(p. 95) Circulatory assessment 

Conscious level

Conscious level is a useful bedside marker of adequate cerebral perfusion and tissue oxygenation, and is often the first and most obvious thing apparent about a patient from the end of the bed. By definition, a fully alert and orientated patient must have a sufficient cardiac output to perfuse the cerebral cortex appropriately. In normal circumstances, cerebral autoregulation ensures a steady cerebral perfusion pressure with changes in blood pressure. However, this process will fail at extremes of range and is also affected by traumatic brain injury.

As cerebral hypoxia increases the level of consciousness will alter, beginning with anxiety, confusion, and agitation, and leading to aggression or combativeness and, if untreated, eventually to coma and death. Focal neurological changes, abnormal posturing, and signs of seizures may also occur.

The level of consciousness may also be affected in patients with a primary brain injury or by drugs (such as opiates or sedatives), thereby preventing further interpretation of the conscious level in relation to the presence, or absence, of shock.

Respiratory rate

The respiratory rate should be measured on arrival and at regular intervals during the initial assessment. This should be done by an observer counting the rate, as bedside physiological monitors that allow continuous respiratory rate measurement by way of transthoracic electrical impedance may give inaccurate results or fail to measure at all, especially where respiratory effort is poor or thoracic injury interferes.

The respiratory rate increases in response to reduced tissue oxygenation due to shock. In adults, a respiratory rate >20 breaths/min is considered abnormal. In children the normal range varies with age as shown in Table 7.1.

The respiratory rate can also be affected by drugs or toxins, or by intrathoracic injury. Tachypnoea may result from pneumothorax or haemothorax, as well as anxiety and pain.

Skin colour and capillary refill

Patients with hypovolaemic shock typically exhibit pale, cool, and clammy skin due to peripheral vasoconstriction although skin may remain warm and vasodilated in sepsis.

Capillary refill time testing is a simple estimate of skin perfusion. This is performed by gentle compression of the skin for 5 s followed by measuring the time in seconds before normal colour returns once this pressure is released. Normal capillary refill time should be less than 2 s. The test is best performed in central areas of the body such as the sternum, in order to minimize the effects of cold on the peripheral circulation.

Heart rate and pulse volume

One of the earliest signs of shock is a relative tachycardia. A heart rate above 90–100/min in an adult may represent shock. Hypovolaemic shock usually presents with a weaker, thready pulse felt as peripheral perfusion diminishes. Septic shock may present with a bounding pulse.

In children, the upper limit of normal heart rate differs with age as shown in Table 7.2.

However, an increased heart rate is an unreliable measure of shock. Tachycardia may have several other causes, including pain and anxiety, and is not always present in significant shock, for example, in young fit patients, those on drugs such as ß–blockers or the elderly.

Pulse points

The traditional view that various pulse points equate to certain systolic blood pressure values has a poor evidence base. However, the presence of a radial pulse does suggest that perfusion is at least sufficient to reach the peripheral circulation and, by implication, organs such as the brain, heart, and kidneys. Vascular injury, such as traumatic arterial transection may affect distal pulses and will therefore prevent any useful estimation of blood pressure in this way.

(p. 97) Pulse points should not be used in isolation when estimating blood pressure or for detecting the presence, or absence, of shock.

Blood pressure

Non-invasive blood pressure (NIBP) monitoring should be carried out with appropriate measurement intervals depending upon the clinical situation. An automated oscillometric system produces numerical values for the systolic, diastolic and mean arterial pressures during a microprocessor controlled sequence of inflation and deflation of the pressure cuff. Failure to measure or false readings can be caused by an incorrectly-sized cuff or by the presence of irregular cardiac rhythms, such as atrial fibrillation.

Normal blood pressure varies with age, gender, and clinical reasons such as cardiovascular drug therapy and medical conditions including hypertension. Normal systolic blood pressure in children (mmHg) can be estimated by the formula 80 + (age in years × 2).

The pulse pressure narrows in the early, compensated stages of hypovolaemic shock, and in cardiogenic shock, due to raised systemic vascular resistance from vasoconstriction. Pulse pressure generally widens in septic, anaphylactic and neurogenic shock, due to reduced peripheral vascular resistance. Postural hypotension may support the diagnosis of shock, especially due to hypovolaemia.

Non-invasive cardiac output estimation

Several non-invasive devices are available that estimate cardiac output at the bedside and may be used to help detect signs of shock. Transcutaneous Doppler, impedance cardiography and aortovelography methods used in such systems should only be relied upon to record changes in cardiac output, rather than providing reliable absolute measurements.

Technically non-invasive (although requiring sedation or anaesthesia to insert the probe), transoesophageal echocardiography (TOE) may also be utilized as a method to estimate cardiac output and demonstrate signs of shock.

Urine output

Urine output may be considered a non-invasive measure of shock in the non-catheterized patient. Failure to produce an adequate urine output may be a delayed sign of shock, although it may also be due to trauma to the urological tract, acute urinary retention due to neurological injury or from other causes of renal failure. A urine output of at least 0.5 mL/kg/h in adults, and at least 1–2 mL/kg/h in children, signifies that there is adequate renal perfusion.

Response to intravenous fluid boluses

Indirect measurement of the presence and extent of shock can be carried out by assessing the physiological response to intravenous fluid boluses. Improvement following fluid administration may support the diagnosis of hypovolaemic, neurogenic, septic, or anaphylactic shock. Deterioration following intravenous fluid therapy may be noted with cardiogenic shock.

A transient response to intravenous fluid therapy may suggest a more severe degree of shock or ongoing haemorrhage.

Causative volume loss estimates

Loss of circulating blood volume may be predictable from the apparent injuries. In addition to external haemorrhage or large open wounds, the two most important examples of apparent fluid losses are due to thermal burns and fractures. Fluid deficit from burn injury can be calcu-lated according to the body surface area affected, and fractures also have predictable blood volume losses. For example, closed femoral fractures may lose up to 1500 mL blood and closed tibial fractures up to 500 mL in adults.

Electromechanical devices: the basics

Common sources of error Confounding errors in measurements can arise from:

• • The system not being calibrated and zeroed.

• • Inappropriate damping of the system.

• • The transducer not being at the level of the heart.

• • The system not being pressurized to 300 mmHg.

(p. 98) Central venous lines

The CVP is the pressure found within the right atrium and great veins of thorax. Normal pressure should be 0-8 cm H₂O. Hypovolaemia and vasodilatation will result in a fall in CVP due to reduced venous return. CVP can also be used to assess the efficacy of fluid resuscitation, suggested to be adequate if a sustained rise in CVP is demonstrated following an appropriate fluid challenge.

Indications For continuous monitoring of haemodynami-cally compromised patients and to enable responsive replacement of circulating volume in accordance with CVP. Central venous access may also be required for inotrope and vasopressor infusions or for other drugs for which peripheral administration is not recommended.

Other indications include:

• • Facilitating the insertion of pacing lines.

• • Regular blood sampling, including mixed venous gases.

• • Provision of renal dialysis.

• • Administration of parenteral nutritional support.

Contraindications Contraindications to the insertion of central venous catheters are generally relative and related to the site of insertion and mechanism of injury. Injury to the upper thorax or neck may prevent use of the internal jugular or subclavian veins, leaving the femoral vein as the most viable option. Maintaining appropriate sterility of the femoral region is difficult, although any risk of infection must be balanced against the urgency of achieving appropriate access. Femoral lines may not truly represent right atrial pressure and must be interpreted with caution.

There is an increased risk of bleeding from the insertion site in patients with coagulopathies, or who are known to be on anticoagulation therapy. Obesity or anatomical abnormalities can make insertion of lines more problematic, and may be more risky in agitated or confused patients without the use of sedation.

Central line insertion may also be difficult in patients whose respiratory function is compromised and who cannot be laid flat. Very rapid respiratory rates may also increase the risk of air embolus from jugular or subclavian line insertion due to lower intrathoracic pressures.

Complications and limitations Central line insertion is associated with a number of potential complications, some of which are potentially life-threatening:

• • Pneumothorax (pleural puncture).

• • Arterial puncture or nerve damage.

• • Cardiac arrhythmias (direct intravascular stimulation).

• • Air embolism.

• • Infection by skin commensals.

• • Occlusion and thrombosis.

Normal central venous lines (triple or quad lumen) are not always the best form of access for rapid fluid administration in emergency situations as their relatively narrow gauge and longer length may restrict maximum flow rates compared with larger peripheral lines. However, insertion of larger lumen lines, such as vascular catheters (normally used for emergency dialysis) or Swan–Ganz catheter introducer sheaths can permit very rapid central infusions.

Technique of insertion The identification and cannulation of central veins may be difficult in hypovolaemic patients. The 2002 NICE guidelines recommend the use of ultrasound guidance where available to facilitate safer insertion. A standard landmark technique may still be appropriate in the emergency situation. ECG monitoring is required in case of arrhythmias.

Once the vein is located, a percutaneous Seldinger technique is used to insert the catheter. The Seldinger technique comprises the following general steps:

• • A ‘seeker’ needle is passed into the vessel.

• • A guide wire is passed through needle into vessel.

• • The needle is removed leaving the guide wire in place.

• • A dilator passed over the guide wire to widen skin the incision.

• • The cannula is introduced into the vessel over the guide wire.

• • The guide wire is removed and the catheter secured.

In case of inadvertent arterial puncture, firm pressure should be applied to the site for 5–10 min or until the site has stopped bleeding completely. The catheter position must be checked by x-ray (i.e. chest x-ray for jugular or subclavian lines, or pelvis x-ray for femoral lines), as well as to exclude a pneumothorax.

Pulmonary artery catheterization Central line access is required in order to introduce this type of catheter. A flow-directed balloon-tipped pulmonary artery catheter is floated into the pulmonary artery via the right atrium and ventricle, usually from a right internal jugular site. Pulmonary capillary wedge pressure (PCWP) is the pressure measurement at the tip of the catheter with the balloon inflated and, in most patients, represents left atrial filling pressure and, therefore, left ventricular end-diastolic pressure.

As with CVP measurements, interpretation of PCWP measurements is more useful when monitoring trends rather than single readings. The response of PCWP to fluid resuscitation may be used to indicate intravascular volume status. The use of pulmonary artery catheters is controversial in critical care, with no clear evidence of any benefit to overall morbidity or mortality.

Arterial lines

Arterial lines provide both measurements of blood pressure and a waveform, the shape of which can also provide useful information regarding the haemodynamic status of the patient. Stroke volume and cardiac output can be derived from the area under the systolic part of the curve. Myocardial contractility may be indicated by rate of pressure change over time. Hypovolaemia is suggested by a low dicrotic notch, narrow waveform, and swinging peak pressures with the respiratory cycle.

Indications The main indication for insertion of an arterial line in trauma patients is to allow continuous direct arterial blood pressure monitoring. Arterial line measurement provides a continuous reading and is more accurate than non-invasive methods. It will also enable regular arterial blood gas sampling and measurements. Arterial BP trend is often more important than single readings. Several variables can affect blood pressure readings including age and the existence of pre-morbid medical conditions. Decreased aortic compliance in the elderly may result in higher peak pressures.

Contraindications As with central lines, there may be an increased risk of bleeding from the insertion site or haematoma formation in patients with coagulopathies. Infection may also occur after insertion, with risk increasing the longer the line remains in situ.

(p. 99) Complications and limitations The potential complica-tions of arterial line insertion are similar to those associated with central lines as listed. User error may minimize the benefit of arterial pressure measurement. Air bubbles, blood clots, a soft diaphragm, or soft tubing may cause damping of the arterial waveform signal, preventing accurate interpretation. Damping is caused by dissipation of stored energy resulting in a progressive diminution of amplitude of oscillations. Increased damping lowers the systolic pressure and elevates the diastolic pressure, although mean arterial pressure is unaltered. The transducer should be at the level of the right atrium; raising or lowering the transducer will result in errors.

Technique of insertion The common sites of insertion of arterial lines are the radial and brachial arteries. Femoral or dorsalis pedis arteries may also be used. Catheters are inserted either using a catheter over needle technique similar to peripheral venous cannula insertion [e.g. Floswitch^™ (BD)], or by a Seldinger wire guided insertion technique similar to that used for inserting central lines [e.g. Leadercath (Vygon)]. Normal catheter sizes are 18–22G. Similar to central lines, the arterial line system consists of the cannula, connecting catheter, transducer and electrical monitor with appropriate connections.

Aerobic respiration

Anaerobic respiration

When oxygen delivery is limited, such as in the case of shock, pyruvate is metabolized by anaerobic respiration. Anaerobic respiration is far less efficient at using the energy from glucose and will produce lactic acid as a waste product. This can occur in skeletal muscle and red blood cells.

As stated above, aerobic metabolism can generate a maximum yield of 36–38 ATP molecules per glucose molecule. If perfusion and oxygen delivery are sufficiently impaired by shock that cells have to rely upon the anaerobic metabolic pathway, only two ATP molecules are generated per molecule of glucose.

Oxygen delivery and consumption

Metabolic (cellular) consequences of shock

Hypoperfusion and subsequent inadequate delivery of substrates and oxygen fails to meet the metabolic requirements of the tissues. Cells are not able to sustain efficient energy production via the aerobic method and respiration will occur anaerobically. This metabolic dysfunction results in production of lactic acid from anaerobic respiration resulting in systemic acidosis. In addition to acidosis, cellular metabolism will no longer be able to generate enough energy to power the vital components of normal cellular homeostasis. The cellular consequences of this include disruption of cell membrane ionic pumps with accumulation of intracellular sodium and cytosolic calcium. Hyperkalaemia occurs due to the subsequent release of intracellular constituents.

An initial rightward shift of the oxyhaemoglobin dissociation curve (ODC) will occur although sustained acidosis will eventually cause the red cell 2,3-DPG to decline and shift the ODC back towards normal. Metabolic acidosis also has negative effects on numerous protein and enzyme functions, such as the coagulation cascade. Cellular gene expression is affected causing deterioration in cell function and signalling.

Tissue injury due to trauma itself causes release of inflammatory mediators resulting in vasodilation, microvascular permeability, and increased metabolic compromise.

If anaerobic conditions continue unchecked, cells swell as water follows the rise in intracellular sodium, cell membranes break down eventually leading to cell death and subsequent organ dysfunction (see below).

Organic (macroscopic) consequences of shock

Compensatory phase

As the signs of shock become more apparent various homeostatic mechanisms attempt to improve tissue perfusion and oxygen delivery. These consist of various neuroendocrine reflexes involving sympathetic activation and renal conservation of salt and water. Increased cardiac output is brought about primarily by vasoconstriction, tachycardia, and reduced renal fluid losses.

As blood pressure falls, arterial baroreceptors detect hypotension and trigger activation of sympathetic chain of the autonomic nervous system. The resulting catecholamine release causes tachycardia and vasoconstriction (skin, viscera, and kidneys), thus improving stroke volume and cardiac output. As a result of the underlying metabolic acidosis, hyperventilation attempts to reduce CO₂ levels and thereby raise the blood pH nearer to normal.

The renin-angiotensin axis is also activated and antidiuretic hormone (ADH) is released in order to conserve intravascular fluid. This causes vasoconstriction of the renal and gastrointestinal systems in order to redistribute blood volume to the heart, lungs and brain. Diminished renal blood flow causes the characteristic oliguria. Corticosteroid secretion also increases as part of the stress response.

(p. 102) Progressive (decompensating) phase

If left untreated, normal compensatory mechanisms will eventually fail, resulting in worsening perfusion, acidosis, and cellular dysfunction. Inflammatory mediators are released and further depress the cardiovascular system, particularly causing myocardial depression and inducing fluid loss from the intravascular compartment.

Hydrostatic pressure increases along with inflammatory mediator release lead to leakage of fluid and protein into the extravascular space. Arteriolar smooth muscle and precapillary sphincters relax such that blood pools in the capillaries and, as fluid is lost, blood concentration and viscosity increases, causing sludging of the micro-circulation and microvascular thrombosis.

As the gastrointestinal tract becomes ischaemic, bacteria and endotoxins (typically lipopolysaccharides, LPS) may enter the blood stream via the portal circulation, which causes further promotion of the systemic inflammatory response. Hypoperfusion-reperfusion injury may represent a second hit as the cardiovascular consequences of shock progress.

Refractory phase

This is also referred to as irreversible shock. As cardiovascular and metabolic function deteriorates further, the resulting organ damage is too severe for recovery to take place, even if appropriate resuscitation is commenced. Signs of multiple organ failure will appear and the later complications of shock may become apparent such as renal failure, ARDS or DIC.

Classes of shock

Haemorrhagic shock has traditionally been classified by the volume of blood loss and the resultant physiological signs and symptoms. However, this classification system does not take into account the multifactorial nature of shock or individual patient factors that may produce variance from these.

Despite its limitation, this classification may be useful when considering the effect of increasing volumes of blood loss on a normal, healthy adult:

• • Even a rapid blood loss of up to 500 mL is likely to be well tolerated and compensated.

• • By 1000 mL the initial signs of tachycardia and postural hypotension are likely to appear.

• • Above 1500–2000 mL shock will definitely be apparent with signs of hypoperfusion and metabolic acidosis.

Later consequences of shock

Physiological parameters

Quantitative measures of shock

Surrogate markers of shock

External haemorrhage

External haemorrhage is usually obvious but can be concealed. Occasionally the cause of haemodynamic instability is only established once the resuscitation trolley is moved, whereby a large pool of blood is apparent on the floor. A thorough physical examination is vital to discover any external sites of bleeding.

The quantity of blood loss externally is extremely difficult to judge by observation alone. A cupful of blood goes a long way on a white floor.

Scalp wounds deserve a particular mention. They can continue to bleed profusely, despite being covered with a dressing, so early attention should be paid to closing the wounds with large sutures (which may be a temporary measure) and achieving haemostasis.

Chest

Bleeding into the chest can occur as a result of lung parenchymal injury, as well as injury to the blood vessels in the chest and the intercostal vessels.

Clinical examination may reveal bruising, pain, reduced expansion, dullness to percussion, and reduced breath sounds. Blood in the chest can be confirmed by a chest X-ray as part of the primary survey. Most thoracic bleeding can be managed with tube thoracostomy.

Abdomen

Bleeding into the abdomen is common, but not always obvious. Clinical clues may be present such as bruising to the abdominal wall, abnormal movement, involuntary muscle guarding, or tenderness to palpation, and absence of bowel sounds. However, in the majority of cases clinical examination needs to be supplemented by further investigation, commonly by ultrasound (FAST), to detect free fluid, and CT if the patient is stable enough.

Concealed intra-abdominal haemorrhage should be assumed if the patient is haemodynamically unstable without any other obvious cause following blunt trauma. Any intra-abdominal bleeding is referred to as non-compressible haemorrhage and is likely to be controlled only by surgery.

Pelvis

Injury to the pelvis should be assumed and excluded on X-ray during the primary survey. In the pre-hospital environment (or emergency department if not already done), when the mechanism of injury suggests a possible pelvic injury, a pelvic splint should be applied and left in place until significant injury is excluded.

Extremities

Significant bleeding can occur from extremity fractures, particularly if they are open or multiple. Long bone fractures should be splinted and, in the case of femoral fractures, traction splints applied to reduce bleeding. Clinical examination and X-ray confirmation give the diagnosis.

Retroperitoneal space

The retroperitoneal space contains the abdominal aorta, inferior vena cava, part of the duodenum, pancreas, kidneys, and ureters, and part of the colon. The lower part of the retroperitoneal space lies within the pelvic cavity.

The retroperitoneum is hidden from view in the resuscitation room. It can only be visualized on CT, where occult haemorrhage into the retroperitoneum is sometimes found.

Direct pressure and limb elevation

Direct pressure and elevation are the first priorities for all compressible external haemorrhage. This approach is most effective for limb and extremity injuries.

Topical haemostatic agents

Tourniquets

Tourniquets are increasingly utilized in the pre-hospital environment in order to arrest bleeding distal to the point of application, although considerable controversy exists about their safety and efficacy. However, the relative risk to the limb is outweighed by the likely risk of death from severe exsanguination.

Surgery

Red cell salvage

Peri-operative red cell salvage is recommended where appropriate in order to minimize blood product use and subsequent complications.

Recombinant factor VIIa (rFVIIa)

The use of rFVIIa has been described in a number of different clinical scenarios including traumatic or post-surgical coagulopathy refractory to conventional therapy with continued haemorrhage. Despite growing peer-reviewed clinical evidence, it is still not yet licensed in any country for this indication. It is also not an alternative to surgical control of haemorrhage and is by no means a magic bullet. Adequate clotting factors, cryoprecipitate and platelets need to be present for its full effect and both significant acidosis (pH<7.2) and hypothermia reduce rFVIIa activity.

The usual rFVIIa dose regime quoted is 90–100 mcg/kg, repeated once only within the next 2 h if required.

Compatibility testing

Full ABO group and cross-match takes up to 45 min to complete. In urgent cases, just ABO and Rhesus group compatibility can be tested more rapidly, although this may still take up to 10–15 min. An antibody screen is then performed retrospectively. Further cross-matching is not required after replacement of one full MNBV.

In life-threatening haemorrhage, where there is established need for immediate blood transfusion before type specific or cross-matched blood is available, group O Rh D-positive blood may be used. Due to limited supplies, group O Rh D-negative blood is usually reserved for pre-menopausal females to avoid haemolytic disease of the newborn in future pregnancies.

Issues and possible complications

Rapid transfusion may result in hyperkalaemia, hypothermia, impaired clotting, and citrate toxicity causing hypocalcaemia. Metabolic alkalosis may occur as citrate is metabolized to bicarbonate. Bacterial contamination of donor blood may result in rapid development of severe sepsis. Elderly patients are more susceptible to fluid overload and cardiac failure, and may require diuretic therapy during, or following, blood transfusion. Stored blood will have impaired oxygen delivery characteristics due to leftward shift of the oxyhaemoglobin dissociation curve as a result of inactivity of 2,3-DPG in the first 24 h. Red cell viability is around 70% at 24 h post-transfusion. Coagulation factor activity in PRC solution is negligible and dilutional thrombocytopenia is to be anticipated during massive blood replacement.

Transfusion reactions

• Life-threatening:

• • immediate haemolysis due to ABO incompatibility;

• • anaphylaxis may occur rarely but can be fatal;

• • transfusion-associated acute lung injury (TRALI).

• Non life-threatening:

• • febrile non-haemolytic transfusion reactions (FNHTR) and delayed haemolysis;

• • urticarial reactions from donor plasma proteins.

Risk of infection

In the UK, donor blood is currently screened for hepatitis B, hepatitis C, HIV, syphilis, HTLV-1, and CMV (for selected recipients). Variant Creutzfeld-Jakob disease (vCJD) risks are thought to be extremely low.

Risk of transmission (per unit transfused):

• • Hepatitis B = 1 in 100,000–400,000

• • Hepatitis C = 1 in 200,000

• • HIV = 1 in 4 000,000

Storage issues

Packed red cell (or red cell concentrate) units and platelets are stored at 2–6°C. FFP and cryoprecipitate require thawing for around 30–40 min before use. PRC units left unrefrigerated for more than 30 min should be transfused within 4 h or discarded.

Massive haemorrhage

Massive haemorrhage may be defined as:

• • Loss of 100% of MNBV in 24 h.

• • Loss of 50% of MNBV in 3 h.

• • Loss of >150mL/min (externally or into drains).

Despite limited evidence, the early use of cryoprecipitate, FFP and platelets may be beneficial and improve survival. Improved survival in massively transfused patients is also associated with more effective and efficient rewarming techniques and aggressive resuscitation. The use of a massive transfusion protocol to activate a pre-determined sequence of events, supply appropriate blood products and monitor their use is recommended.

Administration route

Isotonic solutions may be safely infused via a peripheral venous cannula. Hypertonic solutions are best infused through central venous lines, although they may still be administered peripherally in emergency situations.

The intraosseous route of administration is becoming increasingly common in trauma patients and may be considered a safe route for all isotonic solutions, including plasma and plasma substitutes. However, research into the intra-osseous route for hypertonic solutions has demonstrated a significant risk of local complications including myonecrosis in some animal models. Further research is required before hypertonic solutions are recommended for administration by the intraosseous route in humans.

Electrolyte solutions

Plasma and plasma substitutes

Hypertonic solutions (HS)

There is an increasing enthusiasm for the use of HS in the treatment of hypovolaemic shock in trauma patients. Several cardiovascular advantages are believed to be conferred including:

• • Displacement of fluid into intravascular compartment

• • Vasodilatory effects on pulmonary vasculature

• • Direct positive inotropic effects on myocardium

Other potential advantages include the fact that only small volumes of HS are necessary to achieve the same desired effect of isotonic solutions, thereby less chance of fluid overload and also smaller volumes needed to be carried by pre-hospital personnel.

Various concentrations of HS are available, both alone and in combination with other fluids. Individual vials of sodium chloride are also supplied in 3, 5, 7.5, and 10% strengths, and their use is generally limited to critical care management of severe head injury. The most commonly used combined hypertonic sodium chloride solutions include:

• • RescueFlow^® (Vitaline): 250 mL sodium chloride 7.5%, containing 6% dextran 70 (70,000 D).

Dextrans are glucose polymers available in different molecular weights preparations. Negative adverse effects of dextrans solutions include coagulation abnormalities and severe life-threatening hypersensitivity reactions.

• • HyperHAES^® (Fresenius Kabi): 250 mL sodium chloride 7.2%, containing 6% hydroxyethyl (tetra-) starch (200,000 D).

• • Specific indications:

  • • Hyponatraemia;

  • • traumatic brain injury;

  • • low volume resuscitation of trauma patients.

• • Cautions and complications:

  • • the incidence of serious adverse reactions following the use of Dextran 70 is around 1:4500;

  • • effects of HS alone are reported to be transient;

  • • limited number of clinical trials for high dose HS.

Future developments

Although still at an experimental stage, haemoglobin and synthetic oxygen carrier solutions may have a potential future role in the management of trauma patients.

Examples include:

• • Stroma-free haemoglobin (SFH).

• • Micro-encapsulated haemoglobin (neo red cells).

• • Chelating agents.

• • Perfluorocarbons (PFCs).

The advantages of such products include minimal infection risk, no need for cross-matching, long shelf life, and easier storage at ambient temperature. Of these, haemoglobin-based oxygen carriers (HBOCs) and PFC emulsions are the most likely candidates for general clinical use.

(p. 111) Summary

Overall, there is still no clear evidence to support the use of one fluid over another. Appropriate and early use of blood and blood products should be the priority in the most severely injured patients.

Aetiology

Non-haemorrhagic hypovolaemia can occur due to uncompensated fluid volume loss, from extravascular fluid sequestration (third spacing) of intravascular fluid or following burns. Causes of increased fluid loss include burns, crush injury, and pancreatitis.

Pathophysiology

Intravascular and interstitial compartments are usually held in equilibrium, with losses from one resulting in passage of fluid from the other. Losses of interstitial fluid volume will therefore lead to a reduction in intravascular volume and subsequent shock.

Head injury may result in a deficiency of ADH (vasopressin) production due to hypothalamic or pituitary damage. Termed neurogenic (or cranial) diabetes insipidus, this condition is characterized by excretion of large amounts of highly diluted urine, which will lead to hypovolaemia if untreated. This process may take a few days to develop and in head injury may be temporary, often recovering within a few weeks.

Third spacing of intravascular fluid may occur due to post-traumatic pancreatitis or following injury to the liver or bowel. Increased renal losses of protein from nephrotic syndrome can also lead to increased third spacing.

Specific management

The diagnosis of non-haemorrhagic hypovolaemic shock should only be made by exclusion in the injured patient.

The management of hypovolaemic shock should focus on treating the cause of the volume loss. This will usually only require the replacement of water deficit and restoration of appropriate electrolyte balance. Neurogenic diabetes insipidus can be treated with the vasopressin analogue, desmopressin, although mild cases may be managed appropriately with increased fluid intake alone.

Aetiology

Cardiogenic shock may be divided into intrinsic or extrinsic causes and may co-exist in trauma patients. Intrinsic causes are due to insufficient ejection fraction and cardiac output despite adequate intravascular volume and cardiac filling. Relevant intrinsic causes include myocardial infarction or contusion, traumatic valvular, or ventricular defects, arrhythmias due to ischaemia or toxins, and pre-existing cardiomyopathy.

Extrinsic causes are either due to obstruction of venous return or from external compression preventing adequate cardiac filling and stroke volume. Causes include:

• • Tension pneumothorax.

• • Cardiac tamponade.

• • Mediastinal haemorrhage or pneumo-mediastinum.

• • Massive pulmonary embolus.

• • Diaphragmatic hernia.

• • Positive pressure ventilation.

The most important traumatic causes of cardiogenic shock include cardiac contusion from blunt thoracic trauma, cardiac tamponade from penetrating injury or tension pneumothorax.

Pathophysiology

The most common cause of cardiogenic shock is acute myocardial infarction, leading to a marked decrease in myocardial contractility, reducing the ejection fraction and thereby cardiac output. Cardiogenic shock usually involves some degree of left ventricular dysfunction. Decom-pensation may occur as a result of falling arterial pressure with the subsequent exacerbation of myocardial ischaemia. The heart rate usually increases to compensate for hypotension, exacerbating myocardial oxygen demand.

Direct injury to the heart may result in rupture to the ventricular wall resulting in a pericardial haematoma and cardiac tamponade, valvular rupture reducing forward flow and ejection fraction, or ventricular contusion reducing myocardial contractility.

A tension pneumothorax causes a rise in intrathoracic pressure and may reduce cardiac output. Injury to the mediastinum may result in increased pressure exerted upon the pericardial space and an indirect tamponade effect. The use of positive pressure ventilation, especially when using higher positive end expiratory pressures (PEEP), may also reduce cardiac filling due to the increase in intrathoracic pressure.

Pulmonary embolus is unlikely to present early as a result of trauma, although it may be a later complication. A large pulmonary embolus will obstruct blood flow returning to the left ventricle and thus cause a reduction in cardiac output.

Presentation

Cardiogenic shock is more likely to occur in the elderly and those with known cardiac disease. A history of (p. 113) previous myocardial infarction and atherosclerotic disease increases the likelihood of developing cardiogenic shock.

All forms of cardiogenic shock lead to a fall in cardiac output and a rise in systemic vascular resistance. Central venous pressure is generally increased in cardiogenic shock, although the true CVP falls due to tension pneumothorax from reduced venous return. The CVP may appear falsely raised, reflecting the intrapleural rather than vascular pressure.

ECG complexes may appear small in the presence of a pericardial effusion large enough to result in tamponade.

Specific management

The specific management of cardiogenic shock should focus on treating the cause, particularly in obstructive shock and myocardial infarction, which may include urgent reperfusion therapy in appropriate cases.

The general approach to managing intrinsic cardiogenic shock is to optimize oxygen delivery and left ventricular filling pressures. Fluid resuscitation may be necessary where there are signs of hypotension due to poor cardiac filling. Inotropic and vasodilator therapy may be used with signs of raised left ventricular filling pressures, such as pulmonary oedema. Typical drug therapy involves the use of oxygen, opiates, nitrates, and diuretics. Inotropic agents include dobutamine, which increases myocardial contractility while reducing left ventricular end-diastolic pressure.

The approach to managing obstructive shock involves the restoration of cardiac filling and stroke volume by the removal of external compression forces (in the case of tension pneumothorax for example) or of internal vascular obstruction from pulmonary embolus. In the case of tension pneumothorax, immediate needle decompression is required initially followed by tube thoracostomy. Cardiac tamponade usually requires emergency surgical removal of clotted blood by thoracotomy.

Pathophysiology

Neurogenic shock occurs in spinal injuries above the T6 level and is secondary to the loss of normal sympathetic autonomic outflow below T1. This results in a loss of systemic vascular resistance due to interruption in normal vascular smooth muscle (vasoconstrictor) tone.

The release of catecholamines immediately following a spinal injury may maintain a partial pressor response and therefore the signs of neurogenic shock may take a few minutes to hours to appear.

Presentation

The dominating presenting feature of all causes of distributive shock is due to the loss of systemic vascular resistance. Central venous pressure is often unaffected, unless there is concurrent cause for hypovolaemia, and cardiac output may remain the same or elevated. A spinal injury level above T6 is characterized by hypotension and, above T1, additionally by bradycardia, due to unopposed vagal tone.

Specific management

It is important to exercise caution when dealing with trauma patients with signs of spinal shock as there may also be evidence of hypovolaemic shock requiring urgent surgical intervention. The hypovolaemic trauma patient on ß-blocker therapy may show appearances consistent with an apparent spinal injury.

Where the injury mechanism and clinical signs suggest spinal shock, and there are no signs of a hypovolaemic cause, initial management relies on optimizing oxygen delivery and sufficient fluid volume resuscitation to fill the expanded intravascular space. Subsequent management may require use of an appropriate vasopressor, such as noradrenaline, dopamine, or phenylephrine. Regular bolus therapy with the vasopressor metaraminol may be useful while waiting for an infusion to be commenced. A haemodynamically significant bradycardia may be treated with atropine 500-mcg aliquots up to 3 mg intravenously.

Aetiology

The main causes of sepsis from trauma include translocation of bacteria and endotoxins across the gut wall into the systemic circulation either due to splanchnic hypoperfusion as a result of hypovolaemic shock or from local bowel wall perforation, wound infections, and aspiration of gastric contents.

Pathophysiology

The release of inflammatory mediators into the circulation causes a loss of systemic vascular resistance, venous pooling, reduced venous return, and thereby a fall in cardiac output. Hypovolaemia then follows, causing a further reduction in central venous pressure and cardiac pre-load (p. 114) and subsequently cardiac output. Eventually, falling arterial blood pressure leads to myocardial ischaemia producing a superimposed intrinsic cardiogenic shock.

Most cases of sepsis are due to bacterial sources, traditionally due to Gram-negative organisms, such as E. coli, although Gram-positive organisms are increasingly being implicated (including streptococci and staphylococci). Contributory factors include a loss of immune function due to concomitant therapy or from splenectomy.

Presentation

• • Early:

  • • SIRS clinical state;

  • • hyperdynamic circulation with reduced SVR;

  • • metabolic (lactic) acidosis;

  • • reduced oxygen extraction and utilization;

  • • multiple organ dysfunction.

• • Later:

  • • acute renal and hepatic failure;

  • • pancreatitis and diabetes mellitus;

  • • Acute Respiratory Distress Syndrome (ARDS);

  • • disseminated intravascular coagulation (DIC);

  • • Cardiac failure.

Specific management

Initial management is supportive with appropriate oxygen therapy and fluid resuscitation. Inotropic and vasopressor therapy will be required in the presence of organ dysfunction secondary to ongoing hypoperfusion despite adequate fluid resuscitation. Antibacterial therapy must be instituted as early as possible and the choice of drug must be based upon the most likely causative organism and modified by the results of culture from suitable body fluid and tissue samples. Ideally, such samples should be taken before antibiotic therapy is started. Treatment may also require the use of antiviral or antifungal agents, as guided by culture results.

Early surgical care, including wound debridement and drainage of infected tissue or pus collections will be required to treat the underlying source.

The severe sepsis bundles are a distillation of the evidence-based recommendations from the Surviving Sepsis Campaign and wider critical care community. These are designed to allow medical teams to follow the appropriate timing, sequence, and goals of individual elements in the care of septic patients.

Pathophysiology

Anaphylaxis is a Type I immune reaction, which is characterized by the release of various vasoactive substances (particularly histamine) and results from an antigen-antibody reaction on the surface of mast cells. Release of these substances causes angioedema, as well as vasodilatation with increased capillary permeability and myocardial depression, resulting in shock.

Presentation

• • Angioedema with pharyngeal or laryngeal oedema.

• • Bronchospasm.

• • Vasodilation and subsequent hypotension.

• • Cutaneous erythema and urticaria.

Specific management

The specific management of anaphylaxis requires rapid recognition with airway protection and the early use of adrenaline. Triggers should be removed if possible (stop the antibiotic or colloid infusion if thought to be the cause). (p. 115)