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Understanding hypovolaemic shock
Understanding hypovolaemic shock Julia Kneale
shock.
NMC* CATEGORIES *From April 1st 2002 the United Kingdom Central Council (UKCC) for nurses, midwives and health visitors was replaced by the new Nursing and Midwifery Council (NMC) although PREP categories have remained the same. This article will enable the reader to address PREP categories:
• • • •
Reducing risk. Care enhancement. Practice development. Education development.
Examples of how this may be achieved and possible evidence for your portfolio are given throughout the article. Other ways to demonstrate your professional development may be to:
• Develop a teaching programme based on the article for your ward area to deliver to colleagues and students.
• Develop guidelines for good practice on the assessment and management of patients in hypovolaemic shock.
• Use this article to reflect on other clinical patient problems that relate to the care of orthopaedic and trauma patients.
• Keep a copy of this article together with the notes you make as evidence of completing the reflection items in the text. c 2003 Elsevier Ltd. All rights reserved.
INTRODUCTION Julia Kneale BSc(Hons), RGN, WNB 219 Senior Lecturer, Department of Nursing, Faculty of Health, University of Central Lancashire, Preston, UK. Correspondence to: Julia Kneale Department of Nursing, Faculty of Health, University of Central Lancashire, Preston, PR1 2HU, UK. Tel.: +44-1772-893611; E-mail: [email protected]. uk
Shock is a term with a multitude of interpretations, when related to patients we mean the term to relate to a physiological reaction with its own cascade of events started by a seemingly minor trigger or a catastrophic event. The outcomes can be equally variable from a fast physiological stabilisation that requires no or minimal interventions, to an overwhelming reaction that can end in death. Recognising a patient in shock is a fundamental aspect of assessing the orthopaedic and trauma patient. Many patients are admitted with,
Journal of Orthopaedic Nursing (2003) 7, 207–213 ª 2003 Elsevier Ltd. All rights reserved. doi:10.1016/j.joon.2003.09.002
or because of surgery will incur a reduced circulatory volume and therefore are at risk of hypovolaemic shock. How patients are assessed and managed at this time, will determine their recovery from this potentially life threatening event. This article is a reminder of the main causes of shock, the physiological changes that occur, the specific issues related to hypovolaemic shock, patient assessment and how these inform patient care. The approach taken in this review of care relates to adult patients in shock. The stages of shock, principles of prevention, management and nursing care remain the same for children
P R O F E S S I O N A L
• Understand the causes of hypovolaemic shock and how to recognise a patient at risk. • Identify the different physiological stages of hypovolaemic shock • Support their nursing care decisions and actions relating to the patient in hypovolaemic
C O N T I N U I N G
On completion of the article the reader should be able to:
E D U C A T I O N
LEARNING OUTCOMES
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Journal of Orthopaedic Nursing
although certain aspects, such as the rates of fluid infusion and additional specific issues relating to paediatric care, need further consideration by paediatric nurses.
Table 2 Estimated blood loss from trauma Type of trauma Tibial fracture Femoral shaft fracture Abdominal trauma Thoracic trauma Pelvic fracture
C O N T I N U I N G
P R O F E S S I O N A L
E D U C A T I O N
DEFINING SHOCK Shock is defined as an acute clinical event precipitated by reduced tissue perfusion caused by reduced circulatory output, failure of the heart to pump effectively and a massive peripheral vasoconstriction. These lead to a point where the circulatory volume is insufficient to meet the oxygen and nutrient requirements of tissues. Ineffective removal of the waste products of metabolism, results in further tissue hypoxia the accumulation of metabolites, cell death, organ failure and if untreated death. The principle types of shock (Table 1) illustrate the range of causes including: an infection (septic or endotoxic shock), an antibiotic drug reaction (anaphylatic shock), a nerve injury affecting the sympathetic pathway (neurogenic shock), heart failure (cardiogenic shock) and severe blood loss (hypovolaemic or haemorrhagic shock). All these types of shock occur in trauma and orthopaedic patients, but of particular interest, is hypovolaemic shock, which results from a lack of fluid in the circulation.
Box 1 Reflection item 1 Identify a patient you have recently nursed. At which points in their care, was your patient most at risk of hypovolaemic shock? What risk factors were actually or potentially present on these occasions? 10 min
CAUSES OF HYPOVOLAEMIC SHOCK The most common form of shock seen in clinical practice is hypovolaemic shock where the reduced circulatory volume results in cir-
Blood loss (ml) 500–750 1000–1500 1500–2000 1500–2000 2500–3000
culatory failure, a drop in cardiac output and blood pressure. These lead to reduced oxygen perfusion of the brain, lungs, kidneys and other organs, creating a life-threatening situation. The reduced volume may be caused by:
• Loss of fluid from diarrhoea, vomiting,
• • • • •
thermal injuries from heat stroke or burns, excessive diuresis from diabetes mellitus. Dehydration incurred by an inadequate fluid intake. Internal bleeding from organs, arteries or veins. Collection of fluid within the body as seen in ascites and peritonitis. Extensive blood loss from trauma especially femoral and pelvic fractures (Table 2). Intra and post-operative blood loss that is not adequately or appropriately replaced.
Blood loss remains the principle cause of preventable death in trauma patients. A massive blood loss will pose a threat to the patient’s life, whether the loss is sudden from arterial trauma or slow and undetected from a retroperitoneal haemorrhage in a patient with a pelvic injury. If this blood loss is identified and interventions commenced early and effectively, the risks to the patient’s long-term health and the number of preventable deaths would be reduced. It is therefore safer to assume that all trauma patients are at risk or have hypovolaemic shock to some degree and commence appropriate intravenous fluids. Although not all patients will require large volumes of fluid replacement, it is generally thought better to err on the side of caution, as the risk of death from dehydration is generally greater than the risk of death from fluid overload (Anderson et al. 1998).
Table 1 Definitions of shock Hypovolaemic shock Cardiogenic shock Neurogenic shock Septic shock Anaphylactic shock
A reduced circulatory volume resulting in reduced cardiac output and low perfusion Arises from left ventricular failure, generally following a cardiac problem such as a myocardial infarction or heart failure Caused by the loss of sympathetic nerve activity from a disease, a drug (anaesthetic agent) or trauma (spinal cord injury) An overwhelming infection affecting the body’s ability to defend itself A severe allergic reaction resulting in circulatory collapse
Understanding hypovolaemic shock
Compensatory stage
Rapid shallow breaths (hyperventilation) Rapid thready pulse (tachycardia) Agitation, confusion, drowsiness, restlessness Peripheral vasoconstriction, pallor of skin, cold to touch Cold clammy skin
Progressive stage
Refractory stage
Reduced urine output Possibly oliguria Severe tachycardia Hypotension Notable changes in consciousness and responses to stimuli
The loss of 15–30% of the circulatory volume instigates the compensatory mechanisms and is when the first real symptoms occur.
• The lack of oxygen stimulates
•
Unconsciousness Signs of multiple organ failure
PHYSIOLOGICAL STAGES OF SHOCK
•
All patients will potentially go though the following stages of shock due to the effect of reduced circulatory volume. Early detection of the signs and symptoms at each stage (Table 3) and the implementation of appropriate treatment can prevent the patient from progressing through the four identifiable stages (Collins 2000).
Initial stage
•
The initial loss of 10–15% of the circulatory volume begins the process of deprivation of the tissue cells of oxygen. Many authors suggest that hypovolaemic shock does not develop until 15% of the volume is lost, this equates to about 750 ml.
• In the absence of oxygen the mitrochondria
•
•
use the less effective process of anaerobic rather than aerobic metabolism to produce enough adenosine triphosphate (ATP), essential to create energy in cells, thus the energy within cells is low and they cannot function effectively. The anaerobic metabolism gradually produces a build up of lactic and pyruvic acids in the cells leading to metabolic acidosis. This build up of lactic acid is harmful to the cells. It is normally removed by the circulatory system and broken down by the liver but in the absence of oxygen this cannot occur. As the cell function reduces, the membrane becomes more permeable allowing uncontrolled leakage of electrolytes and fluids in and out of the cells. The cell membrane’s sodium-potassium pump cannot function without ATP and the cell structures are damaged, leading to cellular death.
•
hyperventilation to increase the oxygen supply to the brain and to rid the body of excess carbon dioxide. This raises the pH of the blood with a compensatory respiratory alkalosis (Hand 2001) causing apparent changes in consciousness from agitation, confusion and drowsiness, to total loss of consciousness. The loss of volume reduces the cardiac output; the amount of blood ejected from the heart per minute decreases (Hand 2001). This stimulates the sympathetic branch of the autonomic nervous system, precipitating the ‘fight or flight’ response. The aortic and carotid baroreceptors that control the blood pressure detect hypotension. This precipitates the release of adrenaline and noradrenaline in an attempt to increase the rate and force of the heart contractions and vasoconstriction. This causes a tachycardia and an increase in the blood pressure, resulting in a weak, thready pulse. Although tachycardia may not be present until 30% of the circulating volume is lost (American College of Surgeons 1997). Vasoconstriction affects the blood supply to the skin and organs, concentrating the remaining blood supply to the heart and brain. The cessation of gastrointestinal function leads to the loss of bowel sounds, the sensation of nausea and possibly vomiting. The liver reacts by releasing its store of red blood cells and plasma. The reduced circulation to the kidneys and release of antidiuretic hormone (ADH) from the pituitary gland, leads to the kidneys attempting to conserve water to maintain the circulatory volume, reducing urine output and a possible oliguria. The kidneys also release rennin; this precipitates the production of angiotensin 2, a powerful vasoconstrictor. Angiotensin 2 also promotes the release of aldosterone from the adrenal glands, this results in the reabsorption of sodium in the renal tubules which in turn leads to further water retention (Hand 2001). Peripheral vasoconstriction is seen in the poor rate of capillary refill of the nail beds; the colour taking longer than two seconds to return. The skin especially on the hands and feet is cold from lack of circulating blood. The sweat glands are stimulated increasing their rate of secretion and causing the skin to be moist.
E D U C A T I O N
Few obvious symptoms present External haemorrhage may be seen.
P R O F E S S I O N A L
Initial stage
Compensatory stage
C O N T I N U I N G
Table 3 Summary of the symptoms observed at each stage
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Progressive stage Once 30–40% of the circulating volume is lost, the compensatory mechanisms begin to fail.
• The decreased cell perfusion results in sodium collecting in the cells and potassium leaks out.
C O N T I N U I N G
P R O F E S S I O N A L
E D U C A T I O N
• The continued cellular anaerobic metabolism,
•
•
•
leads to systemic metabolic acidosis, this further constricts the arteriolar and precapillary sphincters, trapping the blood within the capillaries. As a result, the hydrostatic pressure increases, which along with the histamine release, leads to the loss of fluid and protein into the surrounding tissues. This increases the concentration and viscosity of the blood. Any sustained vasoconstriction will compromise the perfusion of the vital organs and their function. The brain is affected leading to unconsciousness, the pupils dilate and are slow to react to light, the kidneys cannot function reducing the urine output to less than 20 ml/h and liver failure leads to jaundice and waste product accumulation in the blood. The gastrointestinal tract is affected by ischaemia, releasing bacteria and endotoxins into the circulation leading to sepsis, gastric ulceration and haemorrhaging. The respiratory system is affected by ischaemia of the alveolar cells resulting in their collapse. The increased permeability of the pulmonary capillaries causes pulmonary oedema. This is observed in reduced arterial oxygen level measured by pulse oximetry and increased carbon dioxide level as measured by blood gases (Hand 2001). These lead to the diagnosis of adult respiratory distress syndrome (ARDS). As the perfusion of each organ is affected, it in turn will affect the function of other organs leading to a state of multi-organ failure. The body can no longer compensate and the systolic blood pressure falls to around 90 mmHg (Porth 1998). The heart becomes ischaemic, the capillaries are more permeable and the refractory stage is reached.
Refractory stage When 40% or more of the fluid volume is lost, the state of shock is irreversible. The cell death leads Box 2 Reflection item 2 Consider the physiological stages of shock and apply these to the patients in your care. What measures are taken to prevent hypovolaemic shock developing? How are the physiological changes identified and acted upon? Which changes tend to be overlooked until a patient’s condition has deteriorated further? 30 min
to multiple organ failure and brain damage; death is imminent or will occur within hours.
MANAGING BLOOD LOSS To detect the early signs of hypovolaemic shock, the orthopaedic nurse must constantly reassess the patients’ fluid balance by maintaining accurate records of fluid input and output to detect a negative balance. This includes accurately estimating the fluid loss at the site of injury, through dressings and insensible loss and intraoperative loss plus loss via chest and wound drains. Any external bleeding is identified and direct pressure exerted where possible to stem the flow. Any estimates of blood loss are recorded, although these can be inaccurate, as a small amount of blood appears to go a long way. The use of a tourniquet is discouraged as further tissue hypoxia can cause irreversible damage to the limb. If the limb is not salvageable then a tourniquet maybe applied in the resuscitation area. When a tourniquet is applied, or a patient is admitted with a tourniquet in place, the time and duration of application are recorded. Care is taken when it is removed as the return of circulation to the distal limb along with the sudden return of toxins from the limb via the circulation, can cause an exacerbation of the patient’s condition. Any internal bleeding will need to be assessed; generally, this requires the patient to go to theatre for surgery to detect and treat the site of haemorrhage and to determine the cause. The difference between the cause and site of the haemorrhage is illustrated by a pelvic fracture, where there is blood loss from the bone but the more significant loss can be from the resultant soft tissue trauma. For example, a deceleration injury can separate the pelvic organs from their arterial blood supply potentially resulting in bruising in the buttocks or scrotum, a retroperitoneal haematoma from an aortic rupture or leg ischaemia from a damaged iliac artery. A patient can rapidly loose 3–4 litres of blood into the abdominal cavity, presenting with abdominal or back pain, a tender abdominal mass and the absence of bowel sounds. The resultant hypovolaemic shock requires emergency treatment to stabilise the patient prior to exploration and suturing of the affected blood vessels and organs, the bone injury being stabilised initially using an emergency external fixation technique, with later internal or external fixation being carried out once the patient is haemodynamically stable.
FLUID REPLACEMENT Treatment of hypovolaemic shock involves the rapid infusion of adequate volumes of appro-
Understanding hypovolaemic shock
Identify a previously hypovolaemic patient from your clinical area and review their medical and nursing records. Are there any physiological indicators of hypovolaemic shock in the records? If present, how were these recognised and patient care managed as a result? 30 min
PATIENT CARE POINTS The aims of patient management and care are to restore the circulatory volume, thus ensuring:
• an appropriate oxygen and nutrient supply to the tissues,
• waste products from the cells are removed and
• normal cellular activity and organ function is restored. These aims are achieved with continual assessment of the patient to identify the early stages of shock and the changes occurring with treatment. Regular physical observations, initially every 15 min, give immediate indicators of changes. Understanding the physiological changes enables early detection and initiation of treatment to manage or correct these. The initial hypoxia from the reduced circulatory volume stimulates the respiratory centre. This increases the respiratory rate and depth to twice the normal tidal volume in an attempt to improve circulating oxygen levels. As the stages of shock progress, the respiratory muscles tire and the patient begins to hyperventilate with rapid, shallow breaths. Ideally, the patient should be on 100% oxygen given via a non-rebreathe mask. Humidifying the oxygen increases expectoration of
P R O F E S S I O N A L
Box 3 1 Reflection item 3 1
E D U C A T I O N
still only increase the circulatory volume not the oxygen supply to the tissues. Human albumin will expand the plasma volume and increase it further by drawing additional fluid from the interstitial spaces risking further dehydration and tissue hypoxia. There has been much debate about the role of albumin for volume replacement; the Cochrane Group of Albumin Reviewers (1998) suggest there is a lack of significant evidence to support its use in practice. The patient needs to be closely monitored as rapid fluid replacement can carry its own risks especially for the elderly and those with pre-existing heart disease.
C O N T I N U I N G
priate fluids. Accurate fluid loss and infusion records are essential for monitoring the patient’s response to fluid replacement. To prevent the progression of shock, measures are needed to treat the cause, prevent further blood loss and replace the circulating volume. Two large bore cannulae are inserted, ideally in the anti-cubital fossa veins for the rapid infusion of large volumes of fluid; at least two litres initially. If insertion of a peripheral line is difficult due to vasoconstriction, a central line is required. The transfusion of whole blood is ideal as this increases the circulatory volume. The oxygen carrying capacity provides a good supply of oxygen and nutrients to the tissues and increases available clotting factors. Consequently, two to three units of blood are cross matched and saved for patients who are expected to loose large amounts of blood in theatre and up to six units are cross matched for a seriously affected patient. In an emergency, if the risks of continued hypovolaemia outweigh the potential risks of reactions and later problems with cross matching, a transfusion of O negative blood is given. Whole blood contains the red and white blood cells, platelets, plasma and electrolytes, making it ideal for replacing fluid, carrying oxygen and nutrients. Units of packed cells are of less value, although they may contain the same volume of red blood cells as a unit of whole blood, these are in concentration with minimal plasma fluid, as a result an infusion of packed cells will further concentrate the circulating blood rather than expanding the over all volume. Plasma is the opposite, as it contains water, electrolytes, proteins, and coagulation factors, it will increase the circulating volume but the lack of red blood cells means the oxygen carrying capacity is severely diminished. Colloid and crystalloid fluids increase the volume but not the oxygen capacity, further diluting the blood. This is seen by changes to the haemoglobin (ideally 12.5–14 g/100 ml) and haematocrit (ideally above 30%) levels. Crystalloid solutions such as saline and Hartmann’s solution are generally considered more effective than colloid solutions such as Haemaccel although none are problem free. In hypovolaemic shock, saline will give a temporary increase in the circulatory volume but the majority will be absorbed from the circulatory system into the extracellular fluid (outside the cells) across the capillary membrane and from here into the cells as intracellular fluid. Saline is therefore useful for replacing fluid loss but in the case of large volume loss, this transfer of solution will not adequately replace the circulatory volume. Hartmann’s solution is similar to plasma and is useful to correct metabolic acidosis but it will
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Table 4 Laboratory and diagnostic tests for hypovolaemic shock
C O N T I N U I N G
P R O F E S S I O N A L
E D U C A T I O N
Arterial blood gases Serum electrolyes Blood glucose concentration Enzyme levels to indicate tissue damage: Creatinine phosphokinase (CPK), serum glutamate oxaloacetate transaminase (SGOT), amylase Renal and hepatic function tests: serum urea nitrogen, creatinine, bilirubin and ammonia For covert bleeding: full blood count and coagulation studies
secretions and prevents damage to the bronchial mucosa and cilia. Monitoring of the respiratory rate, oxygen saturation level and blood gas measurements are essential as indicators of oxygen circulation and perfusion (Table 4). In severe cases respiratory ventilation is required. Emergency equipment should be available in case the lung capacity is restricted, for instance, by:
• a haemopneumothorax, significant blood loss •
•
into the pleural space usually from an open injury, requiring a chest drain, a tension pneumothorax, air in the pleural cavity from a blunt or penetrating chest injury, indicating the need for immediate decompression by the rapid insertion of a needle in the cavity followed by an underwater sealed chest drain rib fractures causing a flail chest necessitating the patient to be ventilated.
Cardiac monitoring is advised to identify any cardiac arrhythmias early. A tachycardia is present, with peripheral pulses being weak and thready from the reduced peripheral flow. Resuscitation equipment must be ready in case of need. The blood pressure is initially normal prior to the compensatory mechanisms starting. The fall in blood pressure relates to a drop in the systolic pressure from the reduced cardiac stroke volume, while the diastolic pressure remains normal due to peripheral vasoconstriction giving a narrower systolic–diastolic range. However, as the circulatory volume decreases, the peripheral blood pressure readings become less accurate and measurements, such as central venous pressure readings, are required. If a patient requires adrenaline, noradrenaline or dopamine to support their circulatory system and blood pressure, they should be transferred to an intensive care or high dependency unit. Core and peripheral temperature observations are required as the loss of blood leads to a lower temperature from reduced circulatory heat, with the potential for severe blood loss to lead to hypothermia. Rapid rewarming is avoided as this risks peripheral vasodilation, affecting the physiological compensatory mechanism. Instead, gradual rewarming and the use of warmed intravenous fluids when large volumes of fluid replacement are required, can reduce further heat loss.
Most drugs that need to be given are administered intravenously to increase their rate of absorption, with the exception of adrenaline, which if required, is given intramuscularly. In the early stages of shock, as the central nervous system is stimulated, this leads to an increased blood supply to the main organs and increased sweat gland activity making the skin cool, pale and clammy. The sustained peripheral vasoconstriction makes the skin appear cyanotic, cold and mottled. As the skin is also dehydrated, there is poor skin turgor while the mucous membranes are dry and pale from the reduced blood supply. These observations are often the initial signs noted by practitioners. Hourly monitoring of fluid balance is essential. Ideally a urethral catheter is inserted but this must only be done when any trauma to the urethra, bladder or perineum has been discounted. If a urethral catheter is contraindicated, a suprapubic catheter may be used. The urine output needs to be greater than 0.5 ml/kg/h or greater than 20 ml/h, less than this indicates reduced renal perfusion. The specific gravity (osmolarity) of the urine increases as the urine concentration increases due to the continued excretion of waste products and fluid retention. As the stages of shock progress, the kidneys excrete fewer waste products and as the volume is also low, the relative concentration remains stable or dilutes because the kidneys are unable to concentrate the urine. The patient’s level of consciousness alters because of the inadequate oxygen supply to the brain cells. Initially there are subtle changes generally presented as restlessness, agitation and irritability. As the cerebral ischemia increases confusion, personality changes, paranoia, poor judgement, loss of memory and altered sleep patterns occur. As the stages of shock progress the patient’s responses to verbal stimulation reduces. The nurse needs to assess their responses to pain; this will also decrease until there is no response to any stimuli. Using the Glasgow Coma Scale enables the early detection of these changes. As the patient is nursed supine, there is a risk of fluid accumulation in the lungs and of pressure sores developing from reduced tissue perfusion and inadequate change of position. Regular pressure area care with correct moving
Understanding hypovolaemic shock
American College of Surgeons Committee on Trauma 1997 Advanced Trauma Life Support programme: student course manual Chicago, ACSCT Anderson ID, Woodford M, de Dombal FT, Irving M (1998) Retrospective study of 100 trauma deaths from injury in England and Wales British. Med. J. 296: 1305–1308 Cochrane Group of Albumin Reviewers (1998) Human albumin administration in critically ill patients. Br Med J 317: 235–240 Collins T (2000) Understanding shock. Nursing Standard 14(49): 35–41 Hand H (2001) Shock. Nursing Standard 15(48): 45–52, pp. 54–55 Porth C (1998) Pathophysiology: concepts of altered health states Lippincott, Philadelphia
E D U C A T I O N
The need for nurses to understand the causes and physiological changes of shock along with how these relate to nursing actions is essential, if appropriate care is to be given. Although this life threatening condition is more often thought of as a trauma related problem, hypovolaemic shock is
REFERENCES
P R O F E S S I O N A L
CONCLUSION
also observed in orthopaedic patients after elective surgery, especially if their care does not include appropriate fluid replacement or haemorrhaging continues after surgery.
C O N T I N U I N G
and handling to prevent fracture site movement is vital. It is advisable for patients in shock to be nilby-mouth in case they need surgery and to reduce their risk of aspiration. Regular mouth care increases the patient’s comfort. Psychological care is needed, especially when the patient is hypoxic, to support both the patient and their relatives. Good verbal communication skills and the provision of information relating to the affects and implications of their injury, condition and nursing care are essential.
213
shock.
NMC* CATEGORIES *From April 1st 2002 the United Kingdom Central Council (UKCC) for nurses, midwives and health visitors was replaced by the new Nursing and Midwifery Council (NMC) although PREP categories have remained the same. This article will enable the reader to address PREP categories:
• • • •
Reducing risk. Care enhancement. Practice development. Education development.
Examples of how this may be achieved and possible evidence for your portfolio are given throughout the article. Other ways to demonstrate your professional development may be to:
• Develop a teaching programme based on the article for your ward area to deliver to colleagues and students.
• Develop guidelines for good practice on the assessment and management of patients in hypovolaemic shock.
• Use this article to reflect on other clinical patient problems that relate to the care of orthopaedic and trauma patients.
• Keep a copy of this article together with the notes you make as evidence of completing the reflection items in the text. c 2003 Elsevier Ltd. All rights reserved.
INTRODUCTION Julia Kneale BSc(Hons), RGN, WNB 219 Senior Lecturer, Department of Nursing, Faculty of Health, University of Central Lancashire, Preston, UK. Correspondence to: Julia Kneale Department of Nursing, Faculty of Health, University of Central Lancashire, Preston, PR1 2HU, UK. Tel.: +44-1772-893611; E-mail: [email protected]. uk
Shock is a term with a multitude of interpretations, when related to patients we mean the term to relate to a physiological reaction with its own cascade of events started by a seemingly minor trigger or a catastrophic event. The outcomes can be equally variable from a fast physiological stabilisation that requires no or minimal interventions, to an overwhelming reaction that can end in death. Recognising a patient in shock is a fundamental aspect of assessing the orthopaedic and trauma patient. Many patients are admitted with,
Journal of Orthopaedic Nursing (2003) 7, 207–213 ª 2003 Elsevier Ltd. All rights reserved. doi:10.1016/j.joon.2003.09.002
or because of surgery will incur a reduced circulatory volume and therefore are at risk of hypovolaemic shock. How patients are assessed and managed at this time, will determine their recovery from this potentially life threatening event. This article is a reminder of the main causes of shock, the physiological changes that occur, the specific issues related to hypovolaemic shock, patient assessment and how these inform patient care. The approach taken in this review of care relates to adult patients in shock. The stages of shock, principles of prevention, management and nursing care remain the same for children
P R O F E S S I O N A L
• Understand the causes of hypovolaemic shock and how to recognise a patient at risk. • Identify the different physiological stages of hypovolaemic shock • Support their nursing care decisions and actions relating to the patient in hypovolaemic
C O N T I N U I N G
On completion of the article the reader should be able to:
E D U C A T I O N
LEARNING OUTCOMES
208
Journal of Orthopaedic Nursing
although certain aspects, such as the rates of fluid infusion and additional specific issues relating to paediatric care, need further consideration by paediatric nurses.
Table 2 Estimated blood loss from trauma Type of trauma Tibial fracture Femoral shaft fracture Abdominal trauma Thoracic trauma Pelvic fracture
C O N T I N U I N G
P R O F E S S I O N A L
E D U C A T I O N
DEFINING SHOCK Shock is defined as an acute clinical event precipitated by reduced tissue perfusion caused by reduced circulatory output, failure of the heart to pump effectively and a massive peripheral vasoconstriction. These lead to a point where the circulatory volume is insufficient to meet the oxygen and nutrient requirements of tissues. Ineffective removal of the waste products of metabolism, results in further tissue hypoxia the accumulation of metabolites, cell death, organ failure and if untreated death. The principle types of shock (Table 1) illustrate the range of causes including: an infection (septic or endotoxic shock), an antibiotic drug reaction (anaphylatic shock), a nerve injury affecting the sympathetic pathway (neurogenic shock), heart failure (cardiogenic shock) and severe blood loss (hypovolaemic or haemorrhagic shock). All these types of shock occur in trauma and orthopaedic patients, but of particular interest, is hypovolaemic shock, which results from a lack of fluid in the circulation.
Box 1 Reflection item 1 Identify a patient you have recently nursed. At which points in their care, was your patient most at risk of hypovolaemic shock? What risk factors were actually or potentially present on these occasions? 10 min
CAUSES OF HYPOVOLAEMIC SHOCK The most common form of shock seen in clinical practice is hypovolaemic shock where the reduced circulatory volume results in cir-
Blood loss (ml) 500–750 1000–1500 1500–2000 1500–2000 2500–3000
culatory failure, a drop in cardiac output and blood pressure. These lead to reduced oxygen perfusion of the brain, lungs, kidneys and other organs, creating a life-threatening situation. The reduced volume may be caused by:
• Loss of fluid from diarrhoea, vomiting,
• • • • •
thermal injuries from heat stroke or burns, excessive diuresis from diabetes mellitus. Dehydration incurred by an inadequate fluid intake. Internal bleeding from organs, arteries or veins. Collection of fluid within the body as seen in ascites and peritonitis. Extensive blood loss from trauma especially femoral and pelvic fractures (Table 2). Intra and post-operative blood loss that is not adequately or appropriately replaced.
Blood loss remains the principle cause of preventable death in trauma patients. A massive blood loss will pose a threat to the patient’s life, whether the loss is sudden from arterial trauma or slow and undetected from a retroperitoneal haemorrhage in a patient with a pelvic injury. If this blood loss is identified and interventions commenced early and effectively, the risks to the patient’s long-term health and the number of preventable deaths would be reduced. It is therefore safer to assume that all trauma patients are at risk or have hypovolaemic shock to some degree and commence appropriate intravenous fluids. Although not all patients will require large volumes of fluid replacement, it is generally thought better to err on the side of caution, as the risk of death from dehydration is generally greater than the risk of death from fluid overload (Anderson et al. 1998).
Table 1 Definitions of shock Hypovolaemic shock Cardiogenic shock Neurogenic shock Septic shock Anaphylactic shock
A reduced circulatory volume resulting in reduced cardiac output and low perfusion Arises from left ventricular failure, generally following a cardiac problem such as a myocardial infarction or heart failure Caused by the loss of sympathetic nerve activity from a disease, a drug (anaesthetic agent) or trauma (spinal cord injury) An overwhelming infection affecting the body’s ability to defend itself A severe allergic reaction resulting in circulatory collapse
Understanding hypovolaemic shock
Compensatory stage
Rapid shallow breaths (hyperventilation) Rapid thready pulse (tachycardia) Agitation, confusion, drowsiness, restlessness Peripheral vasoconstriction, pallor of skin, cold to touch Cold clammy skin
Progressive stage
Refractory stage
Reduced urine output Possibly oliguria Severe tachycardia Hypotension Notable changes in consciousness and responses to stimuli
The loss of 15–30% of the circulatory volume instigates the compensatory mechanisms and is when the first real symptoms occur.
• The lack of oxygen stimulates
•
Unconsciousness Signs of multiple organ failure
PHYSIOLOGICAL STAGES OF SHOCK
•
All patients will potentially go though the following stages of shock due to the effect of reduced circulatory volume. Early detection of the signs and symptoms at each stage (Table 3) and the implementation of appropriate treatment can prevent the patient from progressing through the four identifiable stages (Collins 2000).
Initial stage
•
The initial loss of 10–15% of the circulatory volume begins the process of deprivation of the tissue cells of oxygen. Many authors suggest that hypovolaemic shock does not develop until 15% of the volume is lost, this equates to about 750 ml.
• In the absence of oxygen the mitrochondria
•
•
use the less effective process of anaerobic rather than aerobic metabolism to produce enough adenosine triphosphate (ATP), essential to create energy in cells, thus the energy within cells is low and they cannot function effectively. The anaerobic metabolism gradually produces a build up of lactic and pyruvic acids in the cells leading to metabolic acidosis. This build up of lactic acid is harmful to the cells. It is normally removed by the circulatory system and broken down by the liver but in the absence of oxygen this cannot occur. As the cell function reduces, the membrane becomes more permeable allowing uncontrolled leakage of electrolytes and fluids in and out of the cells. The cell membrane’s sodium-potassium pump cannot function without ATP and the cell structures are damaged, leading to cellular death.
•
hyperventilation to increase the oxygen supply to the brain and to rid the body of excess carbon dioxide. This raises the pH of the blood with a compensatory respiratory alkalosis (Hand 2001) causing apparent changes in consciousness from agitation, confusion and drowsiness, to total loss of consciousness. The loss of volume reduces the cardiac output; the amount of blood ejected from the heart per minute decreases (Hand 2001). This stimulates the sympathetic branch of the autonomic nervous system, precipitating the ‘fight or flight’ response. The aortic and carotid baroreceptors that control the blood pressure detect hypotension. This precipitates the release of adrenaline and noradrenaline in an attempt to increase the rate and force of the heart contractions and vasoconstriction. This causes a tachycardia and an increase in the blood pressure, resulting in a weak, thready pulse. Although tachycardia may not be present until 30% of the circulating volume is lost (American College of Surgeons 1997). Vasoconstriction affects the blood supply to the skin and organs, concentrating the remaining blood supply to the heart and brain. The cessation of gastrointestinal function leads to the loss of bowel sounds, the sensation of nausea and possibly vomiting. The liver reacts by releasing its store of red blood cells and plasma. The reduced circulation to the kidneys and release of antidiuretic hormone (ADH) from the pituitary gland, leads to the kidneys attempting to conserve water to maintain the circulatory volume, reducing urine output and a possible oliguria. The kidneys also release rennin; this precipitates the production of angiotensin 2, a powerful vasoconstrictor. Angiotensin 2 also promotes the release of aldosterone from the adrenal glands, this results in the reabsorption of sodium in the renal tubules which in turn leads to further water retention (Hand 2001). Peripheral vasoconstriction is seen in the poor rate of capillary refill of the nail beds; the colour taking longer than two seconds to return. The skin especially on the hands and feet is cold from lack of circulating blood. The sweat glands are stimulated increasing their rate of secretion and causing the skin to be moist.
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Few obvious symptoms present External haemorrhage may be seen.
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Initial stage
Compensatory stage
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Table 3 Summary of the symptoms observed at each stage
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Progressive stage Once 30–40% of the circulating volume is lost, the compensatory mechanisms begin to fail.
• The decreased cell perfusion results in sodium collecting in the cells and potassium leaks out.
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• The continued cellular anaerobic metabolism,
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leads to systemic metabolic acidosis, this further constricts the arteriolar and precapillary sphincters, trapping the blood within the capillaries. As a result, the hydrostatic pressure increases, which along with the histamine release, leads to the loss of fluid and protein into the surrounding tissues. This increases the concentration and viscosity of the blood. Any sustained vasoconstriction will compromise the perfusion of the vital organs and their function. The brain is affected leading to unconsciousness, the pupils dilate and are slow to react to light, the kidneys cannot function reducing the urine output to less than 20 ml/h and liver failure leads to jaundice and waste product accumulation in the blood. The gastrointestinal tract is affected by ischaemia, releasing bacteria and endotoxins into the circulation leading to sepsis, gastric ulceration and haemorrhaging. The respiratory system is affected by ischaemia of the alveolar cells resulting in their collapse. The increased permeability of the pulmonary capillaries causes pulmonary oedema. This is observed in reduced arterial oxygen level measured by pulse oximetry and increased carbon dioxide level as measured by blood gases (Hand 2001). These lead to the diagnosis of adult respiratory distress syndrome (ARDS). As the perfusion of each organ is affected, it in turn will affect the function of other organs leading to a state of multi-organ failure. The body can no longer compensate and the systolic blood pressure falls to around 90 mmHg (Porth 1998). The heart becomes ischaemic, the capillaries are more permeable and the refractory stage is reached.
Refractory stage When 40% or more of the fluid volume is lost, the state of shock is irreversible. The cell death leads Box 2 Reflection item 2 Consider the physiological stages of shock and apply these to the patients in your care. What measures are taken to prevent hypovolaemic shock developing? How are the physiological changes identified and acted upon? Which changes tend to be overlooked until a patient’s condition has deteriorated further? 30 min
to multiple organ failure and brain damage; death is imminent or will occur within hours.
MANAGING BLOOD LOSS To detect the early signs of hypovolaemic shock, the orthopaedic nurse must constantly reassess the patients’ fluid balance by maintaining accurate records of fluid input and output to detect a negative balance. This includes accurately estimating the fluid loss at the site of injury, through dressings and insensible loss and intraoperative loss plus loss via chest and wound drains. Any external bleeding is identified and direct pressure exerted where possible to stem the flow. Any estimates of blood loss are recorded, although these can be inaccurate, as a small amount of blood appears to go a long way. The use of a tourniquet is discouraged as further tissue hypoxia can cause irreversible damage to the limb. If the limb is not salvageable then a tourniquet maybe applied in the resuscitation area. When a tourniquet is applied, or a patient is admitted with a tourniquet in place, the time and duration of application are recorded. Care is taken when it is removed as the return of circulation to the distal limb along with the sudden return of toxins from the limb via the circulation, can cause an exacerbation of the patient’s condition. Any internal bleeding will need to be assessed; generally, this requires the patient to go to theatre for surgery to detect and treat the site of haemorrhage and to determine the cause. The difference between the cause and site of the haemorrhage is illustrated by a pelvic fracture, where there is blood loss from the bone but the more significant loss can be from the resultant soft tissue trauma. For example, a deceleration injury can separate the pelvic organs from their arterial blood supply potentially resulting in bruising in the buttocks or scrotum, a retroperitoneal haematoma from an aortic rupture or leg ischaemia from a damaged iliac artery. A patient can rapidly loose 3–4 litres of blood into the abdominal cavity, presenting with abdominal or back pain, a tender abdominal mass and the absence of bowel sounds. The resultant hypovolaemic shock requires emergency treatment to stabilise the patient prior to exploration and suturing of the affected blood vessels and organs, the bone injury being stabilised initially using an emergency external fixation technique, with later internal or external fixation being carried out once the patient is haemodynamically stable.
FLUID REPLACEMENT Treatment of hypovolaemic shock involves the rapid infusion of adequate volumes of appro-
Understanding hypovolaemic shock
Identify a previously hypovolaemic patient from your clinical area and review their medical and nursing records. Are there any physiological indicators of hypovolaemic shock in the records? If present, how were these recognised and patient care managed as a result? 30 min
PATIENT CARE POINTS The aims of patient management and care are to restore the circulatory volume, thus ensuring:
• an appropriate oxygen and nutrient supply to the tissues,
• waste products from the cells are removed and
• normal cellular activity and organ function is restored. These aims are achieved with continual assessment of the patient to identify the early stages of shock and the changes occurring with treatment. Regular physical observations, initially every 15 min, give immediate indicators of changes. Understanding the physiological changes enables early detection and initiation of treatment to manage or correct these. The initial hypoxia from the reduced circulatory volume stimulates the respiratory centre. This increases the respiratory rate and depth to twice the normal tidal volume in an attempt to improve circulating oxygen levels. As the stages of shock progress, the respiratory muscles tire and the patient begins to hyperventilate with rapid, shallow breaths. Ideally, the patient should be on 100% oxygen given via a non-rebreathe mask. Humidifying the oxygen increases expectoration of
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Box 3 1 Reflection item 3 1
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still only increase the circulatory volume not the oxygen supply to the tissues. Human albumin will expand the plasma volume and increase it further by drawing additional fluid from the interstitial spaces risking further dehydration and tissue hypoxia. There has been much debate about the role of albumin for volume replacement; the Cochrane Group of Albumin Reviewers (1998) suggest there is a lack of significant evidence to support its use in practice. The patient needs to be closely monitored as rapid fluid replacement can carry its own risks especially for the elderly and those with pre-existing heart disease.
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priate fluids. Accurate fluid loss and infusion records are essential for monitoring the patient’s response to fluid replacement. To prevent the progression of shock, measures are needed to treat the cause, prevent further blood loss and replace the circulating volume. Two large bore cannulae are inserted, ideally in the anti-cubital fossa veins for the rapid infusion of large volumes of fluid; at least two litres initially. If insertion of a peripheral line is difficult due to vasoconstriction, a central line is required. The transfusion of whole blood is ideal as this increases the circulatory volume. The oxygen carrying capacity provides a good supply of oxygen and nutrients to the tissues and increases available clotting factors. Consequently, two to three units of blood are cross matched and saved for patients who are expected to loose large amounts of blood in theatre and up to six units are cross matched for a seriously affected patient. In an emergency, if the risks of continued hypovolaemia outweigh the potential risks of reactions and later problems with cross matching, a transfusion of O negative blood is given. Whole blood contains the red and white blood cells, platelets, plasma and electrolytes, making it ideal for replacing fluid, carrying oxygen and nutrients. Units of packed cells are of less value, although they may contain the same volume of red blood cells as a unit of whole blood, these are in concentration with minimal plasma fluid, as a result an infusion of packed cells will further concentrate the circulating blood rather than expanding the over all volume. Plasma is the opposite, as it contains water, electrolytes, proteins, and coagulation factors, it will increase the circulating volume but the lack of red blood cells means the oxygen carrying capacity is severely diminished. Colloid and crystalloid fluids increase the volume but not the oxygen capacity, further diluting the blood. This is seen by changes to the haemoglobin (ideally 12.5–14 g/100 ml) and haematocrit (ideally above 30%) levels. Crystalloid solutions such as saline and Hartmann’s solution are generally considered more effective than colloid solutions such as Haemaccel although none are problem free. In hypovolaemic shock, saline will give a temporary increase in the circulatory volume but the majority will be absorbed from the circulatory system into the extracellular fluid (outside the cells) across the capillary membrane and from here into the cells as intracellular fluid. Saline is therefore useful for replacing fluid loss but in the case of large volume loss, this transfer of solution will not adequately replace the circulatory volume. Hartmann’s solution is similar to plasma and is useful to correct metabolic acidosis but it will
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Table 4 Laboratory and diagnostic tests for hypovolaemic shock
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Arterial blood gases Serum electrolyes Blood glucose concentration Enzyme levels to indicate tissue damage: Creatinine phosphokinase (CPK), serum glutamate oxaloacetate transaminase (SGOT), amylase Renal and hepatic function tests: serum urea nitrogen, creatinine, bilirubin and ammonia For covert bleeding: full blood count and coagulation studies
secretions and prevents damage to the bronchial mucosa and cilia. Monitoring of the respiratory rate, oxygen saturation level and blood gas measurements are essential as indicators of oxygen circulation and perfusion (Table 4). In severe cases respiratory ventilation is required. Emergency equipment should be available in case the lung capacity is restricted, for instance, by:
• a haemopneumothorax, significant blood loss •
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into the pleural space usually from an open injury, requiring a chest drain, a tension pneumothorax, air in the pleural cavity from a blunt or penetrating chest injury, indicating the need for immediate decompression by the rapid insertion of a needle in the cavity followed by an underwater sealed chest drain rib fractures causing a flail chest necessitating the patient to be ventilated.
Cardiac monitoring is advised to identify any cardiac arrhythmias early. A tachycardia is present, with peripheral pulses being weak and thready from the reduced peripheral flow. Resuscitation equipment must be ready in case of need. The blood pressure is initially normal prior to the compensatory mechanisms starting. The fall in blood pressure relates to a drop in the systolic pressure from the reduced cardiac stroke volume, while the diastolic pressure remains normal due to peripheral vasoconstriction giving a narrower systolic–diastolic range. However, as the circulatory volume decreases, the peripheral blood pressure readings become less accurate and measurements, such as central venous pressure readings, are required. If a patient requires adrenaline, noradrenaline or dopamine to support their circulatory system and blood pressure, they should be transferred to an intensive care or high dependency unit. Core and peripheral temperature observations are required as the loss of blood leads to a lower temperature from reduced circulatory heat, with the potential for severe blood loss to lead to hypothermia. Rapid rewarming is avoided as this risks peripheral vasodilation, affecting the physiological compensatory mechanism. Instead, gradual rewarming and the use of warmed intravenous fluids when large volumes of fluid replacement are required, can reduce further heat loss.
Most drugs that need to be given are administered intravenously to increase their rate of absorption, with the exception of adrenaline, which if required, is given intramuscularly. In the early stages of shock, as the central nervous system is stimulated, this leads to an increased blood supply to the main organs and increased sweat gland activity making the skin cool, pale and clammy. The sustained peripheral vasoconstriction makes the skin appear cyanotic, cold and mottled. As the skin is also dehydrated, there is poor skin turgor while the mucous membranes are dry and pale from the reduced blood supply. These observations are often the initial signs noted by practitioners. Hourly monitoring of fluid balance is essential. Ideally a urethral catheter is inserted but this must only be done when any trauma to the urethra, bladder or perineum has been discounted. If a urethral catheter is contraindicated, a suprapubic catheter may be used. The urine output needs to be greater than 0.5 ml/kg/h or greater than 20 ml/h, less than this indicates reduced renal perfusion. The specific gravity (osmolarity) of the urine increases as the urine concentration increases due to the continued excretion of waste products and fluid retention. As the stages of shock progress, the kidneys excrete fewer waste products and as the volume is also low, the relative concentration remains stable or dilutes because the kidneys are unable to concentrate the urine. The patient’s level of consciousness alters because of the inadequate oxygen supply to the brain cells. Initially there are subtle changes generally presented as restlessness, agitation and irritability. As the cerebral ischemia increases confusion, personality changes, paranoia, poor judgement, loss of memory and altered sleep patterns occur. As the stages of shock progress the patient’s responses to verbal stimulation reduces. The nurse needs to assess their responses to pain; this will also decrease until there is no response to any stimuli. Using the Glasgow Coma Scale enables the early detection of these changes. As the patient is nursed supine, there is a risk of fluid accumulation in the lungs and of pressure sores developing from reduced tissue perfusion and inadequate change of position. Regular pressure area care with correct moving
Understanding hypovolaemic shock
American College of Surgeons Committee on Trauma 1997 Advanced Trauma Life Support programme: student course manual Chicago, ACSCT Anderson ID, Woodford M, de Dombal FT, Irving M (1998) Retrospective study of 100 trauma deaths from injury in England and Wales British. Med. J. 296: 1305–1308 Cochrane Group of Albumin Reviewers (1998) Human albumin administration in critically ill patients. Br Med J 317: 235–240 Collins T (2000) Understanding shock. Nursing Standard 14(49): 35–41 Hand H (2001) Shock. Nursing Standard 15(48): 45–52, pp. 54–55 Porth C (1998) Pathophysiology: concepts of altered health states Lippincott, Philadelphia
E D U C A T I O N
The need for nurses to understand the causes and physiological changes of shock along with how these relate to nursing actions is essential, if appropriate care is to be given. Although this life threatening condition is more often thought of as a trauma related problem, hypovolaemic shock is
REFERENCES
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CONCLUSION
also observed in orthopaedic patients after elective surgery, especially if their care does not include appropriate fluid replacement or haemorrhaging continues after surgery.
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and handling to prevent fracture site movement is vital. It is advisable for patients in shock to be nilby-mouth in case they need surgery and to reduce their risk of aspiration. Regular mouth care increases the patient’s comfort. Psychological care is needed, especially when the patient is hypoxic, to support both the patient and their relatives. Good verbal communication skills and the provision of information relating to the affects and implications of their injury, condition and nursing care are essential.
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