Injury (1990) 21,317-320
Printed in Great Britain
317
Resuscitation Anne J. Sutcliffe Department
of Anaesthetics,
‘Resuscitate: revive (Sykes, 1978).
Birmingham
from unconsciousness
Accident Hospital, Birmingham,
or apparent
death
‘Shock: a term used by clinicians to describe a condition characterized by inadequate cellular perfusion and consequent failure of function of various tissues and organs’ (Hanson, 1978).
Introduction The first clinical description of shock was probably made by O’Shaughnessy in 1831. He studied cholera victims in Sunderland and described accurately and in graphic detail the clinical signs of severe shock. He also analysed the blood and excreta of cholera patients in the laboratory and concluded that the clinical state of the patients was due to loss of water and electrolytes from the blood. He suggested that these patients might be cured by ‘the injection into the veins of tepid water holding a solution of the normal salts of the blood’. This suggestion resulted in the first attempts at intravenous resuscitation. Only moribund patients were treated with intravenous fluids and most died. There were, however, a few survivors (Cosnett, 1989). In 1899, Crile showed that an intravenous infusion of warm saline reduced mortality in experimental haemorrhagic shock. During the First World War doctors began to understand the pathophysiological effects of shock and to appreciate that poor tissue perfusion caused tissue hypoxia (Runciman and Skowronski, 1984), but it was not until stored blood became available in the 1940s that clinicians were able to treat haemorrhagic shock. The value of adequate blood transfusion was demonstrated by army surgeons during the Second World War, and these surgeons continued to give large volume blood transfusions when they returned to civilian practice. The minutes of the Birmingham Accident Hospital Medical Society for 1948 record the fact that it was sometimes necessary to use two drips in order to administer sufficiently large volumes of blood with adequate speed. This policy was not adopted immediately by all doctors. As late as 1953 a standard anaesthetic textbook stated that ‘never more than 500 ml of fluid should be run in at speed under pressure’ (Lee, 1953). The need for the administration of oxygen was less well appreciated. One of the Accident Hospital Surgeons is reported to have said that ‘the value of oxygen is not known but tends to distress the patient and make him restless’! Before 1970, the adequacy of resuscitation was difficult to assess. It was possible to measure blood pressure and to estimate blood volume, but it was not possible routinely to 0 1990 Butterworth-Heinemann 0020-1383/90/050317-4
Ltd
UK
measure blood flow or assess tissue oxygenation. The introduction of the Swan-Ganz pulmonary artery flotation catheter (Swan et al., 1970), and its subsequent development to permit bedside estimation of cardiac output and oxygen delivery and uptake, have dramatically improved the clinician’s ability to resuscitate patients accurately. As resuscitation has improved, survival in the immediate post-injury period has improved. Today, most patients who reach hospital alive should survive the effects of the original injury. However, deaths still occur days or weeks after injury, usually as a result of multiple organ failure (MOF). Evidence is increasing that inadequate resuscitation may contribute to these deaths.
Pathophysiological effects of haemorrhage and hypovolaemia There are a variety of homeostatic responses to acute blood loss which have been reviewed in detail by Runciman and Skowronski (1984). They include activation of the sympathetic nervous system and release of renin, angiotensin, antidiuretic hormone and prostaglandins; all of which cause generalized vasoconstriction. Other humoral mediators such as serotonin, exert a local vasoconstrictor effect and help to stop bleeding. Still others such as components of the complement cascade and fibronectin may play a role in tissue healing. In evolutionary terms these responses are appropriate because blood flow to essential organs is preserved and therefore survival is possible if the total blood loss is not too great. If, however, the loss is great, the response becomes excessive and inappropriate because tissue oxygenation is compromised. In the presence of hypoxia, intracellular metabolism is disrupted and cell membranes cease to function normally. Numerous toxic substances including bradykinin, histamine, thromboxanes and leukotrienes are released. It is thought that these cellular toxins may play a part in the subsequent development of MOF.
Adult respiratory distress syndrome, multiple organ failure and shock years, it has been known that the Adult Respiratory Distress Syndrome (ARDS) may develop following multiple trauma or severe haemorrhage. ARDS becomes apparent z to 6 days after the primary insult. Clinical signs include dyspnoea and cyanosis. Interstitial pulmonary oedema is seen on the chest radiograph as diffuse fluffy For many
Injury: the British Journal of Accident Surgery (1990) Vol. 21/No. 5
318
opacities. Histologically, the lungs show widespread microemboli containing platelets and leucocytes (Harrison et al., 1977). Increased permeability of the pulmonary capillaries can also be demonstrated (Kreuzfelder et al., 1988). The precise cause of these pathological changes is not known, but complement activation (Hammerschmidt et al., 1980), the generation of free oxygen radicals (Baldwin et al., 1986), and the release of toxic humoral mediators (He&man et al., 1984) have all been implicated. Many of these mechanisms are initiated by shock (Runciman and Skowronski, 1984). When ARDS was first described, it was thought to be a discrete clinical entity, but increased capillary permeability also occurs in other organs. Patients with ARDS have increased glomerular permeability (Kreuzfelder et al., 1988) and may have pancreatic microvascular damage (Nicod et al., 1985) or acalculous cholecystitis (Glenn and Becker, 1982). Furthermore, following experimentally induced haemorrhage in animals, myocardial oedema (Holcroft et al., 1976), and capillary endothelial swelling in the liver and skeletal muscle (S&lag and Redl, 1985) have also been noted. It is now thought that ARDS is the pulmonary manifestation of generalized multiple organ failure resulting from systemic damage to vascular endothelia, permeability oedema and impaired oxygen availability to the mitochondria (Goris et al., 1985). As a result of improved resuscitation, MOF following major haemorrhage or multiple trauma is rare. There is, however, no room for complacency. In humans, increased glomerular permeability and pulmonary capillary permeability have been demonstrated following injury (Gosling and Sutcliffe, 1986, Kreuzfelder et al., 1988). These changes are proportional to injury severity and occur even in the presence of minor injury. It seems probable, therefore, that tissue injury can initiate the responses causing increased capillary permeability and that these responses are also induced and possibly compounded by haemorrhage. In order to minimize the effects of injury and haemorrhage, adequate resuscitation is essential. Effective resuscitation is as important for patients with minor injuries and relatively minor haemorrhage as it is for those with multiple injuries and major haemorrhage.
Sepsis in the trauma patient As has already been stated, MOF secondary to trauma and haemorrhage is rare. Most injured patients who survive long enough to reach hospital but who subsequently die, do so as a result of MOF secondary to sepsis. There is increasing evidence that bacteria from the gut are the cause of many infections suffered by injured patients. It is postulated that vasoconstriction in the splanchnic bed causes ischaemia of the. gastrointestinal mucosa which becomes permeable to pathogenic organisms and endotoxins. These enter the portal circulation and damage the Kupffer cells in the liver. These cells compromise 70 per cent of the total population of macrophages which trigger the specific immune response.
If they are damaged the patient is unable to combat infection. This subject is well reviewed by S&lag and Redl (1987). Further evidence that gut pathogens play a role in sepsis following trauma has been provided by Ledingham et al. (1988), who have shown that selective decontamination of the gut reduces the incidence of sepsis. Adequate resuscitation and prevention of severe vasoconstriction of the splanchnic mucosa should, therefore, help to reduce the incidence of infection and late MOF in trauma patients.
Diagnosis of hypovolaemia Fluid resuscitation should begin as soon as possible. In certain circumstances, it may be possible to start an intravenous infusion at the scene of the accident. If this is not possible, large-bore peripheral intravenous cannulae should be inserted as soon as the patient reaches hospital. The amount of fluid given in the first 10 min will depend on the history obtained from ambulancemen or relatives, a rapid survey of the patient noting obvious injuries and clinical signs such as pallor, confusion, the state of the peripheral veins, skin temperature, pulse rate and blood pressure. Table I summarizes the changes which occur as a progressively greater percentage of the patient’s blood volume is lost. Oxygen should also be given from the time of admission and, if necessary, the patient should be intubated and ventilated. When these life-saving measures are complete the patient should be examined in detail. Resuscitation should be guided by the injuries diagnosed and the likely blood loss associated with them (Clarke and Fisher, 1956). Initially, monitoring of pulse, blood pressure and central venous pressure will provide a crude guide to the adequacy of resuscitation. The presence of a normal pulse rate and pressures indicates only adequate volume has been given to fill the vascular space as it exists at the time of these measurements, because a normal pulse rate and blood pressure can occur in the presence of gross vasoconstriction. Clues to the degree of vasoconstriction may be obtained by monitoring skin temperature and urine output. Pressure measurements do not reflect the adequacy of blood flow or the adequacy of tissue oxygenation. Rapid capillary refill and a urine output of 50 ml/h may be used as indicators of adequate flow to the tissues. Arterial blood gas estimations showing a metabolic acidosis indicate anaerobic metabolism and tissue hypoxia. Confusion or inappropriate anxiety are often due to cerebral hypoxia. For many patients, the methods described previously will be sufficient to monitor the adequacy of resuscitation. Their interpretation depends to a certain extent on the age of the patient and pre-existing medical illnesses. Myocardial failure as a result of disease or injury can render the patient less able to compensate for hypovolaemia and can also make the interpretation of clinical information difficult. For patients with major haemorrhage or cardiac problems, the use of a pulmonary artery flotation catheter is helpful (Buchbinder and Ganz, 1976). Measurement of cardiac output and
Table I. Signs of acute blood loss Blood loss Heart rate Systolic BP Peripheral vasoconstriction Urine output Mental status
50 ml/hr Mildly anxious
1500-2000 ml 120-l 40 bpm 70-90 mmHg +++ i 50 ml/hr Anxious or confused
> 2000 ml >140bpm
Printed in Great Britain
317
Resuscitation Anne J. Sutcliffe Department
of Anaesthetics,
‘Resuscitate: revive (Sykes, 1978).
Birmingham
from unconsciousness
Accident Hospital, Birmingham,
or apparent
death
‘Shock: a term used by clinicians to describe a condition characterized by inadequate cellular perfusion and consequent failure of function of various tissues and organs’ (Hanson, 1978).
Introduction The first clinical description of shock was probably made by O’Shaughnessy in 1831. He studied cholera victims in Sunderland and described accurately and in graphic detail the clinical signs of severe shock. He also analysed the blood and excreta of cholera patients in the laboratory and concluded that the clinical state of the patients was due to loss of water and electrolytes from the blood. He suggested that these patients might be cured by ‘the injection into the veins of tepid water holding a solution of the normal salts of the blood’. This suggestion resulted in the first attempts at intravenous resuscitation. Only moribund patients were treated with intravenous fluids and most died. There were, however, a few survivors (Cosnett, 1989). In 1899, Crile showed that an intravenous infusion of warm saline reduced mortality in experimental haemorrhagic shock. During the First World War doctors began to understand the pathophysiological effects of shock and to appreciate that poor tissue perfusion caused tissue hypoxia (Runciman and Skowronski, 1984), but it was not until stored blood became available in the 1940s that clinicians were able to treat haemorrhagic shock. The value of adequate blood transfusion was demonstrated by army surgeons during the Second World War, and these surgeons continued to give large volume blood transfusions when they returned to civilian practice. The minutes of the Birmingham Accident Hospital Medical Society for 1948 record the fact that it was sometimes necessary to use two drips in order to administer sufficiently large volumes of blood with adequate speed. This policy was not adopted immediately by all doctors. As late as 1953 a standard anaesthetic textbook stated that ‘never more than 500 ml of fluid should be run in at speed under pressure’ (Lee, 1953). The need for the administration of oxygen was less well appreciated. One of the Accident Hospital Surgeons is reported to have said that ‘the value of oxygen is not known but tends to distress the patient and make him restless’! Before 1970, the adequacy of resuscitation was difficult to assess. It was possible to measure blood pressure and to estimate blood volume, but it was not possible routinely to 0 1990 Butterworth-Heinemann 0020-1383/90/050317-4
Ltd
UK
measure blood flow or assess tissue oxygenation. The introduction of the Swan-Ganz pulmonary artery flotation catheter (Swan et al., 1970), and its subsequent development to permit bedside estimation of cardiac output and oxygen delivery and uptake, have dramatically improved the clinician’s ability to resuscitate patients accurately. As resuscitation has improved, survival in the immediate post-injury period has improved. Today, most patients who reach hospital alive should survive the effects of the original injury. However, deaths still occur days or weeks after injury, usually as a result of multiple organ failure (MOF). Evidence is increasing that inadequate resuscitation may contribute to these deaths.
Pathophysiological effects of haemorrhage and hypovolaemia There are a variety of homeostatic responses to acute blood loss which have been reviewed in detail by Runciman and Skowronski (1984). They include activation of the sympathetic nervous system and release of renin, angiotensin, antidiuretic hormone and prostaglandins; all of which cause generalized vasoconstriction. Other humoral mediators such as serotonin, exert a local vasoconstrictor effect and help to stop bleeding. Still others such as components of the complement cascade and fibronectin may play a role in tissue healing. In evolutionary terms these responses are appropriate because blood flow to essential organs is preserved and therefore survival is possible if the total blood loss is not too great. If, however, the loss is great, the response becomes excessive and inappropriate because tissue oxygenation is compromised. In the presence of hypoxia, intracellular metabolism is disrupted and cell membranes cease to function normally. Numerous toxic substances including bradykinin, histamine, thromboxanes and leukotrienes are released. It is thought that these cellular toxins may play a part in the subsequent development of MOF.
Adult respiratory distress syndrome, multiple organ failure and shock years, it has been known that the Adult Respiratory Distress Syndrome (ARDS) may develop following multiple trauma or severe haemorrhage. ARDS becomes apparent z to 6 days after the primary insult. Clinical signs include dyspnoea and cyanosis. Interstitial pulmonary oedema is seen on the chest radiograph as diffuse fluffy For many
Injury: the British Journal of Accident Surgery (1990) Vol. 21/No. 5
318
opacities. Histologically, the lungs show widespread microemboli containing platelets and leucocytes (Harrison et al., 1977). Increased permeability of the pulmonary capillaries can also be demonstrated (Kreuzfelder et al., 1988). The precise cause of these pathological changes is not known, but complement activation (Hammerschmidt et al., 1980), the generation of free oxygen radicals (Baldwin et al., 1986), and the release of toxic humoral mediators (He&man et al., 1984) have all been implicated. Many of these mechanisms are initiated by shock (Runciman and Skowronski, 1984). When ARDS was first described, it was thought to be a discrete clinical entity, but increased capillary permeability also occurs in other organs. Patients with ARDS have increased glomerular permeability (Kreuzfelder et al., 1988) and may have pancreatic microvascular damage (Nicod et al., 1985) or acalculous cholecystitis (Glenn and Becker, 1982). Furthermore, following experimentally induced haemorrhage in animals, myocardial oedema (Holcroft et al., 1976), and capillary endothelial swelling in the liver and skeletal muscle (S&lag and Redl, 1985) have also been noted. It is now thought that ARDS is the pulmonary manifestation of generalized multiple organ failure resulting from systemic damage to vascular endothelia, permeability oedema and impaired oxygen availability to the mitochondria (Goris et al., 1985). As a result of improved resuscitation, MOF following major haemorrhage or multiple trauma is rare. There is, however, no room for complacency. In humans, increased glomerular permeability and pulmonary capillary permeability have been demonstrated following injury (Gosling and Sutcliffe, 1986, Kreuzfelder et al., 1988). These changes are proportional to injury severity and occur even in the presence of minor injury. It seems probable, therefore, that tissue injury can initiate the responses causing increased capillary permeability and that these responses are also induced and possibly compounded by haemorrhage. In order to minimize the effects of injury and haemorrhage, adequate resuscitation is essential. Effective resuscitation is as important for patients with minor injuries and relatively minor haemorrhage as it is for those with multiple injuries and major haemorrhage.
Sepsis in the trauma patient As has already been stated, MOF secondary to trauma and haemorrhage is rare. Most injured patients who survive long enough to reach hospital but who subsequently die, do so as a result of MOF secondary to sepsis. There is increasing evidence that bacteria from the gut are the cause of many infections suffered by injured patients. It is postulated that vasoconstriction in the splanchnic bed causes ischaemia of the. gastrointestinal mucosa which becomes permeable to pathogenic organisms and endotoxins. These enter the portal circulation and damage the Kupffer cells in the liver. These cells compromise 70 per cent of the total population of macrophages which trigger the specific immune response.
If they are damaged the patient is unable to combat infection. This subject is well reviewed by S&lag and Redl (1987). Further evidence that gut pathogens play a role in sepsis following trauma has been provided by Ledingham et al. (1988), who have shown that selective decontamination of the gut reduces the incidence of sepsis. Adequate resuscitation and prevention of severe vasoconstriction of the splanchnic mucosa should, therefore, help to reduce the incidence of infection and late MOF in trauma patients.
Diagnosis of hypovolaemia Fluid resuscitation should begin as soon as possible. In certain circumstances, it may be possible to start an intravenous infusion at the scene of the accident. If this is not possible, large-bore peripheral intravenous cannulae should be inserted as soon as the patient reaches hospital. The amount of fluid given in the first 10 min will depend on the history obtained from ambulancemen or relatives, a rapid survey of the patient noting obvious injuries and clinical signs such as pallor, confusion, the state of the peripheral veins, skin temperature, pulse rate and blood pressure. Table I summarizes the changes which occur as a progressively greater percentage of the patient’s blood volume is lost. Oxygen should also be given from the time of admission and, if necessary, the patient should be intubated and ventilated. When these life-saving measures are complete the patient should be examined in detail. Resuscitation should be guided by the injuries diagnosed and the likely blood loss associated with them (Clarke and Fisher, 1956). Initially, monitoring of pulse, blood pressure and central venous pressure will provide a crude guide to the adequacy of resuscitation. The presence of a normal pulse rate and pressures indicates only adequate volume has been given to fill the vascular space as it exists at the time of these measurements, because a normal pulse rate and blood pressure can occur in the presence of gross vasoconstriction. Clues to the degree of vasoconstriction may be obtained by monitoring skin temperature and urine output. Pressure measurements do not reflect the adequacy of blood flow or the adequacy of tissue oxygenation. Rapid capillary refill and a urine output of 50 ml/h may be used as indicators of adequate flow to the tissues. Arterial blood gas estimations showing a metabolic acidosis indicate anaerobic metabolism and tissue hypoxia. Confusion or inappropriate anxiety are often due to cerebral hypoxia. For many patients, the methods described previously will be sufficient to monitor the adequacy of resuscitation. Their interpretation depends to a certain extent on the age of the patient and pre-existing medical illnesses. Myocardial failure as a result of disease or injury can render the patient less able to compensate for hypovolaemia and can also make the interpretation of clinical information difficult. For patients with major haemorrhage or cardiac problems, the use of a pulmonary artery flotation catheter is helpful (Buchbinder and Ganz, 1976). Measurement of cardiac output and
Table I. Signs of acute blood loss Blood loss Heart rate Systolic BP Peripheral vasoconstriction Urine output Mental status
50 ml/hr Mildly anxious
1500-2000 ml 120-l 40 bpm 70-90 mmHg +++ i 50 ml/hr Anxious or confused
> 2000 ml >140bpm
