible. Low fibrinogen levels are v ery common, and fibrinogen is vital to clot formation and stabilisation. Cryoprecipitate can be given empirically or guided by laboratory or point-of-care tests of  clotting (e.g. thr omboelastometry). Similarly platelet con centrates are given for low platelet counts or observed platelet dysfunction. Clotting function should be assayed frequently during haemorrhage and acted upon until bleeding has been controlled.

# Conduct of resuscitation

Conduct of resuscitation

Resuscitation should not be delayed in order to definitively diagnose the source of  the shocked state. However, the timing and nature of  resuscitation will depend on the type of  shock and the timing and severity of  the insult. Rapid clinical exam - ination will provide adequate clues to make an appropriate first determination, even if  a source of  bleeding or sepsis is not immediately identifiable. If there is initial doubt about the cause of shock, it is safer to assume the cause is hypo- volaemia and begin with fluid resuscitation, and then assess the response. Correction of  shock is important in the pre- and peri- operative period for all cases of  urgent surgery . For e xample, a patient with bowel obstruction and hypovolaemic shock must be adequately resuscitated before undergoing surgery . If not, the additional surgical injury and hypovolaemia induced during the procedure will increase the physiological demand on the heart, increasing the risk of  myocardial infarction; will exacerbate the inflammatory activation and thus the incidence and severity of  organ damage (especially acute kidney injury); will increase susceptibility to infection and venous thrombo - - embolism; and will prolong the period of  gut dysfunction and overall recovery from surgery . In all cases of  shock, regardless of  classification, hypovolaemia and inadequate preload must be addressed before other ther apy is instituted. Administration of  inotropic or chronotropic agents to an empty heart will rapidly and permanently deplete the myocardium of  oxygen stores and dramatically reduce diastolic filling and therefore coronary perfusion. Correction of  preload by ensuring adequate volume resuscitation should be prioritised before introducing vasopressors or inotropic agents. First-line therapy , therefore, is intravenous access and administration of  intravenous fluids. Access should be through short, wide-bore catheters that allow rapid infusion of  fluids as necessary . Long, narr ow lines, such as central venous catheters, have too high a resistance to allow rapid infusion and are more appropriate for monitoring than fluid replacement therapy . Type of fluids As a general rule, the ideal replacement fluid is one that approximates the fluid lost by the underlying cause of  shock. If  blood is being lost, the replacement fluid is whole blood or its equivalent in components /uni00A0 – /uni00A0 although crystalloid therapy may be required while awaiting blood products. Other causes of  shock will require crystalloid resuscitation with appropriate electrolyte supplementation. In most studies of  shock resuscitation there is no overt dif ference in response or outcome between crystalloid solutions (normal saline, Hartmann’s solution, Ringer’s lactate) and colloids (albumin or commercially available products). Fur ther more, there is less volume benefit to the administration of colloids than had previously been thought, with only 1.3 times more crystalloid than colloid administered in blinded trials. On balance, there is little evidence to support the administration of colloids, which are more expensive and have worse side-e ff ect profiles. Hypotonic solutions (e.g. dextrose) are poor volume expand ers and should not be used in the treatment of  shock unless the deficit is free water loss (e.g. diabetes insipidus) or patients are sodium overloaded (e.g. cirrhosis). Conduct of resuscitation

Resuscitation should not be delayed in order to definitively diagnose the source of  the shocked state. However, the timing and nature of  resuscitation will depend on the type of  shock and the timing and severity of  the insult. Rapid clinical exam - ination will provide adequate clues to make an appropriate first determination, even if  a source of  bleeding or sepsis is not immediately identifiable. If there is initial doubt about the cause of shock, it is safer to assume the cause is hypo- volaemia and begin with fluid resuscitation, and then assess the response. Correction of  shock is important in the pre- and peri- operative period for all cases of  urgent surgery . For e xample, a patient with bowel obstruction and hypovolaemic shock must be adequately resuscitated before undergoing surgery . If not, the additional surgical injury and hypovolaemia induced during the procedure will increase the physiological demand on the heart, increasing the risk of  myocardial infarction; will exacerbate the inflammatory activation and thus the incidence and severity of  organ damage (especially acute kidney injury); will increase susceptibility to infection and venous thrombo - - embolism; and will prolong the period of  gut dysfunction and overall recovery from surgery . In all cases of  shock, regardless of  classification, hypovolaemia and inadequate preload must be addressed before other ther apy is instituted. Administration of  inotropic or chronotropic agents to an empty heart will rapidly and permanently deplete the myocardium of  oxygen stores and dramatically reduce diastolic filling and therefore coronary perfusion. Correction of  preload by ensuring adequate volume resuscitation should be prioritised before introducing vasopressors or inotropic agents. First-line therapy , therefore, is intravenous access and administration of  intravenous fluids. Access should be through short, wide-bore catheters that allow rapid infusion of  fluids as necessary . Long, narr ow lines, such as central venous catheters, have too high a resistance to allow rapid infusion and are more appropriate for monitoring than fluid replacement therapy . Type of fluids As a general rule, the ideal replacement fluid is one that approximates the fluid lost by the underlying cause of  shock. If  blood is being lost, the replacement fluid is whole blood or its equivalent in components /uni00A0 – /uni00A0 although crystalloid therapy may be required while awaiting blood products. Other causes of  shock will require crystalloid resuscitation with appropriate electrolyte supplementation. In most studies of  shock resuscitation there is no overt dif ference in response or outcome between crystalloid solutions (normal saline, Hartmann’s solution, Ringer’s lactate) and colloids (albumin or commercially available products). Fur ther more, there is less volume benefit to the administration of colloids than had previously been thought, with only 1.3 times more crystalloid than colloid administered in blinded trials. On balance, there is little evidence to support the administration of colloids, which are more expensive and have worse side-e ff ect profiles. Hypotonic solutions (e.g. dextrose) are poor volume expand ers and should not be used in the treatment of  shock unless the deficit is free water loss (e.g. diabetes insipidus) or patients are sodium overloaded (e.g. cirrhosis). Conduct of resuscitation

Resuscitation should not be delayed in order to definitively diagnose the source of  the shocked state. However, the timing and nature of  resuscitation will depend on the type of  shock and the timing and severity of  the insult. Rapid clinical exam - ination will provide adequate clues to make an appropriate first determination, even if  a source of  bleeding or sepsis is not immediately identifiable. If there is initial doubt about the cause of shock, it is safer to assume the cause is hypo- volaemia and begin with fluid resuscitation, and then assess the response. Correction of  shock is important in the pre- and peri- operative period for all cases of  urgent surgery . For e xample, a patient with bowel obstruction and hypovolaemic shock must be adequately resuscitated before undergoing surgery . If not, the additional surgical injury and hypovolaemia induced during the procedure will increase the physiological demand on the heart, increasing the risk of  myocardial infarction; will exacerbate the inflammatory activation and thus the incidence and severity of  organ damage (especially acute kidney injury); will increase susceptibility to infection and venous thrombo - - embolism; and will prolong the period of  gut dysfunction and overall recovery from surgery . In all cases of  shock, regardless of  classification, hypovolaemia and inadequate preload must be addressed before other ther apy is instituted. Administration of  inotropic or chronotropic agents to an empty heart will rapidly and permanently deplete the myocardium of  oxygen stores and dramatically reduce diastolic filling and therefore coronary perfusion. Correction of  preload by ensuring adequate volume resuscitation should be prioritised before introducing vasopressors or inotropic agents. First-line therapy , therefore, is intravenous access and administration of  intravenous fluids. Access should be through short, wide-bore catheters that allow rapid infusion of  fluids as necessary . Long, narr ow lines, such as central venous catheters, have too high a resistance to allow rapid infusion and are more appropriate for monitoring than fluid replacement therapy . Type of fluids As a general rule, the ideal replacement fluid is one that approximates the fluid lost by the underlying cause of  shock. If  blood is being lost, the replacement fluid is whole blood or its equivalent in components /uni00A0 – /uni00A0 although crystalloid therapy may be required while awaiting blood products. Other causes of  shock will require crystalloid resuscitation with appropriate electrolyte supplementation. In most studies of  shock resuscitation there is no overt dif ference in response or outcome between crystalloid solutions (normal saline, Hartmann’s solution, Ringer’s lactate) and colloids (albumin or commercially available products). Fur ther more, there is less volume benefit to the administration of colloids than had previously been thought, with only 1.3 times more crystalloid than colloid administered in blinded trials. On balance, there is little evidence to support the administration of colloids, which are more expensive and have worse side-e ff ect profiles. Hypotonic solutions (e.g. dextrose) are poor volume expand ers and should not be used in the treatment of  shock unless the deficit is free water loss (e.g. diabetes insipidus) or patients are sodium overloaded (e.g. cirrhosis).

# Cross-matching

Cross-matching

To prevent transfusion reactions, all transfusions are preceded by ABO and rhesus typing of  both donor and recipient blood to ensure compatibility . The recipient’s serum is then mixed with the donor’s cells to confirm ABO compatibility and to test for rhesus and any other blood group antigen–antibody reaction. Full cross-matching of  blood may take up to 45 minutes in most laboratories. In more urgent situations, ‘type-specific’ blood is provided; this is only ABO/rhesus matched and can be issued within 10–15 minutes . Where blood must be given in an emergency , group O (universal donor) blood is given (O– to - females, O+ to males). When blood transfusion is prescribed and blood is admin - istered, it is essential that the correct patient receives the cor - rect transfusion. Two healthcare personnel should check the patient’s details against the prescription and the label of the donor blood. In addition, the donor blood serial number should also be checked against the issue slip for that patient. Provided these principles are strictly adhered to, the number of  severe and fatal ABO incompatibility reactions can be minimised. 

Antibodies
Frequency (%)
Anti-A, anti-B
46
Anti-B
42
Anti-A
9
None
3

Cross-matching

To prevent transfusion reactions, all transfusions are preceded by ABO and rhesus typing of  both donor and recipient blood to ensure compatibility . The recipient’s serum is then mixed with the donor’s cells to confirm ABO compatibility and to test for rhesus and any other blood group antigen–antibody reaction. Full cross-matching of  blood may take up to 45 minutes in most laboratories. In more urgent situations, ‘type-specific’ blood is provided; this is only ABO/rhesus matched and can be issued within 10–15 minutes . Where blood must be given in an emergency , group O (universal donor) blood is given (O– to - females, O+ to males). When blood transfusion is prescribed and blood is admin - istered, it is essential that the correct patient receives the cor - rect transfusion. Two healthcare personnel should check the patient’s details against the prescription and the label of the donor blood. In addition, the donor blood serial number should also be checked against the issue slip for that patient. Provided these principles are strictly adhered to, the number of  severe and fatal ABO incompatibility reactions can be minimised. 

Antibodies
Frequency (%)
Anti-A, anti-B
46
Anti-B
42
Anti-A
9
None
3

Cross-matching

To prevent transfusion reactions, all transfusions are preceded by ABO and rhesus typing of  both donor and recipient blood to ensure compatibility . The recipient’s serum is then mixed with the donor’s cells to confirm ABO compatibility and to test for rhesus and any other blood group antigen–antibody reaction. Full cross-matching of  blood may take up to 45 minutes in most laboratories. In more urgent situations, ‘type-specific’ blood is provided; this is only ABO/rhesus matched and can be issued within 10–15 minutes . Where blood must be given in an emergency , group O (universal donor) blood is given (O– to - females, O+ to males). When blood transfusion is prescribed and blood is admin - istered, it is essential that the correct patient receives the cor - rect transfusion. Two healthcare personnel should check the patient’s details against the prescription and the label of the donor blood. In addition, the donor blood serial number should also be checked against the issue slip for that patient. Provided these principles are strictly adhered to, the number of  severe and fatal ABO incompatibility reactions can be minimised. 

Antibodies
Frequency (%)
Anti-A, anti-B
46
Anti-B
42
Anti-A
9
None
3

# Damage control resuscitation

Damage control resuscitation

Damage control resuscitation (DCR), also known as haemo - static resuscitation, is a paradigm that prioritises haemorrhage control in patients who are still actively bleeding. The rationale is that no aspect of  the shock state /uni00A0 – /uni00A0 end-organ perfusion, blood pressure, temperature, lactic acidosis /uni00A0 – /uni00A0 can be corrected 

Haemostasis
Time
Prioritise perfusion
Perfusion-targeted resuscitation
Goal: End-organ perfusion
Adequate preload and afterload (
/f_l
uids and pressors)
Thromboprophylaxis
Monitor
:
Cardiovascular: BP , HR, CO, SVR
Perfusion: base excess, lactate, S
O
v
2
Organ function: PaO
/F
O
, UO, GCS
2
i
2
Abdominal compartment: IAP
O
, fraction of inspired oxygen;
i
2
, arterial oxygen tension; PT, prothrombin time; RBC, red
2
O
, mixed venous oxygen saturation; TEG, thrombo
-
v
2

resuscitation will exacerbate coagulopathy , hypothermia and metabolic derangements (acidosis, hyperkalaemia, hypocal caemia). The introduction of  DCR has been associated with substantial reductions in mortality from haemorrhagic shock in the last decade. DCR applies only while patients are bleeding and is based on four key principles /uni00A0 – /uni00A0 rapid haemorrhage control; permissive hypotension; avoiding dilutional coagulopathy; and trea existing coagulation deficits ( Figure 2.2 ). Rapid haemorrhage control At all times, control of  bleeding is the priority . Direct pres sure should be placed over the site of external haemorrhage. Temporary bleeding control should be achieved with tour niquets, balloon occlusion or other techniques. Intracavitary haemorrhage should be suspected and searched for, and the pathway should actively move patients forwards to the oper ating theatre or interventional radiology room to achieve this. The damage control approach is extended to the conduct of  surgery to prioritise rapid bleeding control. In damage con trol surgery , surgical intervention is limited to the minimum necessary to stop bleeding and contr ol sepsis, in order to avoid additional tissue damage, bleeding and physiological stress. More definitive repairs can be delayed until the patient is hae modynamically stable and physiologically capable of  sustain ing the procedure. Thus the operation is tailored to match the patient’s physiology , and is not focused on reconstructing anat omy . ‘Damage control’ is a term borrowed from the military: it ensures continued functioning of  a damaged ship above con ducting complete repairs, which would prevent rapid return to battle. Summary box 2.3 Damage control surgery /uni25CF /uni25CF /uni25CF /uni25CF Permissive hypotension Permissive hypotension allows the patient to set their own blood pressure while bleeding and avoids continued volume resuscitation in the vain attempt to normalise perfusion while bleeding. This reduces blood loss from bleeding sites and reduces dilutional coagulopathy and hypothermia induced by fluids. It is important to maintain baseline perfusion of the coronary arteries at minimum, and thus a palpable central pulse (mean arterial pressure above ~50 /uni00A0 mmHg) must be maintained by whatever means are available. Avoid dilutional coagulopathy Avoid dilutional coagulopathy by avoiding clear fluids (crystal loids or colloids) and by giving a transfusion that approximates red blood cells and plasma. - Treat existing coagulation deficits Treat existing coagulopathies either empirically or by regular coagulation testing and acting on the results. Tranexamic acid should be given as soon as possible in almost all bleeding patients to stop hyperfibrinolysis. Blood component concen - ting trates should be given to correct existing deficits, such as cryoprecipitate for low fibrinogen levels or platelet transfusions for platelet dysfunctions. - 

Arrest haemorrhage
Control sepsis
Protect from further injury
Nothing else

Damage control resuscitation

Damage control resuscitation (DCR), also known as haemo - static resuscitation, is a paradigm that prioritises haemorrhage control in patients who are still actively bleeding. The rationale is that no aspect of  the shock state /uni00A0 – /uni00A0 end-organ perfusion, blood pressure, temperature, lactic acidosis /uni00A0 – /uni00A0 can be corrected 

Haemostasis
Time
Prioritise perfusion
Perfusion-targeted resuscitation
Goal: End-organ perfusion
Adequate preload and afterload (
/f_l
uids and pressors)
Thromboprophylaxis
Monitor
:
Cardiovascular: BP , HR, CO, SVR
Perfusion: base excess, lactate, S
O
v
2
Organ function: PaO
/F
O
, UO, GCS
2
i
2
Abdominal compartment: IAP
O
, fraction of inspired oxygen;
i
2
, arterial oxygen tension; PT, prothrombin time; RBC, red
2
O
, mixed venous oxygen saturation; TEG, thrombo
-
v
2

resuscitation will exacerbate coagulopathy , hypothermia and metabolic derangements (acidosis, hyperkalaemia, hypocal caemia). The introduction of  DCR has been associated with substantial reductions in mortality from haemorrhagic shock in the last decade. DCR applies only while patients are bleeding and is based on four key principles /uni00A0 – /uni00A0 rapid haemorrhage control; permissive hypotension; avoiding dilutional coagulopathy; and trea existing coagulation deficits ( Figure 2.2 ). Rapid haemorrhage control At all times, control of  bleeding is the priority . Direct pres sure should be placed over the site of external haemorrhage. Temporary bleeding control should be achieved with tour niquets, balloon occlusion or other techniques. Intracavitary haemorrhage should be suspected and searched for, and the pathway should actively move patients forwards to the oper ating theatre or interventional radiology room to achieve this. The damage control approach is extended to the conduct of  surgery to prioritise rapid bleeding control. In damage con trol surgery , surgical intervention is limited to the minimum necessary to stop bleeding and contr ol sepsis, in order to avoid additional tissue damage, bleeding and physiological stress. More definitive repairs can be delayed until the patient is hae modynamically stable and physiologically capable of  sustain ing the procedure. Thus the operation is tailored to match the patient’s physiology , and is not focused on reconstructing anat omy . ‘Damage control’ is a term borrowed from the military: it ensures continued functioning of  a damaged ship above con ducting complete repairs, which would prevent rapid return to battle. Summary box 2.3 Damage control surgery /uni25CF /uni25CF /uni25CF /uni25CF Permissive hypotension Permissive hypotension allows the patient to set their own blood pressure while bleeding and avoids continued volume resuscitation in the vain attempt to normalise perfusion while bleeding. This reduces blood loss from bleeding sites and reduces dilutional coagulopathy and hypothermia induced by fluids. It is important to maintain baseline perfusion of the coronary arteries at minimum, and thus a palpable central pulse (mean arterial pressure above ~50 /uni00A0 mmHg) must be maintained by whatever means are available. Avoid dilutional coagulopathy Avoid dilutional coagulopathy by avoiding clear fluids (crystal loids or colloids) and by giving a transfusion that approximates red blood cells and plasma. - Treat existing coagulation deficits Treat existing coagulopathies either empirically or by regular coagulation testing and acting on the results. Tranexamic acid should be given as soon as possible in almost all bleeding patients to stop hyperfibrinolysis. Blood component concen - ting trates should be given to correct existing deficits, such as cryoprecipitate for low fibrinogen levels or platelet transfusions for platelet dysfunctions. - 

Arrest haemorrhage
Control sepsis
Protect from further injury
Nothing else

Damage control resuscitation

Damage control resuscitation (DCR), also known as haemo - static resuscitation, is a paradigm that prioritises haemorrhage control in patients who are still actively bleeding. The rationale is that no aspect of  the shock state /uni00A0 – /uni00A0 end-organ perfusion, blood pressure, temperature, lactic acidosis /uni00A0 – /uni00A0 can be corrected 

Haemostasis
Time
Prioritise perfusion
Perfusion-targeted resuscitation
Goal: End-organ perfusion
Adequate preload and afterload (
/f_l
uids and pressors)
Thromboprophylaxis
Monitor
:
Cardiovascular: BP , HR, CO, SVR
Perfusion: base excess, lactate, S
O
v
2
Organ function: PaO
/F
O
, UO, GCS
2
i
2
Abdominal compartment: IAP
O
, fraction of inspired oxygen;
i
2
, arterial oxygen tension; PT, prothrombin time; RBC, red
2
O
, mixed venous oxygen saturation; TEG, thrombo
-
v
2

resuscitation will exacerbate coagulopathy , hypothermia and metabolic derangements (acidosis, hyperkalaemia, hypocal caemia). The introduction of  DCR has been associated with substantial reductions in mortality from haemorrhagic shock in the last decade. DCR applies only while patients are bleeding and is based on four key principles /uni00A0 – /uni00A0 rapid haemorrhage control; permissive hypotension; avoiding dilutional coagulopathy; and trea existing coagulation deficits ( Figure 2.2 ). Rapid haemorrhage control At all times, control of  bleeding is the priority . Direct pres sure should be placed over the site of external haemorrhage. Temporary bleeding control should be achieved with tour niquets, balloon occlusion or other techniques. Intracavitary haemorrhage should be suspected and searched for, and the pathway should actively move patients forwards to the oper ating theatre or interventional radiology room to achieve this. The damage control approach is extended to the conduct of  surgery to prioritise rapid bleeding control. In damage con trol surgery , surgical intervention is limited to the minimum necessary to stop bleeding and contr ol sepsis, in order to avoid additional tissue damage, bleeding and physiological stress. More definitive repairs can be delayed until the patient is hae modynamically stable and physiologically capable of  sustain ing the procedure. Thus the operation is tailored to match the patient’s physiology , and is not focused on reconstructing anat omy . ‘Damage control’ is a term borrowed from the military: it ensures continued functioning of  a damaged ship above con ducting complete repairs, which would prevent rapid return to battle. Summary box 2.3 Damage control surgery /uni25CF /uni25CF /uni25CF /uni25CF Permissive hypotension Permissive hypotension allows the patient to set their own blood pressure while bleeding and avoids continued volume resuscitation in the vain attempt to normalise perfusion while bleeding. This reduces blood loss from bleeding sites and reduces dilutional coagulopathy and hypothermia induced by fluids. It is important to maintain baseline perfusion of the coronary arteries at minimum, and thus a palpable central pulse (mean arterial pressure above ~50 /uni00A0 mmHg) must be maintained by whatever means are available. Avoid dilutional coagulopathy Avoid dilutional coagulopathy by avoiding clear fluids (crystal loids or colloids) and by giving a transfusion that approximates red blood cells and plasma. - Treat existing coagulation deficits Treat existing coagulopathies either empirically or by regular coagulation testing and acting on the results. Tranexamic acid should be given as soon as possible in almost all bleeding patients to stop hyperfibrinolysis. Blood component concen - ting trates should be given to correct existing deficits, such as cryoprecipitate for low fibrinogen levels or platelet transfusions for platelet dysfunctions. - 

Arrest haemorrhage
Control sepsis
Protect from further injury
Nothing else

# Degree of haemorrhage and classification

Degree of haemorrhage and classification

The adult human has approximately 5 litres of  blood (70 /uni00A0 mL/kg for children and adults, 80 /uni00A0 mL/kg for neonates). Estimation of the amount of  blood that has been lost is di ffi cult, inaccurate and usually underestimates the actual value. External haemorrhage is obvious, but it may be di ffi cult to estimate the actual volume lost. In the operating theatre, blood collected in suction apparatus can be measur ed and swabs soaked in blood weighed. - The haemoglobin level is a poor indicator of  the degree of haemorrhage because it represents a concentration and not an absolute amount. In the early stages of rapid haemorrhage, the haemoglobin concentra tion is unchanged (as whole blood is lost). Later, as fluid shifts from the intracellular and interstitial - spaces into the vascular compartment, the haemoglobin and haematocrit levels will fall. 

Class
2
3
4
15–30%
30–40%
>40%

classes 1–4 based on the estimated blood loss required to pro duce certain physiological compensatory changes ( Table 2.3 Although conceptually useful, this classification system is never applied clinically , and indeed is di ffi cult if  not impossible to determine. There is variation in clinical response across ages (the young compensate well, the old very poorly), variation among individuals (e.g. athletes versus the obese) and variation owing to confounding factors (e.g. concomitant medications, pain). Degree of haemorrhage and classification

The adult human has approximately 5 litres of  blood (70 /uni00A0 mL/kg for children and adults, 80 /uni00A0 mL/kg for neonates). Estimation of the amount of  blood that has been lost is di ffi cult, inaccurate and usually underestimates the actual value. External haemorrhage is obvious, but it may be di ffi cult to estimate the actual volume lost. In the operating theatre, blood collected in suction apparatus can be measur ed and swabs soaked in blood weighed. - The haemoglobin level is a poor indicator of  the degree of haemorrhage because it represents a concentration and not an absolute amount. In the early stages of rapid haemorrhage, the haemoglobin concentra tion is unchanged (as whole blood is lost). Later, as fluid shifts from the intracellular and interstitial - spaces into the vascular compartment, the haemoglobin and haematocrit levels will fall. 

Class
2
3
4
15–30%
30–40%
>40%

classes 1–4 based on the estimated blood loss required to pro duce certain physiological compensatory changes ( Table 2.3 Although conceptually useful, this classification system is never applied clinically , and indeed is di ffi cult if  not impossible to determine. There is variation in clinical response across ages (the young compensate well, the old very poorly), variation among individuals (e.g. athletes versus the obese) and variation owing to confounding factors (e.g. concomitant medications, pain). Degree of haemorrhage and classification

The adult human has approximately 5 litres of  blood (70 /uni00A0 mL/kg for children and adults, 80 /uni00A0 mL/kg for neonates). Estimation of the amount of  blood that has been lost is di ffi cult, inaccurate and usually underestimates the actual value. External haemorrhage is obvious, but it may be di ffi cult to estimate the actual volume lost. In the operating theatre, blood collected in suction apparatus can be measur ed and swabs soaked in blood weighed. - The haemoglobin level is a poor indicator of  the degree of haemorrhage because it represents a concentration and not an absolute amount. In the early stages of rapid haemorrhage, the haemoglobin concentra tion is unchanged (as whole blood is lost). Later, as fluid shifts from the intracellular and interstitial - spaces into the vascular compartment, the haemoglobin and haematocrit levels will fall. 

Class
2
3
4
15–30%
30–40%
>40%

classes 1–4 based on the estimated blood loss required to pro duce certain physiological compensatory changes ( Table 2.3 Although conceptually useful, this classification system is never applied clinically , and indeed is di ffi cult if  not impossible to determine. There is variation in clinical response across ages (the young compensate well, the old very poorly), variation among individuals (e.g. athletes versus the obese) and variation owing to confounding factors (e.g. concomitant medications, pain).

# Definitions

Definitions

Revealed and concealed haemorrhage Haemorrhage may be revealed or concealed. Revealed haemorrhage is obvious external haemorrhage, such as exsanguination from an open arterial wound or from massive haematemesis from a duodenal ulcer. Concealed haemorrhage is contained within the body cav ity and must be suspected, actively investigated and controlled. In trauma, haemorrhage may be concealed within the chest, abdomen, pelvis, r etroperitoneum or in the limbs with con tained vascular injury or associated with long-bone fractures. Examples of  non-traumatic concealed haemorrhage include occult gastrointestinal bleeding or ruptured aortic aneurysm. Primary, reactionary and secondary haemorrhage Primary haemorrhage is haemorrhage occurring immediately as a result of  an injury (or surgery). Reactionary haemorrhage is delayed haemorrhage (within 24 hours) and is usually due to dislodgement of  a clot by resus citation, normalisation of  blood pressure and vasodilatation. Reactionary haemorrhage may also be due to technical failure, such as slippage of  a ligature. Secondary haemorrhage is due to sloughing of  the wall of a vessel. It usually occurs 7–14 days after injury and is precip itated by factors such as infection, pressure necrosis (such as from a drain) or malignancy . Surgical haemorrhage is due to a direct injury and is amenable to surgical control (e.g. suture ligation) or other techniques such as angioembolisation. Non-surgical haemorrhage is general bleeding from raw surfaces and mucous membranes due to coagulopathy and cannot be stopped by surgical means (except packing). Treat - ment requires correction of  the coagula tion abnormalities. Diagnosis of active bleeding: response to fluid therapy The mode of resuscitation is determined by whether patients are actively bleeding, which requires a dynamic assessment of the blood pressure response to volume infusion. Patients who are ‘non-responders’ or ‘transient responders’ are still bleeding and must have the site of  haemorrhage identified and controlled. Responder There is a good and sustained improvement in blood pressure in response to a bolus transfusion. Transient responder There is an improvement in the blood pressure but this is not sustained. The rate of  haemorrhage is less than the rate of volume administration. Non-responder There is no improvement in the blood pressure to a bolus transfusion. The rate of  haemorrhage is greater than the rate - of  volume administration. - 

TABLE 2.3
Traditional classi
/f_i
cation of haemorrhagic shock.
1
Blood volume lost as percentage of total <15%

Definitions

Revealed and concealed haemorrhage Haemorrhage may be revealed or concealed. Revealed haemorrhage is obvious external haemorrhage, such as exsanguination from an open arterial wound or from massive haematemesis from a duodenal ulcer. Concealed haemorrhage is contained within the body cav ity and must be suspected, actively investigated and controlled. In trauma, haemorrhage may be concealed within the chest, abdomen, pelvis, r etroperitoneum or in the limbs with con tained vascular injury or associated with long-bone fractures. Examples of  non-traumatic concealed haemorrhage include occult gastrointestinal bleeding or ruptured aortic aneurysm. Primary, reactionary and secondary haemorrhage Primary haemorrhage is haemorrhage occurring immediately as a result of  an injury (or surgery). Reactionary haemorrhage is delayed haemorrhage (within 24 hours) and is usually due to dislodgement of  a clot by resus citation, normalisation of  blood pressure and vasodilatation. Reactionary haemorrhage may also be due to technical failure, such as slippage of  a ligature. Secondary haemorrhage is due to sloughing of  the wall of a vessel. It usually occurs 7–14 days after injury and is precip itated by factors such as infection, pressure necrosis (such as from a drain) or malignancy . Surgical haemorrhage is due to a direct injury and is amenable to surgical control (e.g. suture ligation) or other techniques such as angioembolisation. Non-surgical haemorrhage is general bleeding from raw surfaces and mucous membranes due to coagulopathy and cannot be stopped by surgical means (except packing). Treat - ment requires correction of  the coagula tion abnormalities. Diagnosis of active bleeding: response to fluid therapy The mode of resuscitation is determined by whether patients are actively bleeding, which requires a dynamic assessment of the blood pressure response to volume infusion. Patients who are ‘non-responders’ or ‘transient responders’ are still bleeding and must have the site of  haemorrhage identified and controlled. Responder There is a good and sustained improvement in blood pressure in response to a bolus transfusion. Transient responder There is an improvement in the blood pressure but this is not sustained. The rate of  haemorrhage is less than the rate of volume administration. Non-responder There is no improvement in the blood pressure to a bolus transfusion. The rate of  haemorrhage is greater than the rate - of  volume administration. - 

TABLE 2.3
Traditional classi
/f_i
cation of haemorrhagic shock.
1
Blood volume lost as percentage of total <15%

Definitions

Revealed and concealed haemorrhage Haemorrhage may be revealed or concealed. Revealed haemorrhage is obvious external haemorrhage, such as exsanguination from an open arterial wound or from massive haematemesis from a duodenal ulcer. Concealed haemorrhage is contained within the body cav ity and must be suspected, actively investigated and controlled. In trauma, haemorrhage may be concealed within the chest, abdomen, pelvis, r etroperitoneum or in the limbs with con tained vascular injury or associated with long-bone fractures. Examples of  non-traumatic concealed haemorrhage include occult gastrointestinal bleeding or ruptured aortic aneurysm. Primary, reactionary and secondary haemorrhage Primary haemorrhage is haemorrhage occurring immediately as a result of  an injury (or surgery). Reactionary haemorrhage is delayed haemorrhage (within 24 hours) and is usually due to dislodgement of  a clot by resus citation, normalisation of  blood pressure and vasodilatation. Reactionary haemorrhage may also be due to technical failure, such as slippage of  a ligature. Secondary haemorrhage is due to sloughing of  the wall of a vessel. It usually occurs 7–14 days after injury and is precip itated by factors such as infection, pressure necrosis (such as from a drain) or malignancy . Surgical haemorrhage is due to a direct injury and is amenable to surgical control (e.g. suture ligation) or other techniques such as angioembolisation. Non-surgical haemorrhage is general bleeding from raw surfaces and mucous membranes due to coagulopathy and cannot be stopped by surgical means (except packing). Treat - ment requires correction of  the coagula tion abnormalities. Diagnosis of active bleeding: response to fluid therapy The mode of resuscitation is determined by whether patients are actively bleeding, which requires a dynamic assessment of the blood pressure response to volume infusion. Patients who are ‘non-responders’ or ‘transient responders’ are still bleeding and must have the site of  haemorrhage identified and controlled. Responder There is a good and sustained improvement in blood pressure in response to a bolus transfusion. Transient responder There is an improvement in the blood pressure but this is not sustained. The rate of  haemorrhage is less than the rate of volume administration. Non-responder There is no improvement in the blood pressure to a bolus transfusion. The rate of  haemorrhage is greater than the rate - of  volume administration. - 

TABLE 2.3
Traditional classi
/f_i
cation of haemorrhagic shock.
1
Blood volume lost as percentage of total <15%

# End points of resuscitation

End points of resuscitation

It is much easier to know when to start resuscitation than when to stop. Traditionally , patients have been resuscitated until they have a normal pulse, blood pressure and urine output. However, these parameters are monitoring organ systems whose blood flow is preserved until the late stages of  shock. A patient therefore may be resuscitated to restore central perfusion to the brain, lungs and kidneys and yet continue to underperfuse the gut and muscle beds. Thus, activation of inflammation and coagulation may be ongoing and lead to reperfusion injury when these organs are finally perfused, and ultimately multiple organ failure. This state of  normal vital signs and continued underperfu sion is termed ‘occult hypoperfusion’. With current monitoring techniques, it is manifested only by a persistent lactic acidosis and low mixed venous oxygen saturation. T he time spent by patients in this hypoperfused state has a dramatic e ff ect on outcome. Patients with occult hypoperfusion for more than 12 /uni00A0 hours have two to three times the mortality of  patients with a limited duration of  shock. Resuscitation algorithms directed at correcting global perfusion end points (base deficit, lactate, mixed venous oxygen saturation) rather than traditional end points have been shown to improve mortality and morbidity in high-risk surgical patients. However, it is also clear that aggressive crystalloid resus citation regimens can lead to tissue oedema and organ fail ure, especially acute respira tory distress syndrome, abdominal compartment syndrome and cerebral oedema. Some patients cannot be resuscitated to normal parameters within 12 hours Karl Landsteiner , 1868–1943, Professor of  Pathological Anatomy , University of  Vienna, Austria. In 1909 he classified the human blood groups into A, B, AB and O. For this he was awarded the Nobel Prize in Physiology or Medicine in 1930. Hans Gerhard Creutzfeldt , 1885–1946, neurologist, Kiel, Germany . Alfons Maria Jakob , 1884–1931, neurologist, Hamburg, Germany . patients to be judicious in the approach to all therapies as end points are approached. End points of resuscitation

It is much easier to know when to start resuscitation than when to stop. Traditionally , patients have been resuscitated until they have a normal pulse, blood pressure and urine output. However, these parameters are monitoring organ systems whose blood flow is preserved until the late stages of  shock. A patient therefore may be resuscitated to restore central perfusion to the brain, lungs and kidneys and yet continue to underperfuse the gut and muscle beds. Thus, activation of inflammation and coagulation may be ongoing and lead to reperfusion injury when these organs are finally perfused, and ultimately multiple organ failure. This state of  normal vital signs and continued underperfu sion is termed ‘occult hypoperfusion’. With current monitoring techniques, it is manifested only by a persistent lactic acidosis and low mixed venous oxygen saturation. T he time spent by patients in this hypoperfused state has a dramatic e ff ect on outcome. Patients with occult hypoperfusion for more than 12 /uni00A0 hours have two to three times the mortality of  patients with a limited duration of  shock. Resuscitation algorithms directed at correcting global perfusion end points (base deficit, lactate, mixed venous oxygen saturation) rather than traditional end points have been shown to improve mortality and morbidity in high-risk surgical patients. However, it is also clear that aggressive crystalloid resus citation regimens can lead to tissue oedema and organ fail ure, especially acute respira tory distress syndrome, abdominal compartment syndrome and cerebral oedema. Some patients cannot be resuscitated to normal parameters within 12 hours Karl Landsteiner , 1868–1943, Professor of  Pathological Anatomy , University of  Vienna, Austria. In 1909 he classified the human blood groups into A, B, AB and O. For this he was awarded the Nobel Prize in Physiology or Medicine in 1930. Hans Gerhard Creutzfeldt , 1885–1946, neurologist, Kiel, Germany . Alfons Maria Jakob , 1884–1931, neurologist, Hamburg, Germany . patients to be judicious in the approach to all therapies as end points are approached. End points of resuscitation

It is much easier to know when to start resuscitation than when to stop. Traditionally , patients have been resuscitated until they have a normal pulse, blood pressure and urine output. However, these parameters are monitoring organ systems whose blood flow is preserved until the late stages of  shock. A patient therefore may be resuscitated to restore central perfusion to the brain, lungs and kidneys and yet continue to underperfuse the gut and muscle beds. Thus, activation of inflammation and coagulation may be ongoing and lead to reperfusion injury when these organs are finally perfused, and ultimately multiple organ failure. This state of  normal vital signs and continued underperfu sion is termed ‘occult hypoperfusion’. With current monitoring techniques, it is manifested only by a persistent lactic acidosis and low mixed venous oxygen saturation. T he time spent by patients in this hypoperfused state has a dramatic e ff ect on outcome. Patients with occult hypoperfusion for more than 12 /uni00A0 hours have two to three times the mortality of  patients with a limited duration of  shock. Resuscitation algorithms directed at correcting global perfusion end points (base deficit, lactate, mixed venous oxygen saturation) rather than traditional end points have been shown to improve mortality and morbidity in high-risk surgical patients. However, it is also clear that aggressive crystalloid resus citation regimens can lead to tissue oedema and organ fail ure, especially acute respira tory distress syndrome, abdominal compartment syndrome and cerebral oedema. Some patients cannot be resuscitated to normal parameters within 12 hours Karl Landsteiner , 1868–1943, Professor of  Pathological Anatomy , University of  Vienna, Austria. In 1909 he classified the human blood groups into A, B, AB and O. For this he was awarded the Nobel Prize in Physiology or Medicine in 1930. Hans Gerhard Creutzfeldt , 1885–1946, neurologist, Kiel, Germany . Alfons Maria Jakob , 1884–1931, neurologist, Hamburg, Germany . patients to be judicious in the approach to all therapies as end points are approached.

# FURTHER READING

FURTHER READING

- Cole E, Weaver A, Gall L et al . A decade of  damage control resusci - tation: new transfusion practice, new survivors, new directions. Ann Surg 2019; 273 (6): 1215–20. Duchesne JC, McSwain NE Jr, Cotton BA et al. Damage control resuscitation: the new face of  damage control. J Trauma 2010; 69 : 976–90. - Glen J, Constanti M, Brohi K; Guideline Development Group. Assessment and initial management of  major trauma: summary of NICE guidance. BMJ 2016; 353 : i3051. Harris T , Thomas GO, Brohi K. Early fluid resuscitation in severe trauma. BMJ 2012; 345 : e5752. Nguyen HB, Jaehne AK, Jayaprakash N et al . Early goal-directed therapy in severe sepsis and septic shock: insights and comparisons to ProCESS, ProMISe, and ARISE. Crit Care 2016; 20 (1): 160. Pearse RM, Ackland GL. Perioperative fluid therapy . BMJ 2012; 344 : e2865. Semler MW , Rice TW . Sepsis resuscitation: fluid choice and dose. Clin Chest Med 2016; 37 : 241–50. - Sihler KC, Nathans AB. Management of  severe sepsis in the surgical patient. Surg Clin N Am 2006; 86 : 1457–81. Spahn DR, Bouillon B, Cerny V et al . The European guideline on management of  major bleeding and coagulopathy following trauma: fifth edition. Crit Care 2019; 23 : 98. FURTHER READING

- Cole E, Weaver A, Gall L et al . A decade of  damage control resusci - tation: new transfusion practice, new survivors, new directions. Ann Surg 2019; 273 (6): 1215–20. Duchesne JC, McSwain NE Jr, Cotton BA et al. Damage control resuscitation: the new face of  damage control. J Trauma 2010; 69 : 976–90. - Glen J, Constanti M, Brohi K; Guideline Development Group. Assessment and initial management of  major trauma: summary of NICE guidance. BMJ 2016; 353 : i3051. Harris T , Thomas GO, Brohi K. Early fluid resuscitation in severe trauma. BMJ 2012; 345 : e5752. Nguyen HB, Jaehne AK, Jayaprakash N et al . Early goal-directed therapy in severe sepsis and septic shock: insights and comparisons to ProCESS, ProMISe, and ARISE. Crit Care 2016; 20 (1): 160. Pearse RM, Ackland GL. Perioperative fluid therapy . BMJ 2012; 344 : e2865. Semler MW , Rice TW . Sepsis resuscitation: fluid choice and dose. Clin Chest Med 2016; 37 : 241–50. - Sihler KC, Nathans AB. Management of  severe sepsis in the surgical patient. Surg Clin N Am 2006; 86 : 1457–81. Spahn DR, Bouillon B, Cerny V et al . The European guideline on management of  major bleeding and coagulopathy following trauma: fifth edition. Crit Care 2019; 23 : 98. FURTHER READING

- Cole E, Weaver A, Gall L et al . A decade of  damage control resusci - tation: new transfusion practice, new survivors, new directions. Ann Surg 2019; 273 (6): 1215–20. Duchesne JC, McSwain NE Jr, Cotton BA et al. Damage control resuscitation: the new face of  damage control. J Trauma 2010; 69 : 976–90. - Glen J, Constanti M, Brohi K; Guideline Development Group. Assessment and initial management of  major trauma: summary of NICE guidance. BMJ 2016; 353 : i3051. Harris T , Thomas GO, Brohi K. Early fluid resuscitation in severe trauma. BMJ 2012; 345 : e5752. Nguyen HB, Jaehne AK, Jayaprakash N et al . Early goal-directed therapy in severe sepsis and septic shock: insights and comparisons to ProCESS, ProMISe, and ARISE. Crit Care 2016; 20 (1): 160. Pearse RM, Ackland GL. Perioperative fluid therapy . BMJ 2012; 344 : e2865. Semler MW , Rice TW . Sepsis resuscitation: fluid choice and dose. Clin Chest Med 2016; 37 : 241–50. - Sihler KC, Nathans AB. Management of  severe sepsis in the surgical patient. Surg Clin N Am 2006; 86 : 1457–81. Spahn DR, Bouillon B, Cerny V et al . The European guideline on management of  major bleeding and coagulopathy following trauma: fifth edition. Crit Care 2019; 23 : 98.

# HAEMORRHAGE RESUSCITATION

HAEMORRHAGE RESUSCITATION

The conduct and goals of  resuscitation change depending on whether the patient is actively bleeding. In this case, the resusci tation focuses on achieving rapid haemostasis and maintaining the ability of  the blood to clot. This paradigm is called damage control resuscitation (see Damage control resuscitation If  the patient is not actively bleeding, has stopped bleeding or the cause of  shock is not haemorrhage, then resuscitation is directed at correcting the shock state and restoring perfusion to end organs. HAEMORRHAGE RESUSCITATION

The conduct and goals of  resuscitation change depending on whether the patient is actively bleeding. In this case, the resusci tation focuses on achieving rapid haemostasis and maintaining the ability of  the blood to clot. This paradigm is called damage control resuscitation (see Damage control resuscitation If  the patient is not actively bleeding, has stopped bleeding or the cause of  shock is not haemorrhage, then resuscitation is directed at correcting the shock state and restoring perfusion to end organs. HAEMORRHAGE RESUSCITATION

The conduct and goals of  resuscitation change depending on whether the patient is actively bleeding. In this case, the resusci tation focuses on achieving rapid haemostasis and maintaining the ability of  the blood to clot. This paradigm is called damage control resuscitation (see Damage control resuscitation If  the patient is not actively bleeding, has stopped bleeding or the cause of  shock is not haemorrhage, then resuscitation is directed at correcting the shock state and restoring perfusion to end organs.

# HAEMORRHAGE

HAEMORRHAGE

Uncontrolled bleeding will lead to a hypovolaemic shock - state, or haemorrhagic shock. While haemorrhage and shock often coexist, they are not the same. Patients who are actively bleeding may not yet be in shock. Conversely , patients may be in shock as a consequence of  haemorrhage, but they may no longer be actively bleeding. ) are Resuscitation is very di ff erent if  patients are actively bleed - - ing or if they are not bleeding. In patients who are bleeding, the priority is to stop bleeding. In patients who are not bleeding, the priority shifts to normalising end-organ perfusion (correct - ing the shock state). Thus it is vital to recognise patients who are actively bleeding, and this is di ff erent from recognising that a patient is in shock. Haemorrhage must be recognised and managed rapidly and decisively to reduce the severity and duration of  shock. Haemorrhage is treated by arresting the bleeding /uni00A0 – /uni00A0 not by fluid resuscita tion or blood transfusion. Although necessary as supportive measures to maintain organ (especially cardiac) perfusion, repeated volume resuscitation of  patients who have ongoing haemorrhage will lead to physiological exhaustion (profound coagulopathy , acidosis and hypothermia) and sub - sequently death. HAEMORRHAGE

Uncontrolled bleeding will lead to a hypovolaemic shock - state, or haemorrhagic shock. While haemorrhage and shock often coexist, they are not the same. Patients who are actively bleeding may not yet be in shock. Conversely , patients may be in shock as a consequence of  haemorrhage, but they may no longer be actively bleeding. ) are Resuscitation is very di ff erent if  patients are actively bleed - - ing or if they are not bleeding. In patients who are bleeding, the priority is to stop bleeding. In patients who are not bleeding, the priority shifts to normalising end-organ perfusion (correct - ing the shock state). Thus it is vital to recognise patients who are actively bleeding, and this is di ff erent from recognising that a patient is in shock. Haemorrhage must be recognised and managed rapidly and decisively to reduce the severity and duration of  shock. Haemorrhage is treated by arresting the bleeding /uni00A0 – /uni00A0 not by fluid resuscita tion or blood transfusion. Although necessary as supportive measures to maintain organ (especially cardiac) perfusion, repeated volume resuscitation of  patients who have ongoing haemorrhage will lead to physiological exhaustion (profound coagulopathy , acidosis and hypothermia) and sub - sequently death. HAEMORRHAGE

Uncontrolled bleeding will lead to a hypovolaemic shock - state, or haemorrhagic shock. While haemorrhage and shock often coexist, they are not the same. Patients who are actively bleeding may not yet be in shock. Conversely , patients may be in shock as a consequence of  haemorrhage, but they may no longer be actively bleeding. ) are Resuscitation is very di ff erent if  patients are actively bleed - - ing or if they are not bleeding. In patients who are bleeding, the priority is to stop bleeding. In patients who are not bleeding, the priority shifts to normalising end-organ perfusion (correct - ing the shock state). Thus it is vital to recognise patients who are actively bleeding, and this is di ff erent from recognising that a patient is in shock. Haemorrhage must be recognised and managed rapidly and decisively to reduce the severity and duration of  shock. Haemorrhage is treated by arresting the bleeding /uni00A0 – /uni00A0 not by fluid resuscita tion or blood transfusion. Although necessary as supportive measures to maintain organ (especially cardiac) perfusion, repeated volume resuscitation of  patients who have ongoing haemorrhage will lead to physiological exhaustion (profound coagulopathy , acidosis and hypothermia) and sub - sequently death.

# Identify haemorrhage

Identify haemorrhage

External haemorrhage may be obvious, but the diagnosis of concealed haemorrhage may be more di ffi cult. Any shock should be assumed to be hypovolaemic until proven otherwise and, similarly , hypovolaemia should be assumed to be due to haemorrhage until this has been excluded. Once haemorrhage has been identified, the institution’s major haemorrhage protocol should be activated, which will Figure 2.2 - ate resuscitative measures include the assessment of airway and ). breathing and control of  life-threatening issues as necessary . Large-bore intra venous access should be instituted and blood drawn for cross-matching (see Cross-matching ). Transfusion should start with emergency (type O) blood (see Transfusion ). Once haemorrhage has been considered, the site of  hae - morrhage must be rapidly identified. Note that this is not to identify the exact location definitively , but rather to define the next step in haemorrhage control (operation, angioembolisa - tion, endoscopic control). Clues may be in the histor y (previous episodes, known aneurysm, non-steroidal therapy for gastro - intestinal bleeding) or examination (nature of  blood /uni00A0 – /uni00A0 fresh, melaena; abdominal tenderness, etc.). For shocked trauma - patients, the external signs of  injury may suggest internal hae - morrhage, but haemorrhage into a body cavity (thorax, abdo - men) must be excluded with rapid investigations (chest and ). pelvis radiographs, abdominal ultrasound). Investigations for blood loss must be appropriate to the patient’s physiological condition. Rapid bedside tests such as ultrasound are more appropriate for profound shock and exsanguinating haemorrhage than investiga tions such as com - puted tomography . Patients who are not actively bleeding can have a more methodical, definitive work-up. 

Bleeding
Prioritise coagulation
Recognise active bleeding
Hypotension. Transient/Non-responder
Damage control resuscitation
Goal: Coagulation function. Coronary perfusion
Damage control surgery
Permissive hypotension
Balanced transfusion (1:1 RBC and FFP)
Treat coagulopathy (tranexamic acid, platelets,
/f_i
brinogen)
Monitor
:
Cardiovascular: BP , HR
2+
+
Electrolytes: Ca
, K
Coagulation: PT,
/f_i
brinogen, ROTEM/TEG
Perfusion: pH, base excess, lactate, temperature
Haemorrhage resuscitation. BP , blood pressure; CO, cardiac output; FFP , fresh-frozen plasma; F
GCS, Glasgow Coma Scale score; HR, heart rate; IAP , intra-abdominal pressure; PaO
blood cells; ROTEM, rotational thromboelastometry; SVR, systemic vascular resistance; S
elastography; UO, urine output.

Identify haemorrhage

External haemorrhage may be obvious, but the diagnosis of concealed haemorrhage may be more di ffi cult. Any shock should be assumed to be hypovolaemic until proven otherwise and, similarly , hypovolaemia should be assumed to be due to haemorrhage until this has been excluded. Once haemorrhage has been identified, the institution’s major haemorrhage protocol should be activated, which will Figure 2.2 - ate resuscitative measures include the assessment of airway and ). breathing and control of  life-threatening issues as necessary . Large-bore intra venous access should be instituted and blood drawn for cross-matching (see Cross-matching ). Transfusion should start with emergency (type O) blood (see Transfusion ). Once haemorrhage has been considered, the site of  hae - morrhage must be rapidly identified. Note that this is not to identify the exact location definitively , but rather to define the next step in haemorrhage control (operation, angioembolisa - tion, endoscopic control). Clues may be in the histor y (previous episodes, known aneurysm, non-steroidal therapy for gastro - intestinal bleeding) or examination (nature of  blood /uni00A0 – /uni00A0 fresh, melaena; abdominal tenderness, etc.). For shocked trauma - patients, the external signs of  injury may suggest internal hae - morrhage, but haemorrhage into a body cavity (thorax, abdo - men) must be excluded with rapid investigations (chest and ). pelvis radiographs, abdominal ultrasound). Investigations for blood loss must be appropriate to the patient’s physiological condition. Rapid bedside tests such as ultrasound are more appropriate for profound shock and exsanguinating haemorrhage than investiga tions such as com - puted tomography . Patients who are not actively bleeding can have a more methodical, definitive work-up. 

Bleeding
Prioritise coagulation
Recognise active bleeding
Hypotension. Transient/Non-responder
Damage control resuscitation
Goal: Coagulation function. Coronary perfusion
Damage control surgery
Permissive hypotension
Balanced transfusion (1:1 RBC and FFP)
Treat coagulopathy (tranexamic acid, platelets,
/f_i
brinogen)
Monitor
:
Cardiovascular: BP , HR
2+
+
Electrolytes: Ca
, K
Coagulation: PT,
/f_i
brinogen, ROTEM/TEG
Perfusion: pH, base excess, lactate, temperature
Haemorrhage resuscitation. BP , blood pressure; CO, cardiac output; FFP , fresh-frozen plasma; F
GCS, Glasgow Coma Scale score; HR, heart rate; IAP , intra-abdominal pressure; PaO
blood cells; ROTEM, rotational thromboelastometry; SVR, systemic vascular resistance; S
elastography; UO, urine output.

Identify haemorrhage

External haemorrhage may be obvious, but the diagnosis of concealed haemorrhage may be more di ffi cult. Any shock should be assumed to be hypovolaemic until proven otherwise and, similarly , hypovolaemia should be assumed to be due to haemorrhage until this has been excluded. Once haemorrhage has been identified, the institution’s major haemorrhage protocol should be activated, which will Figure 2.2 - ate resuscitative measures include the assessment of airway and ). breathing and control of  life-threatening issues as necessary . Large-bore intra venous access should be instituted and blood drawn for cross-matching (see Cross-matching ). Transfusion should start with emergency (type O) blood (see Transfusion ). Once haemorrhage has been considered, the site of  hae - morrhage must be rapidly identified. Note that this is not to identify the exact location definitively , but rather to define the next step in haemorrhage control (operation, angioembolisa - tion, endoscopic control). Clues may be in the histor y (previous episodes, known aneurysm, non-steroidal therapy for gastro - intestinal bleeding) or examination (nature of  blood /uni00A0 – /uni00A0 fresh, melaena; abdominal tenderness, etc.). For shocked trauma - patients, the external signs of  injury may suggest internal hae - morrhage, but haemorrhage into a body cavity (thorax, abdo - men) must be excluded with rapid investigations (chest and ). pelvis radiographs, abdominal ultrasound). Investigations for blood loss must be appropriate to the patient’s physiological condition. Rapid bedside tests such as ultrasound are more appropriate for profound shock and exsanguinating haemorrhage than investiga tions such as com - puted tomography . Patients who are not actively bleeding can have a more methodical, definitive work-up. 

Bleeding
Prioritise coagulation
Recognise active bleeding
Hypotension. Transient/Non-responder
Damage control resuscitation
Goal: Coagulation function. Coronary perfusion
Damage control surgery
Permissive hypotension
Balanced transfusion (1:1 RBC and FFP)
Treat coagulopathy (tranexamic acid, platelets,
/f_i
brinogen)
Monitor
:
Cardiovascular: BP , HR
2+
+
Electrolytes: Ca
, K
Coagulation: PT,
/f_i
brinogen, ROTEM/TEG
Perfusion: pH, base excess, lactate, temperature
Haemorrhage resuscitation. BP , blood pressure; CO, cardiac output; FFP , fresh-frozen plasma; F
GCS, Glasgow Coma Scale score; HR, heart rate; IAP , intra-abdominal pressure; PaO
blood cells; ROTEM, rotational thromboelastometry; SVR, systemic vascular resistance; S
elastography; UO, urine output.

# Indications for blood transfusion

Indications for blood transfusion

Blood transfusions should be avoided if  possible, and many previous uses of blood and blood products are now no longer considered appropriate. The indications for blood transfusion are as follows: /uni25CF Acute blood loss, to replace circulating volume and main - tain oxygen delivery; /uni25CF Perioperative anaemia, to ensure adequate oxygen delivery during the perioperative phase; /uni25CF Symptomatic chronic anaemia, without haemorrhage or impending surgery . Transfusion trigger Historically , patients were transfused to achieve a haemoglobin >10 /uni00A0 g/dL. This has now been shown not only to be unneces - sary but also to be associated with an increased morbidity and - mortality compared with lower target values. A haemoglobin level of  6 /uni00A0 g/dL is acceptable in patients who are not actively bleeding, those who are not about to undergo major surgery and those who are not symptomatic. There is some controversy as to the optimal haemoglobin level in some patient groups, such as those with cardiovascular disease, sepsis and traumatic brain injury . Although, conceptually , a higher haemoglobin level improves oxygen delivery , there is little clinical evidence at this stage to support higher levels in these groups ( Table 2.6 ). - - 

TABLE 2.6
Perioperative red blood cell transfusion
criteria.
Haemoglobin level (g/dL)
Indications
<6
Probably will bene
/f_i
t from transfusion
6–8
Transfusion unlikely to be of bene
/f_i
t in
the absence of bleeding or impending
surgery
>8
No indication for transfusion in the
absence of other risk factors

Indications for blood transfusion

Blood transfusions should be avoided if  possible, and many previous uses of blood and blood products are now no longer considered appropriate. The indications for blood transfusion are as follows: /uni25CF Acute blood loss, to replace circulating volume and main - tain oxygen delivery; /uni25CF Perioperative anaemia, to ensure adequate oxygen delivery during the perioperative phase; /uni25CF Symptomatic chronic anaemia, without haemorrhage or impending surgery . Transfusion trigger Historically , patients were transfused to achieve a haemoglobin >10 /uni00A0 g/dL. This has now been shown not only to be unneces - sary but also to be associated with an increased morbidity and - mortality compared with lower target values. A haemoglobin level of  6 /uni00A0 g/dL is acceptable in patients who are not actively bleeding, those who are not about to undergo major surgery and those who are not symptomatic. There is some controversy as to the optimal haemoglobin level in some patient groups, such as those with cardiovascular disease, sepsis and traumatic brain injury . Although, conceptually , a higher haemoglobin level improves oxygen delivery , there is little clinical evidence at this stage to support higher levels in these groups ( Table 2.6 ). - - 

TABLE 2.6
Perioperative red blood cell transfusion
criteria.
Haemoglobin level (g/dL)
Indications
<6
Probably will bene
/f_i
t from transfusion
6–8
Transfusion unlikely to be of bene
/f_i
t in
the absence of bleeding or impending
surgery
>8
No indication for transfusion in the
absence of other risk factors

Indications for blood transfusion

Blood transfusions should be avoided if  possible, and many previous uses of blood and blood products are now no longer considered appropriate. The indications for blood transfusion are as follows: /uni25CF Acute blood loss, to replace circulating volume and main - tain oxygen delivery; /uni25CF Perioperative anaemia, to ensure adequate oxygen delivery during the perioperative phase; /uni25CF Symptomatic chronic anaemia, without haemorrhage or impending surgery . Transfusion trigger Historically , patients were transfused to achieve a haemoglobin >10 /uni00A0 g/dL. This has now been shown not only to be unneces - sary but also to be associated with an increased morbidity and - mortality compared with lower target values. A haemoglobin level of  6 /uni00A0 g/dL is acceptable in patients who are not actively bleeding, those who are not about to undergo major surgery and those who are not symptomatic. There is some controversy as to the optimal haemoglobin level in some patient groups, such as those with cardiovascular disease, sepsis and traumatic brain injury . Although, conceptually , a higher haemoglobin level improves oxygen delivery , there is little clinical evidence at this stage to support higher levels in these groups ( Table 2.6 ). - - 

TABLE 2.6
Perioperative red blood cell transfusion
criteria.
Haemoglobin level (g/dL)
Indications
<6
Probably will bene
/f_i
t from transfusion
6–8
Transfusion unlikely to be of bene
/f_i
t in
the absence of bleeding or impending
surgery
>8
No indication for transfusion in the
absence of other risk factors

# Introduction

INTRODUCTION

Shock is the most common cause of  death of  surgical patients. Death may occur rapidly because of  a profound state of  shock or may occur later because of  the consequences of  organ ischaemia and reperfusion injury . It is important therefore that every surgeon understands the pathophysiology , diagnosis and priorities in management of  shock and haemorrhage.

# Learning objectives

Learning objectives

To understand: The pathophysiology of shock • The different patterns of shock and the principles and • priorities of resuscitation Appropriate monitoring and end points of resuscitation • Learning objectives

To understand: The pathophysiology of shock • The different patterns of shock and the principles and • priorities of resuscitation Appropriate monitoring and end points of resuscitation • Learning objectives

To understand: The pathophysiology of shock • The different patterns of shock and the principles and • priorities of resuscitation Appropriate monitoring and end points of resuscitation •

# Monitoring

Monitoring

The minimum standard for monitoring of  the patient in shock is continuous heart rate and oxygen saturation moni - toring, frequent non-invasive blood pressure monitoring and hourly urine output measurements. Most patients will need more aggressive invasive monitoring, including central venous pressure (CVP) and invasive blood pressure monitoring. Summary box 2.4 Monitoring for patients in shock /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF - Cardiovascular - Cardiovascular monitoring at minimum should include continuous heart rate (electrocardiogram, oxygen saturation and pulse waveform and non-invasive blood pressure). Patients whose state of  shock is not rapidly corrected with a small amount of  fluid should have CVP monitoring and continuous blood pressure monitoring through an arterial line. - Central venous pressure There is no ‘normal’ CVP for a shocked patient, and reliance cannot be placed on an individual pressure measurement to assess volume status. Some patients may require a CVP of 5 /uni00A0 cmH O, whereas some may require a CVP of  15 /uni00A0 cmH O 2 2 or higher. Further, ventricular compliance can change from minute to minute in the shocked state, and CVP is a poor reflection of  end-diastolic volume (preload). CVP measurements should be assessed dynamically as the - response to a fluid challenge. A fluid bolus (250–500 /uni00A0 mL) is infused rapidly over 5–10 minutes. - The normal CVP response is a rise of  2–5 /uni00A0 cmH O, which 2 gradually drifts back to the original level over 10–20 minutes. tion Patients with no change in their CVP are empty and require further fluid resuscitation. Patients with a large, sustained rise - in CVP have high preload and an element of  cardiac insu ffi - - ciency or volume overload. 

Minimum
Additional modalities
ECG
Central venous pressure
Pulse oximetry
Invasive blood pressure
Blood pressure
Cardiac output
Urine output
Base de
/f_i
cit and serum
lactate

Cardiac output monitoring allows assessment of  not only the cardiac output but also the systemic vascular resistance and, depending on the technique used, end-diastolic volume (preload) and blood volume. Use of  invasive cardiac monitor ing with pulmonary artery catheters is becoming less frequent as new non-invasive monitoring techniques, such as Doppler ultrasound, pulse waveform analysis and indicator dilution methods, provide similar information without many of  the drawbacks of  more invasive techniques. Measurement of cardiac output, systemic vascular resis tance and preload can help distinguish the types of  shock present (hypovolaemia, distributive, cardiogenic), especially when they coexist. The information pr ovided guides fluid and vasopressor therapy by providing real-time monitoring of  the cardiovascular response. Measurement of  cardiac output is desirable in patients who do not respond as expected to first-line therapy or who have evidence of  cardiogenic shock or myocardial dysfunction. Early consideration should be giv en to instituting cardiac out put monitoring for patients who require vasopressor or inotro pic support. Systemic and organ perfusion Ultimately , the goal of  treatment is to restore cellular and organ perfusion. Ideally , therefore, monitoring of  organ perfusion should guide the management of shock. The best measure of  organ perfusion and the best monitor of  the adequacy of shock therapy remains the urine output. However, this is an hourly measure and does not give a minute-to-minute view of the shocked state. The level of  consciousness is an important marker of  cerebral perfusion, but brain perfusion is maintained until the very late stages of  shock and hence is a poor marker of  adequacy of  resuscitation ( Table 2.4 ). Currently , the only clinical indicators of  perfusion of the gastrointestinal tract and muscular beds are the global Christian Johann Doppler , 1803–1853, Professor of  Experimental Physics, Vienna, Austria, en mixed venous oxygen saturation. Base deficit and lactate Lactic acid is generated by cells undergoing anaerobic respi - - ration. The degree of  lactic acidosis, as measured by serum lactate level and/or the base deficit, is sensitive for both diagnosis of  shock and monitoring the response to therapy . Patients with a base deficit of  more than 6 /uni00A0 mmol/L have a much higher morbidity and mortality than those with no metabolic acidosis. Furthermore, the length of  time in shock - with an increased base deficit is important, even if  all other vital signs have returned to normal (see occult hypoperfusion below under End points of resuscitation ). These parameters are measured from arterial blood gas analyses, and therefore the frequency of  measurements is limited and they do not pr ovide minute-to-minute data on systemic perfusion or the response to therapy . Nevertheless, the base deficit and/or lactate should be measured routinely in these patients until they have returned to normal levels. - - Mixed venous oxygen saturation The percentage saturation of  oxygen returning to the heart from the body is a measure of  the oxygen delivery and extraction by the tissues. Accurate measurement is via analysis of  blood drawn from a long central line placed in the right atrium. Estimations can be made from blood drawn from lines in the superior vena cava, but these values will be slightly higher than those of  a mixed venous sample (as there is rela - tively more oxygen extraction from the lower half  of  the body). Normal mixed venous oxygen saturation levels are 50–70%. Levels below 50% indicate inadequate oxygen delivery and increased oxygen extraction by the cells. This is consistent with hypovolaemic or cardiogenic shock. High mixed venous saturations (>70%) are seen in sepsis and some other forms of  distributive shock. In sepsis, there is disordered utilisation of  oxygen at the cellular level and unciated the Doppler principle in 1842. 

TABLE 2.4
Monitors for organ/systemic perfusion.
Clinical
Systemic perfusion
Organ perfusion
Muscle
–
Gut
–
Kidney
Urine output
Brain
Conscious level
Investigational
Base de
/f_i
cit
Lactate
Mixed venous oxygen saturation
Near-infrared spectroscopy
Tissue oxygen electrode
Sublingual capnometry
Gut mucosal pH
Laser Doppler
/f_l
owmetry
–
Tissue oxygen electrode
Near-infrared spectroscopy

Therefore, less oxygen is presented to the cells, and those cells cannot utilise what little oxygen is presented. Thus, venous blood has a higher oxygen concentration than normal. Patients who are septic should therefore have mixed venous oxygen saturations above 70%; below this level, they are not only in septic shock but also in hypovolaemic or cardiogenic shock. Although the S O level is in the ‘normal’ range, it is low v 2 for the septic state, and inadequate oxygen is being supplied to cells that cannot utilise oxygen appropriately . This must be cor rected rapidly . Hypovolaemia should be corrected with fluid therapy , and low cardiac output due to myocardial depression or failure should be treated with inotropes (dobutamine) to achieve a mixed venous saturation greater than 70% (normal for the septic state). New methods for monitoring regional tissue perfusion and oxygenation are becoming available, the most promising of whic h are muscle tissue oxygen probes, near-infrared spectros copy and sublingual capnometry . While these techniques pro vide information regarding perfusion of  specific tissue beds, it is as yet unclear whether there are significant advantages over existing measurements of  global hypoperfusion (base deficit, lactate). Monitoring

The minimum standard for monitoring of  the patient in shock is continuous heart rate and oxygen saturation moni - toring, frequent non-invasive blood pressure monitoring and hourly urine output measurements. Most patients will need more aggressive invasive monitoring, including central venous pressure (CVP) and invasive blood pressure monitoring. Summary box 2.4 Monitoring for patients in shock /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF - Cardiovascular - Cardiovascular monitoring at minimum should include continuous heart rate (electrocardiogram, oxygen saturation and pulse waveform and non-invasive blood pressure). Patients whose state of  shock is not rapidly corrected with a small amount of  fluid should have CVP monitoring and continuous blood pressure monitoring through an arterial line. - Central venous pressure There is no ‘normal’ CVP for a shocked patient, and reliance cannot be placed on an individual pressure measurement to assess volume status. Some patients may require a CVP of 5 /uni00A0 cmH O, whereas some may require a CVP of  15 /uni00A0 cmH O 2 2 or higher. Further, ventricular compliance can change from minute to minute in the shocked state, and CVP is a poor reflection of  end-diastolic volume (preload). CVP measurements should be assessed dynamically as the - response to a fluid challenge. A fluid bolus (250–500 /uni00A0 mL) is infused rapidly over 5–10 minutes. - The normal CVP response is a rise of  2–5 /uni00A0 cmH O, which 2 gradually drifts back to the original level over 10–20 minutes. tion Patients with no change in their CVP are empty and require further fluid resuscitation. Patients with a large, sustained rise - in CVP have high preload and an element of  cardiac insu ffi - - ciency or volume overload. 

Minimum
Additional modalities
ECG
Central venous pressure
Pulse oximetry
Invasive blood pressure
Blood pressure
Cardiac output
Urine output
Base de
/f_i
cit and serum
lactate

Cardiac output monitoring allows assessment of  not only the cardiac output but also the systemic vascular resistance and, depending on the technique used, end-diastolic volume (preload) and blood volume. Use of  invasive cardiac monitor ing with pulmonary artery catheters is becoming less frequent as new non-invasive monitoring techniques, such as Doppler ultrasound, pulse waveform analysis and indicator dilution methods, provide similar information without many of  the drawbacks of  more invasive techniques. Measurement of cardiac output, systemic vascular resis tance and preload can help distinguish the types of  shock present (hypovolaemia, distributive, cardiogenic), especially when they coexist. The information pr ovided guides fluid and vasopressor therapy by providing real-time monitoring of  the cardiovascular response. Measurement of  cardiac output is desirable in patients who do not respond as expected to first-line therapy or who have evidence of  cardiogenic shock or myocardial dysfunction. Early consideration should be giv en to instituting cardiac out put monitoring for patients who require vasopressor or inotro pic support. Systemic and organ perfusion Ultimately , the goal of  treatment is to restore cellular and organ perfusion. Ideally , therefore, monitoring of  organ perfusion should guide the management of shock. The best measure of  organ perfusion and the best monitor of  the adequacy of shock therapy remains the urine output. However, this is an hourly measure and does not give a minute-to-minute view of the shocked state. The level of  consciousness is an important marker of  cerebral perfusion, but brain perfusion is maintained until the very late stages of  shock and hence is a poor marker of  adequacy of  resuscitation ( Table 2.4 ). Currently , the only clinical indicators of  perfusion of the gastrointestinal tract and muscular beds are the global Christian Johann Doppler , 1803–1853, Professor of  Experimental Physics, Vienna, Austria, en mixed venous oxygen saturation. Base deficit and lactate Lactic acid is generated by cells undergoing anaerobic respi - - ration. The degree of  lactic acidosis, as measured by serum lactate level and/or the base deficit, is sensitive for both diagnosis of  shock and monitoring the response to therapy . Patients with a base deficit of  more than 6 /uni00A0 mmol/L have a much higher morbidity and mortality than those with no metabolic acidosis. Furthermore, the length of  time in shock - with an increased base deficit is important, even if  all other vital signs have returned to normal (see occult hypoperfusion below under End points of resuscitation ). These parameters are measured from arterial blood gas analyses, and therefore the frequency of  measurements is limited and they do not pr ovide minute-to-minute data on systemic perfusion or the response to therapy . Nevertheless, the base deficit and/or lactate should be measured routinely in these patients until they have returned to normal levels. - - Mixed venous oxygen saturation The percentage saturation of  oxygen returning to the heart from the body is a measure of  the oxygen delivery and extraction by the tissues. Accurate measurement is via analysis of  blood drawn from a long central line placed in the right atrium. Estimations can be made from blood drawn from lines in the superior vena cava, but these values will be slightly higher than those of  a mixed venous sample (as there is rela - tively more oxygen extraction from the lower half  of  the body). Normal mixed venous oxygen saturation levels are 50–70%. Levels below 50% indicate inadequate oxygen delivery and increased oxygen extraction by the cells. This is consistent with hypovolaemic or cardiogenic shock. High mixed venous saturations (>70%) are seen in sepsis and some other forms of  distributive shock. In sepsis, there is disordered utilisation of  oxygen at the cellular level and unciated the Doppler principle in 1842. 

TABLE 2.4
Monitors for organ/systemic perfusion.
Clinical
Systemic perfusion
Organ perfusion
Muscle
–
Gut
–
Kidney
Urine output
Brain
Conscious level
Investigational
Base de
/f_i
cit
Lactate
Mixed venous oxygen saturation
Near-infrared spectroscopy
Tissue oxygen electrode
Sublingual capnometry
Gut mucosal pH
Laser Doppler
/f_l
owmetry
–
Tissue oxygen electrode
Near-infrared spectroscopy

Therefore, less oxygen is presented to the cells, and those cells cannot utilise what little oxygen is presented. Thus, venous blood has a higher oxygen concentration than normal. Patients who are septic should therefore have mixed venous oxygen saturations above 70%; below this level, they are not only in septic shock but also in hypovolaemic or cardiogenic shock. Although the S O level is in the ‘normal’ range, it is low v 2 for the septic state, and inadequate oxygen is being supplied to cells that cannot utilise oxygen appropriately . This must be cor rected rapidly . Hypovolaemia should be corrected with fluid therapy , and low cardiac output due to myocardial depression or failure should be treated with inotropes (dobutamine) to achieve a mixed venous saturation greater than 70% (normal for the septic state). New methods for monitoring regional tissue perfusion and oxygenation are becoming available, the most promising of whic h are muscle tissue oxygen probes, near-infrared spectros copy and sublingual capnometry . While these techniques pro vide information regarding perfusion of  specific tissue beds, it is as yet unclear whether there are significant advantages over existing measurements of  global hypoperfusion (base deficit, lactate). Monitoring

The minimum standard for monitoring of  the patient in shock is continuous heart rate and oxygen saturation moni - toring, frequent non-invasive blood pressure monitoring and hourly urine output measurements. Most patients will need more aggressive invasive monitoring, including central venous pressure (CVP) and invasive blood pressure monitoring. Summary box 2.4 Monitoring for patients in shock /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF - Cardiovascular - Cardiovascular monitoring at minimum should include continuous heart rate (electrocardiogram, oxygen saturation and pulse waveform and non-invasive blood pressure). Patients whose state of  shock is not rapidly corrected with a small amount of  fluid should have CVP monitoring and continuous blood pressure monitoring through an arterial line. - Central venous pressure There is no ‘normal’ CVP for a shocked patient, and reliance cannot be placed on an individual pressure measurement to assess volume status. Some patients may require a CVP of 5 /uni00A0 cmH O, whereas some may require a CVP of  15 /uni00A0 cmH O 2 2 or higher. Further, ventricular compliance can change from minute to minute in the shocked state, and CVP is a poor reflection of  end-diastolic volume (preload). CVP measurements should be assessed dynamically as the - response to a fluid challenge. A fluid bolus (250–500 /uni00A0 mL) is infused rapidly over 5–10 minutes. - The normal CVP response is a rise of  2–5 /uni00A0 cmH O, which 2 gradually drifts back to the original level over 10–20 minutes. tion Patients with no change in their CVP are empty and require further fluid resuscitation. Patients with a large, sustained rise - in CVP have high preload and an element of  cardiac insu ffi - - ciency or volume overload. 

Minimum
Additional modalities
ECG
Central venous pressure
Pulse oximetry
Invasive blood pressure
Blood pressure
Cardiac output
Urine output
Base de
/f_i
cit and serum
lactate

Cardiac output monitoring allows assessment of  not only the cardiac output but also the systemic vascular resistance and, depending on the technique used, end-diastolic volume (preload) and blood volume. Use of  invasive cardiac monitor ing with pulmonary artery catheters is becoming less frequent as new non-invasive monitoring techniques, such as Doppler ultrasound, pulse waveform analysis and indicator dilution methods, provide similar information without many of  the drawbacks of  more invasive techniques. Measurement of cardiac output, systemic vascular resis tance and preload can help distinguish the types of  shock present (hypovolaemia, distributive, cardiogenic), especially when they coexist. The information pr ovided guides fluid and vasopressor therapy by providing real-time monitoring of  the cardiovascular response. Measurement of  cardiac output is desirable in patients who do not respond as expected to first-line therapy or who have evidence of  cardiogenic shock or myocardial dysfunction. Early consideration should be giv en to instituting cardiac out put monitoring for patients who require vasopressor or inotro pic support. Systemic and organ perfusion Ultimately , the goal of  treatment is to restore cellular and organ perfusion. Ideally , therefore, monitoring of  organ perfusion should guide the management of shock. The best measure of  organ perfusion and the best monitor of  the adequacy of shock therapy remains the urine output. However, this is an hourly measure and does not give a minute-to-minute view of the shocked state. The level of  consciousness is an important marker of  cerebral perfusion, but brain perfusion is maintained until the very late stages of  shock and hence is a poor marker of  adequacy of  resuscitation ( Table 2.4 ). Currently , the only clinical indicators of  perfusion of the gastrointestinal tract and muscular beds are the global Christian Johann Doppler , 1803–1853, Professor of  Experimental Physics, Vienna, Austria, en mixed venous oxygen saturation. Base deficit and lactate Lactic acid is generated by cells undergoing anaerobic respi - - ration. The degree of  lactic acidosis, as measured by serum lactate level and/or the base deficit, is sensitive for both diagnosis of  shock and monitoring the response to therapy . Patients with a base deficit of  more than 6 /uni00A0 mmol/L have a much higher morbidity and mortality than those with no metabolic acidosis. Furthermore, the length of  time in shock - with an increased base deficit is important, even if  all other vital signs have returned to normal (see occult hypoperfusion below under End points of resuscitation ). These parameters are measured from arterial blood gas analyses, and therefore the frequency of  measurements is limited and they do not pr ovide minute-to-minute data on systemic perfusion or the response to therapy . Nevertheless, the base deficit and/or lactate should be measured routinely in these patients until they have returned to normal levels. - - Mixed venous oxygen saturation The percentage saturation of  oxygen returning to the heart from the body is a measure of  the oxygen delivery and extraction by the tissues. Accurate measurement is via analysis of  blood drawn from a long central line placed in the right atrium. Estimations can be made from blood drawn from lines in the superior vena cava, but these values will be slightly higher than those of  a mixed venous sample (as there is rela - tively more oxygen extraction from the lower half  of  the body). Normal mixed venous oxygen saturation levels are 50–70%. Levels below 50% indicate inadequate oxygen delivery and increased oxygen extraction by the cells. This is consistent with hypovolaemic or cardiogenic shock. High mixed venous saturations (>70%) are seen in sepsis and some other forms of  distributive shock. In sepsis, there is disordered utilisation of  oxygen at the cellular level and unciated the Doppler principle in 1842. 

TABLE 2.4
Monitors for organ/systemic perfusion.
Clinical
Systemic perfusion
Organ perfusion
Muscle
–
Gut
–
Kidney
Urine output
Brain
Conscious level
Investigational
Base de
/f_i
cit
Lactate
Mixed venous oxygen saturation
Near-infrared spectroscopy
Tissue oxygen electrode
Sublingual capnometry
Gut mucosal pH
Laser Doppler
/f_l
owmetry
–
Tissue oxygen electrode
Near-infrared spectroscopy

Therefore, less oxygen is presented to the cells, and those cells cannot utilise what little oxygen is presented. Thus, venous blood has a higher oxygen concentration than normal. Patients who are septic should therefore have mixed venous oxygen saturations above 70%; below this level, they are not only in septic shock but also in hypovolaemic or cardiogenic shock. Although the S O level is in the ‘normal’ range, it is low v 2 for the septic state, and inadequate oxygen is being supplied to cells that cannot utilise oxygen appropriately . This must be cor rected rapidly . Hypovolaemia should be corrected with fluid therapy , and low cardiac output due to myocardial depression or failure should be treated with inotropes (dobutamine) to achieve a mixed venous saturation greater than 70% (normal for the septic state). New methods for monitoring regional tissue perfusion and oxygenation are becoming available, the most promising of whic h are muscle tissue oxygen probes, near-infrared spectros copy and sublingual capnometry . While these techniques pro vide information regarding perfusion of  specific tissue beds, it is as yet unclear whether there are significant advantages over existing measurements of  global hypoperfusion (base deficit, lactate).

# Pathophysiology

Pathophysiology

Cellular As perfusion to the tissues is reduced, cells are deprived of oxygen and must switch from aerobic to anaerobic metabolism. The product of  anaerobic respiration is not carbon dioxide but lactic acid. When enough tissue is underperfused the accumulation of  lactic acid in the blood produces a systemic metabolic acidosis. As glucose within cells is exhausted, anaerobic respiration ceases and there is failure of sodium/potassium pumps in the cell membrane and intracellular organelles. Intracellular lysosomes release autodigestive enzymes and cell lysis ensues. Intracellular contents , including potassium, are released into the bloodstream. Microvascular As tissue ischaemia progresses, changes in the local milieu result in activation of the immune and coagulation systems. Hypoxia and acidosis activate complement and prime leuko cytes, resulting in the generation of  oxygen free radicals and cytokine release. These mechanisms lead to injury of  the capillary endothelial cells. These, in turn, further activate the immune and coagulation systems. Damaged endothelium loses its integrity and becomes ‘leaky’. Spaces between endothelial cells allow fluid to leak out and tissue oedema ensues, exacer - bating cellular hypoxia. Ischaemic cell death releases potassium into the circula - tion, leading to systemic hyperkalaemia and acidosis, as well as further damage to molecules that systemically activate the immune system. - Systemic Cardiovascular As preload and afterload decrease, there is a compensatory baroreceptor response, resulting in increased sympathetic activity and release of  catecholamines into the circulation. This results in tachycardia and systemic vasoconstriction (except in sepsis /uni00A0 – /uni00A0 see Distributive shock ). Respiratory The metabolic acidosis and increased sympathetic response result in an increased respiratory rate and minute ventilation to increase the excretion of  carbon dioxide (and so produce a compensatory respiratory alkalosis). Renal Decreased perfusion pressure in the kidney leads to reduced filtration at the glomerulus and a decreased urine output. The renin–angiotensin–aldosterone axis is stimulated, resulting in further vasoconstriction and increased sodium and water reabsorption by the kidney . Endocrine As well as activation of the adrenal and renin–angiotensin systems, vasopressin (antidiuretic hormone) is released in - 

Recognition and management of bleeding
•
Use of blood and blood products, the bene
/f_i
ts and risks of
•
blood transfusion

and resorption of  water in the renal collecting system. Cortisol is also released from the adrenal cortex, contributing to the sodium and water resorption and sensitising cells to catechol amines. Pathophysiology

In trauma and surgery , the combination of  tissue trauma and hypovolaemic shock leads to the development of  an endog - enous coagulopathy called acute traumatic coagulopathy - (ATC). Up to 25% of  all trauma patients develop ATC within minutes of  injury and it is associated with a fourfold increase in mortality . ATC is characterised by systemic hyperfibrinolysis, low fibrinogen levels and platelet dysfunction. ATC evolves into a more complex, multifactorial ‘trauma- - induced coagulopathy’ owing to further derangements induced by resuscitation ( Figure 2.1 ). Fluid and red b lood cell trans- fusions lead to dilution of  coagulation factors, which worsens the pre-existing coagulopathy . Underperfused muscle is unable to generate hea t and hypothermia ensues, again worsened by cold fluid or blood transfusion. Further heat is lost by opening Figure 2.1 body cavities during surgery . Severe acidosis and hypothermia both inhibit coagulation proteases and reduce coagulation function. These then lead to further bleeding and a downward spiral, leading to physiological exhaustion and death. 

ATC
Haemorrhage
Acidaemia
Hypothermia
In
/f_l
ammation
Fibrinolysis
Genetics
Loss, dilution
TRAUMA-INDUCED
COAGULOPATHY (TIC)
Trauma-induced coagulopathy. ATC, acute traumatic
coagulopathy.

Pathophysiology

Cellular As perfusion to the tissues is reduced, cells are deprived of oxygen and must switch from aerobic to anaerobic metabolism. The product of  anaerobic respiration is not carbon dioxide but lactic acid. When enough tissue is underperfused the accumulation of  lactic acid in the blood produces a systemic metabolic acidosis. As glucose within cells is exhausted, anaerobic respiration ceases and there is failure of sodium/potassium pumps in the cell membrane and intracellular organelles. Intracellular lysosomes release autodigestive enzymes and cell lysis ensues. Intracellular contents , including potassium, are released into the bloodstream. Microvascular As tissue ischaemia progresses, changes in the local milieu result in activation of the immune and coagulation systems. Hypoxia and acidosis activate complement and prime leuko cytes, resulting in the generation of  oxygen free radicals and cytokine release. These mechanisms lead to injury of  the capillary endothelial cells. These, in turn, further activate the immune and coagulation systems. Damaged endothelium loses its integrity and becomes ‘leaky’. Spaces between endothelial cells allow fluid to leak out and tissue oedema ensues, exacer - bating cellular hypoxia. Ischaemic cell death releases potassium into the circula - tion, leading to systemic hyperkalaemia and acidosis, as well as further damage to molecules that systemically activate the immune system. - Systemic Cardiovascular As preload and afterload decrease, there is a compensatory baroreceptor response, resulting in increased sympathetic activity and release of  catecholamines into the circulation. This results in tachycardia and systemic vasoconstriction (except in sepsis /uni00A0 – /uni00A0 see Distributive shock ). Respiratory The metabolic acidosis and increased sympathetic response result in an increased respiratory rate and minute ventilation to increase the excretion of  carbon dioxide (and so produce a compensatory respiratory alkalosis). Renal Decreased perfusion pressure in the kidney leads to reduced filtration at the glomerulus and a decreased urine output. The renin–angiotensin–aldosterone axis is stimulated, resulting in further vasoconstriction and increased sodium and water reabsorption by the kidney . Endocrine As well as activation of the adrenal and renin–angiotensin systems, vasopressin (antidiuretic hormone) is released in - 

Recognition and management of bleeding
•
Use of blood and blood products, the bene
/f_i
ts and risks of
•
blood transfusion

and resorption of  water in the renal collecting system. Cortisol is also released from the adrenal cortex, contributing to the sodium and water resorption and sensitising cells to catechol amines. Pathophysiology

In trauma and surgery , the combination of  tissue trauma and hypovolaemic shock leads to the development of  an endog - enous coagulopathy called acute traumatic coagulopathy - (ATC). Up to 25% of  all trauma patients develop ATC within minutes of  injury and it is associated with a fourfold increase in mortality . ATC is characterised by systemic hyperfibrinolysis, low fibrinogen levels and platelet dysfunction. ATC evolves into a more complex, multifactorial ‘trauma- - induced coagulopathy’ owing to further derangements induced by resuscitation ( Figure 2.1 ). Fluid and red b lood cell trans- fusions lead to dilution of  coagulation factors, which worsens the pre-existing coagulopathy . Underperfused muscle is unable to generate hea t and hypothermia ensues, again worsened by cold fluid or blood transfusion. Further heat is lost by opening Figure 2.1 body cavities during surgery . Severe acidosis and hypothermia both inhibit coagulation proteases and reduce coagulation function. These then lead to further bleeding and a downward spiral, leading to physiological exhaustion and death. 

ATC
Haemorrhage
Acidaemia
Hypothermia
In
/f_l
ammation
Fibrinolysis
Genetics
Loss, dilution
TRAUMA-INDUCED
COAGULOPATHY (TIC)
Trauma-induced coagulopathy. ATC, acute traumatic
coagulopathy.

Pathophysiology

Cellular As perfusion to the tissues is reduced, cells are deprived of oxygen and must switch from aerobic to anaerobic metabolism. The product of  anaerobic respiration is not carbon dioxide but lactic acid. When enough tissue is underperfused the accumulation of  lactic acid in the blood produces a systemic metabolic acidosis. As glucose within cells is exhausted, anaerobic respiration ceases and there is failure of sodium/potassium pumps in the cell membrane and intracellular organelles. Intracellular lysosomes release autodigestive enzymes and cell lysis ensues. Intracellular contents , including potassium, are released into the bloodstream. Microvascular As tissue ischaemia progresses, changes in the local milieu result in activation of the immune and coagulation systems. Hypoxia and acidosis activate complement and prime leuko cytes, resulting in the generation of  oxygen free radicals and cytokine release. These mechanisms lead to injury of  the capillary endothelial cells. These, in turn, further activate the immune and coagulation systems. Damaged endothelium loses its integrity and becomes ‘leaky’. Spaces between endothelial cells allow fluid to leak out and tissue oedema ensues, exacer - bating cellular hypoxia. Ischaemic cell death releases potassium into the circula - tion, leading to systemic hyperkalaemia and acidosis, as well as further damage to molecules that systemically activate the immune system. - Systemic Cardiovascular As preload and afterload decrease, there is a compensatory baroreceptor response, resulting in increased sympathetic activity and release of  catecholamines into the circulation. This results in tachycardia and systemic vasoconstriction (except in sepsis /uni00A0 – /uni00A0 see Distributive shock ). Respiratory The metabolic acidosis and increased sympathetic response result in an increased respiratory rate and minute ventilation to increase the excretion of  carbon dioxide (and so produce a compensatory respiratory alkalosis). Renal Decreased perfusion pressure in the kidney leads to reduced filtration at the glomerulus and a decreased urine output. The renin–angiotensin–aldosterone axis is stimulated, resulting in further vasoconstriction and increased sodium and water reabsorption by the kidney . Endocrine As well as activation of the adrenal and renin–angiotensin systems, vasopressin (antidiuretic hormone) is released in - 

Recognition and management of bleeding
•
Use of blood and blood products, the bene
/f_i
ts and risks of
•
blood transfusion

and resorption of  water in the renal collecting system. Cortisol is also released from the adrenal cortex, contributing to the sodium and water resorption and sensitising cells to catechol amines. Pathophysiology

In trauma and surgery , the combination of  tissue trauma and hypovolaemic shock leads to the development of  an endog - enous coagulopathy called acute traumatic coagulopathy - (ATC). Up to 25% of  all trauma patients develop ATC within minutes of  injury and it is associated with a fourfold increase in mortality . ATC is characterised by systemic hyperfibrinolysis, low fibrinogen levels and platelet dysfunction. ATC evolves into a more complex, multifactorial ‘trauma- - induced coagulopathy’ owing to further derangements induced by resuscitation ( Figure 2.1 ). Fluid and red b lood cell trans- fusions lead to dilution of  coagulation factors, which worsens the pre-existing coagulopathy . Underperfused muscle is unable to generate hea t and hypothermia ensues, again worsened by cold fluid or blood transfusion. Further heat is lost by opening Figure 2.1 body cavities during surgery . Severe acidosis and hypothermia both inhibit coagulation proteases and reduce coagulation function. These then lead to further bleeding and a downward spiral, leading to physiological exhaustion and death. 

ATC
Haemorrhage
Acidaemia
Hypothermia
In
/f_l
ammation
Fibrinolysis
Genetics
Loss, dilution
TRAUMA-INDUCED
COAGULOPATHY (TIC)
Trauma-induced coagulopathy. ATC, acute traumatic
coagulopathy.

# Recognition and diagnosis of shock

Recognition and diagnosis of shock

Shock may be profound and easily recognised or it may be - subtle and only diagnosed with directed clinical examination and cardiovascular and metabolic monitoring. Compensated shock As shock progresses, the body’s cardiovascular and endocrine compensatory responses reduce flow to non-essential organs to preserve preload and flow to the lungs and brain. In compen - sated shock, there is adequate cardiovascular compensation to maintain central blood volume and preserve flow to the kidneys, lungs and brain. Apart from a tachycardia and cool peripheries (vasoconstriction, circulating catecholamines), there may be no other clinical signs of  hypovolaemia. However, this cardiovascular state is only maintained by reducing perfusion to the skin, muscle and gastrointestinal tract. These organs are underperfused: their cells are respiring anaerobically and sustaining ischaemic damage. There is sys - temic metabolic acidosis and both local and systemic activation of  humoral and cellular inflammation. - Although clinically occult, this state will lead to multiple organ failure and death if  prolonged. Patients with occult hypoperfusion (metabolic acidosis despite normal urine output and cardiorespiratory vital signs) for more than 12 hours have a significantly higher mortality , infection rate and incidence of - multiple organ failure (see Multiple organ failure ). Decompensation Further loss of  circulating volume overloads the body’s compensatory mechanisms and there is progressive renal, respiratory and cardiovascular decompensation. In general, loss of  around 15% of  the circulating blood volume is within normal compensatory mechanisms. Blood pressure is usually well maintained and only falls after 30–40% of  circulating volume has been lost. Mild (compensated) shock - Initially there is tachycardia, tachypnoea, a mild reduction in urine output and the patient may exhibit mild anxiety . Blood pressure is maintained, although there is a decrease in pulse pressure. The peripheries are cool and sweaty with prolonged capillary refill times (except in septic distributive shock). Moderate shock As shock progresses, renal compensatory mechanisms fail, renal perfusion falls and urine output dips below 0.5 /uni00A0 mL/kg/hour. There is further tachycardia, and now the blood pressure starts to fall. Patients become drowsy and mildly confused. Severe shock In severe shock, there is profound tachycardia and hypoten sion. Urine output falls to zero and patients are unconscious with laboured respiration. Clinical features The classic cardiovascular responses described ( Table 2.2 not seen in every patient. It is important to recognise the limita tions of  the clinical examination and to recognise patients who are in shock despite the absence of  classic signs. Capillary refill Most patients in hypovolaemic shock will have cool, pale peripheries, with prolonged capillary refill times. However, the actual capillary refill time varies so much in adults that it is not a specific marker of  whether a patient is shocked, and patients with short capillary refill times may be in the early stages of shock. In distributive (septic) shock, the peripheries will be warm and capillary refill will be brisk, despite profound shock. Tachycardia Tachycardia may not always accompany shock. Patients who are on β -blockers or who have implanted pacemakers are unable to mount a tachycardia. A pulse rate of  80 in a fit young adult who normally has a pulse rate of  50 is very abnormal. Furthermore, in some young patients with penetrating trauma, where there is haemorrhage but little tissue damage, there may be a paradoxical bradycardia rather than tachycardia accom panying the shocked state. Blood pressure It is important to recognise that hypotension is one of  the last signs of  shock. Children and fit young adults are able to main tain blood pressure until the final stages of shock by dramatic increases in stroke volume and peripheral vasoconstriction. These patients can be in profound shock with a normal blood pressure. Elderly patients who are normally hypertensive may present with a ‘normal’ blood pressure for the general population but be hypovolaemic and hypotensive relative to their usual blood pressur e. β -blockers or other medications may prevent a tachy - cardic response. T he diagnosis of  shock may be di ffi cult unless one is alert to these pitfalls. 

Compensated
Mild
Lactic acidosis
+
Urine output
Normal
Conscious level
Mild anxiety
Respiratory rate
Increased
Pulse rate
Increased
Blood pressure
Normal
Uncompensated
Moderate
Severe
++
+++
Reduced
Anuric
Drowsy
Comatose
Increased
Laboured
Increased
Increased
Mild hypotension
Severe hypotension

Recognition and diagnosis of shock

Shock may be profound and easily recognised or it may be - subtle and only diagnosed with directed clinical examination and cardiovascular and metabolic monitoring. Compensated shock As shock progresses, the body’s cardiovascular and endocrine compensatory responses reduce flow to non-essential organs to preserve preload and flow to the lungs and brain. In compen - sated shock, there is adequate cardiovascular compensation to maintain central blood volume and preserve flow to the kidneys, lungs and brain. Apart from a tachycardia and cool peripheries (vasoconstriction, circulating catecholamines), there may be no other clinical signs of  hypovolaemia. However, this cardiovascular state is only maintained by reducing perfusion to the skin, muscle and gastrointestinal tract. These organs are underperfused: their cells are respiring anaerobically and sustaining ischaemic damage. There is sys - temic metabolic acidosis and both local and systemic activation of  humoral and cellular inflammation. - Although clinically occult, this state will lead to multiple organ failure and death if  prolonged. Patients with occult hypoperfusion (metabolic acidosis despite normal urine output and cardiorespiratory vital signs) for more than 12 hours have a significantly higher mortality , infection rate and incidence of - multiple organ failure (see Multiple organ failure ). Decompensation Further loss of  circulating volume overloads the body’s compensatory mechanisms and there is progressive renal, respiratory and cardiovascular decompensation. In general, loss of  around 15% of  the circulating blood volume is within normal compensatory mechanisms. Blood pressure is usually well maintained and only falls after 30–40% of  circulating volume has been lost. Mild (compensated) shock - Initially there is tachycardia, tachypnoea, a mild reduction in urine output and the patient may exhibit mild anxiety . Blood pressure is maintained, although there is a decrease in pulse pressure. The peripheries are cool and sweaty with prolonged capillary refill times (except in septic distributive shock). Moderate shock As shock progresses, renal compensatory mechanisms fail, renal perfusion falls and urine output dips below 0.5 /uni00A0 mL/kg/hour. There is further tachycardia, and now the blood pressure starts to fall. Patients become drowsy and mildly confused. Severe shock In severe shock, there is profound tachycardia and hypoten sion. Urine output falls to zero and patients are unconscious with laboured respiration. Clinical features The classic cardiovascular responses described ( Table 2.2 not seen in every patient. It is important to recognise the limita tions of  the clinical examination and to recognise patients who are in shock despite the absence of  classic signs. Capillary refill Most patients in hypovolaemic shock will have cool, pale peripheries, with prolonged capillary refill times. However, the actual capillary refill time varies so much in adults that it is not a specific marker of  whether a patient is shocked, and patients with short capillary refill times may be in the early stages of shock. In distributive (septic) shock, the peripheries will be warm and capillary refill will be brisk, despite profound shock. Tachycardia Tachycardia may not always accompany shock. Patients who are on β -blockers or who have implanted pacemakers are unable to mount a tachycardia. A pulse rate of  80 in a fit young adult who normally has a pulse rate of  50 is very abnormal. Furthermore, in some young patients with penetrating trauma, where there is haemorrhage but little tissue damage, there may be a paradoxical bradycardia rather than tachycardia accom panying the shocked state. Blood pressure It is important to recognise that hypotension is one of  the last signs of  shock. Children and fit young adults are able to main tain blood pressure until the final stages of shock by dramatic increases in stroke volume and peripheral vasoconstriction. These patients can be in profound shock with a normal blood pressure. Elderly patients who are normally hypertensive may present with a ‘normal’ blood pressure for the general population but be hypovolaemic and hypotensive relative to their usual blood pressur e. β -blockers or other medications may prevent a tachy - cardic response. T he diagnosis of  shock may be di ffi cult unless one is alert to these pitfalls. 

Compensated
Mild
Lactic acidosis
+
Urine output
Normal
Conscious level
Mild anxiety
Respiratory rate
Increased
Pulse rate
Increased
Blood pressure
Normal
Uncompensated
Moderate
Severe
++
+++
Reduced
Anuric
Drowsy
Comatose
Increased
Laboured
Increased
Increased
Mild hypotension
Severe hypotension

Recognition and diagnosis of shock

Shock may be profound and easily recognised or it may be - subtle and only diagnosed with directed clinical examination and cardiovascular and metabolic monitoring. Compensated shock As shock progresses, the body’s cardiovascular and endocrine compensatory responses reduce flow to non-essential organs to preserve preload and flow to the lungs and brain. In compen - sated shock, there is adequate cardiovascular compensation to maintain central blood volume and preserve flow to the kidneys, lungs and brain. Apart from a tachycardia and cool peripheries (vasoconstriction, circulating catecholamines), there may be no other clinical signs of  hypovolaemia. However, this cardiovascular state is only maintained by reducing perfusion to the skin, muscle and gastrointestinal tract. These organs are underperfused: their cells are respiring anaerobically and sustaining ischaemic damage. There is sys - temic metabolic acidosis and both local and systemic activation of  humoral and cellular inflammation. - Although clinically occult, this state will lead to multiple organ failure and death if  prolonged. Patients with occult hypoperfusion (metabolic acidosis despite normal urine output and cardiorespiratory vital signs) for more than 12 hours have a significantly higher mortality , infection rate and incidence of - multiple organ failure (see Multiple organ failure ). Decompensation Further loss of  circulating volume overloads the body’s compensatory mechanisms and there is progressive renal, respiratory and cardiovascular decompensation. In general, loss of  around 15% of  the circulating blood volume is within normal compensatory mechanisms. Blood pressure is usually well maintained and only falls after 30–40% of  circulating volume has been lost. Mild (compensated) shock - Initially there is tachycardia, tachypnoea, a mild reduction in urine output and the patient may exhibit mild anxiety . Blood pressure is maintained, although there is a decrease in pulse pressure. The peripheries are cool and sweaty with prolonged capillary refill times (except in septic distributive shock). Moderate shock As shock progresses, renal compensatory mechanisms fail, renal perfusion falls and urine output dips below 0.5 /uni00A0 mL/kg/hour. There is further tachycardia, and now the blood pressure starts to fall. Patients become drowsy and mildly confused. Severe shock In severe shock, there is profound tachycardia and hypoten sion. Urine output falls to zero and patients are unconscious with laboured respiration. Clinical features The classic cardiovascular responses described ( Table 2.2 not seen in every patient. It is important to recognise the limita tions of  the clinical examination and to recognise patients who are in shock despite the absence of  classic signs. Capillary refill Most patients in hypovolaemic shock will have cool, pale peripheries, with prolonged capillary refill times. However, the actual capillary refill time varies so much in adults that it is not a specific marker of  whether a patient is shocked, and patients with short capillary refill times may be in the early stages of shock. In distributive (septic) shock, the peripheries will be warm and capillary refill will be brisk, despite profound shock. Tachycardia Tachycardia may not always accompany shock. Patients who are on β -blockers or who have implanted pacemakers are unable to mount a tachycardia. A pulse rate of  80 in a fit young adult who normally has a pulse rate of  50 is very abnormal. Furthermore, in some young patients with penetrating trauma, where there is haemorrhage but little tissue damage, there may be a paradoxical bradycardia rather than tachycardia accom panying the shocked state. Blood pressure It is important to recognise that hypotension is one of  the last signs of  shock. Children and fit young adults are able to main tain blood pressure until the final stages of shock by dramatic increases in stroke volume and peripheral vasoconstriction. These patients can be in profound shock with a normal blood pressure. Elderly patients who are normally hypertensive may present with a ‘normal’ blood pressure for the general population but be hypovolaemic and hypotensive relative to their usual blood pressur e. β -blockers or other medications may prevent a tachy - cardic response. T he diagnosis of  shock may be di ffi cult unless one is alert to these pitfalls. 

Compensated
Mild
Lactic acidosis
+
Urine output
Normal
Conscious level
Mild anxiety
Respiratory rate
Increased
Pulse rate
Increased
Blood pressure
Normal
Uncompensated
Moderate
Severe
++
+++
Reduced
Anuric
Drowsy
Comatose
Increased
Laboured
Increased
Increased
Mild hypotension
Severe hypotension

# SHOCK RESUSCITATION

SHOCK RESUSCITATION

- Immediate resuscitation manoeuvres for patients presenting in - shock are to ensure a patent airway and adequate oxygenation and ventilation. Once ‘airway’ and ‘breathing’ are assessed and - controlled, attention is directed to cardiovascular resuscitation. Haemorrhagic shock resuscitation should proceed as damage - control resuscitation while bleeding continues (as discussed earlier). After bleeding is controlled, and for all other causes, shock resuscitation is guided by measures of  tissue perfusion, as described in Monitoring . SHOCK RESUSCITATION

- Immediate resuscitation manoeuvres for patients presenting in - shock are to ensure a patent airway and adequate oxygenation and ventilation. Once ‘airway’ and ‘breathing’ are assessed and - controlled, attention is directed to cardiovascular resuscitation. Haemorrhagic shock resuscitation should proceed as damage - control resuscitation while bleeding continues (as discussed earlier). After bleeding is controlled, and for all other causes, shock resuscitation is guided by measures of  tissue perfusion, as described in Monitoring . SHOCK RESUSCITATION

- Immediate resuscitation manoeuvres for patients presenting in - shock are to ensure a patent airway and adequate oxygenation and ventilation. Once ‘airway’ and ‘breathing’ are assessed and - controlled, attention is directed to cardiovascular resuscitation. Haemorrhagic shock resuscitation should proceed as damage - control resuscitation while bleeding continues (as discussed earlier). After bleeding is controlled, and for all other causes, shock resuscitation is guided by measures of  tissue perfusion, as described in Monitoring .

# SHOCK

SHOCK

Shock is a systemic state of  low tissue perfusion that is inade quate for normal cellular respiration. With insu ffi cient delivery of  oxygen and glucose, cells switch from aerobic to anaerobic metabolism. If  perfusion is not restored in a timely fashion, cell death ensues. SHOCK

Shock is a systemic state of  low tissue perfusion that is inade quate for normal cellular respiration. With insu ffi cient delivery of  oxygen and glucose, cells switch from aerobic to anaerobic metabolism. If  perfusion is not restored in a timely fashion, cell death ensues. SHOCK

Shock is a systemic state of  low tissue perfusion that is inade quate for normal cellular respiration. With insu ffi cient delivery of  oxygen and glucose, cells switch from aerobic to anaerobic metabolism. If  perfusion is not restored in a timely fashion, cell death ensues.

# TRANSFUSION

TRANSFUSION

The transfusion of  blood and blood products has become commonplace since the first successful transfusion in 1818. Although the incidence of  severe transfusion reactions and infections is now very low , in recent years it has become - apparent that there is an immunological price to be paid for the transfusion of  heterologous blood, leading to increased morbidity and decreased survival in certain population groups (trauma, malignancy). Supplies are also limited, and therefore the use of  blood and blood products must always be judicious and justifiable for clinical need ( Table 2.5 ). - - - 

TABLE 2.5
History of blood transfusion.
1492
Pope Innocent VIII suffers a stroke and receives a
blood transfusion from three 10-year-old boys (paid a
ducat each). All three boys died, as did the pope later
that year
1665
Richard Lower in Oxford conducts the
/f_i
rst successful
canine transfusions
1667
Jean-Baptiste Denis reports successful sheep–human
transfusions
1678
Animal–human transfusions are banned in France
because of the poor results
1818
James Blundell performs the
/f_i
rst successful
documented human transfusion in a woman suffering
postpartum haemorrhage. She received blood from her
husband and survived
1901
Karl Landsteiner discovers the ABO system
1914
The Belgian physician Albert Hustin performed the
/f_i
rst non-direct transfusion, using sodium citrate as an
anticoagulant
1926
The British Red Cross instituted the
/f_i
rst blood
transfusion service in the world
1939
The rhesus system was identi
/f_i
ed and recognised as
the major cause of transfusion reactions

TRANSFUSION

The transfusion of  blood and blood products has become commonplace since the first successful transfusion in 1818. Although the incidence of  severe transfusion reactions and infections is now very low , in recent years it has become - apparent that there is an immunological price to be paid for the transfusion of  heterologous blood, leading to increased morbidity and decreased survival in certain population groups (trauma, malignancy). Supplies are also limited, and therefore the use of  blood and blood products must always be judicious and justifiable for clinical need ( Table 2.5 ). - - - 

TABLE 2.5
History of blood transfusion.
1492
Pope Innocent VIII suffers a stroke and receives a
blood transfusion from three 10-year-old boys (paid a
ducat each). All three boys died, as did the pope later
that year
1665
Richard Lower in Oxford conducts the
/f_i
rst successful
canine transfusions
1667
Jean-Baptiste Denis reports successful sheep–human
transfusions
1678
Animal–human transfusions are banned in France
because of the poor results
1818
James Blundell performs the
/f_i
rst successful
documented human transfusion in a woman suffering
postpartum haemorrhage. She received blood from her
husband and survived
1901
Karl Landsteiner discovers the ABO system
1914
The Belgian physician Albert Hustin performed the
/f_i
rst non-direct transfusion, using sodium citrate as an
anticoagulant
1926
The British Red Cross instituted the
/f_i
rst blood
transfusion service in the world
1939
The rhesus system was identi
/f_i
ed and recognised as
the major cause of transfusion reactions

TRANSFUSION

The transfusion of  blood and blood products has become commonplace since the first successful transfusion in 1818. Although the incidence of  severe transfusion reactions and infections is now very low , in recent years it has become - apparent that there is an immunological price to be paid for the transfusion of  heterologous blood, leading to increased morbidity and decreased survival in certain population groups (trauma, malignancy). Supplies are also limited, and therefore the use of  blood and blood products must always be judicious and justifiable for clinical need ( Table 2.5 ). - - - 

TABLE 2.5
History of blood transfusion.
1492
Pope Innocent VIII suffers a stroke and receives a
blood transfusion from three 10-year-old boys (paid a
ducat each). All three boys died, as did the pope later
that year
1665
Richard Lower in Oxford conducts the
/f_i
rst successful
canine transfusions
1667
Jean-Baptiste Denis reports successful sheep–human
transfusions
1678
Animal–human transfusions are banned in France
because of the poor results
1818
James Blundell performs the
/f_i
rst successful
documented human transfusion in a woman suffering
postpartum haemorrhage. She received blood from her
husband and survived
1901
Karl Landsteiner discovers the ABO system
1914
The Belgian physician Albert Hustin performed the
/f_i
rst non-direct transfusion, using sodium citrate as an
anticoagulant
1926
The British Red Cross instituted the
/f_i
rst blood
transfusion service in the world
1939
The rhesus system was identi
/f_i
ed and recognised as
the major cause of transfusion reactions

# Transfusion reactions

Transfusion reactions

If  antibodies present in the recipient’s serum are incompatible with the donor’s cells, a transfusion reaction will result. This usually takes the form of  an acute haemolytic reaction. Severe immune-related transfusion reactions due to ABO incompat ibility result in potentially fatal complement-mediated intra vascular haemolysis and multiple organ failure. Transfusion reactions from other antigen systems are usually milder and self-limiting. Febrile transfusion reactions are non-haemolytic and are usually caused by a graft-versus-host-response from leukocytes in transfused components. Such reactions are associated with fe ver, chills or rigors. The blood transfusion should be stopped immediately . This form of  transfusion reaction is rare with leukodepleted blood. Transfusion reactions

If  antibodies present in the recipient’s serum are incompatible with the donor’s cells, a transfusion reaction will result. This usually takes the form of  an acute haemolytic reaction. Severe immune-related transfusion reactions due to ABO incompat ibility result in potentially fatal complement-mediated intra vascular haemolysis and multiple organ failure. Transfusion reactions from other antigen systems are usually milder and self-limiting. Febrile transfusion reactions are non-haemolytic and are usually caused by a graft-versus-host-response from leukocytes in transfused components. Such reactions are associated with fe ver, chills or rigors. The blood transfusion should be stopped immediately . This form of  transfusion reaction is rare with leukodepleted blood. Transfusion reactions

If  antibodies present in the recipient’s serum are incompatible with the donor’s cells, a transfusion reaction will result. This usually takes the form of  an acute haemolytic reaction. Severe immune-related transfusion reactions due to ABO incompat ibility result in potentially fatal complement-mediated intra vascular haemolysis and multiple organ failure. Transfusion reactions from other antigen systems are usually milder and self-limiting. Febrile transfusion reactions are non-haemolytic and are usually caused by a graft-versus-host-response from leukocytes in transfused components. Such reactions are associated with fe ver, chills or rigors. The blood transfusion should be stopped immediately . This form of  transfusion reaction is rare with leukodepleted blood.

# Vasopressor and inotropic support

Vasopressor and inotropic support

Vasopressor or inotropic therapy is not indicated as first-line therapy in hypovolaemia. Administration of  these agents in the absence of adequate preload rapidly leads to decreased coro nary perfusion and depletion of  myocardial oxygen reserves. Vasopressor agents (phenylephrine, noradrenaline [nor epinephrine]) are indicated in distributive shock states (sepsis, neurogenic shock) where there is peripheral vasodilata and a low systemic vascular resistance, leading to hypotension despite a high cardiac output. Where the vasodilatation is resis tant to catecholamines (e.g. absolute or relative steroid defi ciency), vasopressin may be used as an alternative vasopressor. Alexis Frank Hartmann , 1898–1964, paediatrician, St Louis, MO, USA, described the solution; should not be confused with the name of  Henri Albert Charles Antoine Hartmann, French surgeon, who described the operation that goes by his name. Sidney Ringer , 1835–1910, Professor of  Clinical Medicine, University College Hospital, London, UK. complicated a shock state (e.g. severe septic shock with low car - diac output), inotropic therapy ma y be required to increase - cardiac output and therefore oxygen delivery . The inodilator dobutamine is the agent of  choice. Vasopressor and inotropic support

Vasopressor or inotropic therapy is not indicated as first-line therapy in hypovolaemia. Administration of  these agents in the absence of adequate preload rapidly leads to decreased coro nary perfusion and depletion of  myocardial oxygen reserves. Vasopressor agents (phenylephrine, noradrenaline [nor epinephrine]) are indicated in distributive shock states (sepsis, neurogenic shock) where there is peripheral vasodilata and a low systemic vascular resistance, leading to hypotension despite a high cardiac output. Where the vasodilatation is resis tant to catecholamines (e.g. absolute or relative steroid defi ciency), vasopressin may be used as an alternative vasopressor. Alexis Frank Hartmann , 1898–1964, paediatrician, St Louis, MO, USA, described the solution; should not be confused with the name of  Henri Albert Charles Antoine Hartmann, French surgeon, who described the operation that goes by his name. Sidney Ringer , 1835–1910, Professor of  Clinical Medicine, University College Hospital, London, UK. complicated a shock state (e.g. severe septic shock with low car - diac output), inotropic therapy ma y be required to increase - cardiac output and therefore oxygen delivery . The inodilator dobutamine is the agent of  choice. Vasopressor and inotropic support

Vasopressor or inotropic therapy is not indicated as first-line therapy in hypovolaemia. Administration of  these agents in the absence of adequate preload rapidly leads to decreased coro nary perfusion and depletion of  myocardial oxygen reserves. Vasopressor agents (phenylephrine, noradrenaline [nor epinephrine]) are indicated in distributive shock states (sepsis, neurogenic shock) where there is peripheral vasodilata and a low systemic vascular resistance, leading to hypotension despite a high cardiac output. Where the vasodilatation is resis tant to catecholamines (e.g. absolute or relative steroid defi ciency), vasopressin may be used as an alternative vasopressor. Alexis Frank Hartmann , 1898–1964, paediatrician, St Louis, MO, USA, described the solution; should not be confused with the name of  Henri Albert Charles Antoine Hartmann, French surgeon, who described the operation that goes by his name. Sidney Ringer , 1835–1910, Professor of  Clinical Medicine, University College Hospital, London, UK. complicated a shock state (e.g. severe septic shock with low car - diac output), inotropic therapy ma y be required to increase - cardiac output and therefore oxygen delivery . The inodilator dobutamine is the agent of  choice.