The Intensive Care Unit

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The Intensive Care Unit

Historically, critical care medicine can be traced as far back as the Crimean war and Florence Nightingale’s pioneering work in monitoring the critically ill patient. The poliomyelitis outbreak in Denmark in the 1950s saw the onset of positive pressure ventilation in specific designated areas, and continued evolution has led to what we recognize as intensive care medicine today. This chapter aims to provide an overview of the provision of general adult intensive care.

The key components of intensive care are resuscitation and stabilization, physiological optimization to prevent organ failure, support of the failing organ systems and recognition of futility of treatment. The Department of Health NHS Executive defines intensive care as ‘a service for patients with potentially recoverable conditions who can benefit from more detailed observation and treatment than can safely be provided in general wards or high dependency areas’. Levels of care within the hospital can be described from level 0 (ward-based care) to level 3 (patients requiring advanced respiratory support alone or a minimum of 2 organs being supported) (Table 45.1). There is now a move towards a comprehensive critical care system, where the needs of all patients who are critically ill, rather than just those who are admitted to designated intensive care or high dependency beds, are met with consistency.

TABLE 45.1

Levels of ICU Care

image

In the UK, intensive care beds generally account for 1–2% of the total number of acute beds. The design of ICUs varies from hospital to hospital but they are characterized by being designated areas in which traditionally there is a minimum nurse:patient ratio of 1:1 in addition to a nurse in charge at all times, 24 h cover by resident medical staff (without commitments elsewhere) and the facilities to support organ system failures. High-dependency units (HDUs) are designated areas with a nurse:patient ratio of 1:2 in addition to a nurse in charge at all times, continuous availability of medical staff either from the admitting specialty, or from the ICU, and an appropriate level of monitoring and other equipment. While ICU and HDU may be situated separately in the hospital, all critical care beds should ideally be in adjacent locations.

The physical floor space for each bed in an ICU should be greater than 20 m2, more than on an ordinary ward because several nurses may need to treat a patient simultaneously and bulky items of equipment often need to be accommodated. Increased bed spacing and the presence of isolated side rooms may help to reduce the risk of nosocomial infection. Each bed area is supplied with piped oxygen, suction, and medical compressed air. The plethora of electronic monitors requires at least 12 electric power sockets (with emergency backup electrical supply) at each bed. Sufficient bedside storage space, at least 5 m2, is needed for drugs and disposable equipment. Each bed area should be equipped with a self-inflating resuscitation bag to enable staff to maintain artificial ventilation if the mechanical ventilator, gas or electricity supply fails.

STAFFING AN INTENSIVE CARE UNIT

Care of the individual patient in an ICU is increasingly complex and involves contributions from a variety of medical staff, as well as high standards of care from nurses, physiotherapists, dieticians, pharmacists and other health professionals. Each member of the multidisciplinary team has a broad spectrum of experience and skills and it is worth remembering the value of good teamwork to ensure that high standards of quality patient care are provided. Often the consultant in the specialty under which the patient was admitted may still be nominally in charge, but confusion is minimized if day to day decisions are made through the ICU team, in close liaison with the parent specialty. Good communication is paramount, both within the ICU environment and with the various other teams.

The ICU Consultant

There must be twenty-four hour cover of the ICU by a named consultant who has appropriate experience and competencies. Difficult therapeutic and ethical policy decisions may be required at any time in the ICU and it is essential that they are taken by an individual whose previous experience allows a reasonable assessment of the likely outcome, and whose therapeutic expertise is likely to give the patient the optimal chance of recovery. The ICU consultant, if not physically present in the unit, must always be available by telephone and should not be involved in any activity which precludes his or her attendance there within 30 min. Because of the critical nature of ICU patients’ illnesses, the ICU consultant expects to be informed immediately of any significant change in their condition. Similarly they should be informed of any potential admissions and all new patients should be seen within 12 hours. The consultant’s base specialty is less important than appropriate training and experience.

The ICU Resident

The junior medical staff in ICU have a pivotal role in the co-ordination of all aspects of patient care, particularly to maintain good lines of communication between the different teams involved. Because of their continuous presence in the unit, the ICU resident is best informed about the patient’s recent diagnostic results, physiological status and therapeutic responses and should attempt to use current knowledge to guide treatment along rational lines. Daily work comprises at least one main ward round, usually in the presence of the multidisciplinary team, whereby clinical decisions are made. Following patient assessment, findings should be documented, the results of relevant investigations reviewed and appropriate actions taken. Because of the potential to change, the patients’ clinical state should be frequently reassessed. Other duties may include discussion with relatives, but as with all aspects of intensive care, both clinical and non-clinical duties should fall within the expertise and remit as set by both the junior and consultant. There is a broad range of training opportunities to be had with time spent on the unit, and training in intensive care should be focused on a competency-based programme.

Nursing Staff

It should be appreciated that the nursing staff provide most of the care that patients receive in ICU. ICU nurses have greatly extended roles, experience and responsibility. They have undergone specific training to enable them to perform titration of fluid replacement, analgesia, vasoactive drug therapy and weaning from mechanical ventilation. The route by which complex instructions and information are transmitted between medical and nursing staff is of vital importance. A system in which a relatively junior clinician serves as a ‘final common pathway’ for all instructions works well in practice, provided that the doctor involved is present within the unit at all times so that the nurses may obtain clarification of instructions, report changes in status and receive immediate help in emergencies. It is essential that a nurse is present and takes part when discussions take place with the patient, or their relatives or friends. The content of such discussions must be recorded accurately in the patient’s notes. The resident should remember that the majority of ICU nurses (especially the senior nurses) have an enormous amount of ‘bedside’ experience with critically ill patients and considerable reliance should be placed on their observations.

The Microbiologist

Critically ill patients are immunocompromised as a result of the underlying pathological process, the impact of treatments (such as steroids) and the presence of surgical/traumatic wounds, multiple vascular catheters and other invasive tubing. This predisposes them to hospital-acquired infections. Prolonged use of broad-spectrum antibiotics encourages the development of resistant pathogens and overgrowth of other organisms. In order to effectively treat sepsis and prevent resistance, there is usually a nominated microbiologist, who is familiar with the flora and resistance patterns of the unit, and who visits the ICU daily to advise on microbiology results and antibiotic therapy. It is also essential to adhere to local policies aimed at reducing cross infection and minimizing the number of hospital-acquired infections. The National Patient Safety Agency (NPSA) also has a number of helpful guidelines for personnel working on ICU (www.npsa.nhs.uk).

OUTREACH/FOLLOW-UP

The critical care outreach team collaborates between the ICU and other areas of the hospital. The aims of the outreach team are to identify the deteriorating patient early with the aim of averting ICU admission, to facilitate timely admission to ICU if required, and to assist in the timely and appropriate discharge from ICU. It is important to identify those patients who are unlikely to benefit from further resuscitation or critical care support due to the nature of their acute illness or underlying diseases, to prevent futile interventions and ensure equitable use of scarce ICU resources. By following up patients discharged from ICU/HDU, a level of continuity of care can be provided and in addition critical care skills may be shared between the team and ward-based staff. The team may comprise of senior members of medical, nursing and physiotherapy staff.

A number of scoring systems based on abnormal physiological variables, such as the modified early warning score (MEWS) (Table 45.2), can be recorded by ward staff; the outreach team can be contacted accordingly once a trigger score has been reached. Care needs to be taken with younger fitter patients, who have good physiological reserve and who may not deteriorate in terms of MEWS score until a peri-arrest situation develops (e.g. in presence of bleeding or severe sepsis). Children, obstetric, neurological, renal and other sub-specialty groups have adapted scores to allow for altered background physiological status.

ADMISSION TO THE INTENSIVE CARE UNIT

The decision to admit a patient to the intensive care unit may be straightforward, but is often difficult and confounded by increasing expectations in an ever increasing elderly population with multiple co-morbidities. ICU resources are finite and costs high, so in the face of limited prospects for benefit or survival of an individual patient, a number of complex ethical issues can arise surrounding admission, provision and discontinuation of intensive care therapy. It is therefore necessary that all individual cases are discussed with the ICU consultant, as the decision regarding whether to admit the patient often comes down to multidisciplinary team discussion and clinical expertise. Blanket admission policies may be unhelpful, and decisions should consider the individual patient, taking into account their wishes and values. Senior staff should discuss with the patient (where possible) and/or their relatives potential treatment options and possible outcomes and alternatives. However, acutely ill patients can rarely discuss details of their care, and relatives may find it difficult to make an objective judgement. If a patient has made an Advance Directive (‘Living Will’) then its contents must be respected.

In essence, the aim of intensive care is to support patients while they recover. It is not to prolong life when there is no hope of recovery. In many cases, unless the outlook is obviously futile, patients will be admitted for a trial of treatment to see whether they will stabilize and improve over time. Patients with little or no prospect of survival may occasionally be admitted to intensive care. This can facilitate more appropriate terminal care, or to allow the relatives time to visit and the bereavement process to be better managed. In the very short term this is a justifiable and appropriate use of a critical care facility.

Assessment of Patients

When dealing with a newly admitted patient with acute disease, assessment and resuscitation often take place simultaneously and follow the standard pattern of recognizing and dealing with problems in the order of airway, breathing and circulation. The resident should heed all the patient’s problems and the responses to the treatments instigated and to do this, it is essential to approach the assessment of the patient in a systematic manner.

Formulating a Plan

Finally an action plan needs to be formulated, with special regard to both active and ongoing problems. A plan for each organ system requiring support should be put into place as well as a ventilation and/or weaning proposal. A review of nutrition, 24 h fluid balance and changes to drug therapy should also be undertaken and any planned procedures/interventions should be discussed with the consultant. Communicate back any change in plans to the relevant nursing staff and bear in mind that relatives appreciate honest, up to date progress reports. It is important to note that patient confidentiality should never be compromised via discussion or documentation. Full assessment and examination should be repeated at least daily even in stable patients, because the physiological state of critically ill patients can change rapidly.

MONITORING IN ICU

There is a plethora of monitoring equipment in ICU, which may at first be daunting. It is important to know that all equipment is working, and accurate and calibrated correctly. Always question whether additional monitoring is necessary and whether it would safely provide further information.

Invasive Monitoring

Pulmonary Artery Catheter

Pulmonary artery (PA) catheterization was for a number of years considered the ‘gold standard’ for cardiovascular monitoring in ICU. This technique enabled the measurement of pulmonary artery pressure, pulmonary artery occlusion pressure (wedge pressure, PAOP) and CO, and also allowed many other haemodynamic variables to be derived. The value of pulmonary artery catheters has been questioned and its use has fallen significantly with the introduction of alternative forms of monitoring. Given the controversy regarding its potential advantages, its use should be based on the risk/benefit ratio for each individual patient.

Pulse Contour Analysis: The peripheral arterial pulse waveform is a function of the cardiac output, the peripheral vascular resistance, peripheral vascular compliance and the arterial pressure. If the cardiac output is measured for a given peripheral arterial waveform, then after calibration, changes in the peripheral pulse waveform can be used to calculate changes in the cardiac output. To calibrate the system an indicator is injected into a venous catheter and is detected by an arterial line producing a standard dilutional CO measurement. Systems such as PiCCO and LiDCO use thermodilution and lithium respectively as the indicators. Aside from cardiac output, stroke volume and systemic vascular resistance, other variables available with PiCCO include global end diastolic volume (cardiac preload) and intrathoracic blood volume. Dynamic measures, using heart–lung interactions to predict fluid responsiveness, can also be widely determined using beat to beat cardiac output monitoring.

Other Technologies

ICP/Jugular Venous Saturation/Compressed Spectral Array/BIS

Indications for ICP monitoring vary between units, but may include any cause of coma, commonly head injury and intracranial head injury. Types of monitoring may include extradural fibreoptic probes, a subarachnoid screw, ventricular drain or intracerebral transducer. ICP monitoring allows calculation of cerebral perfusion pressure; both variables can then be used to guide management.

Jugular venous bulb oxygen saturation is an indirect indicator of cerebral oxygen utilization and provides a measure of global cerebral oxygenation. It involves a catheter being placed retrogradely up the internal jugular vein.

Compressed spectral array and bispectral index (BIS) are computerized assessments of EEG signals, which allow depth of anaesthesia and sedation to be assessed. The former will allow seizure activity to be seen and the presence of burst suppression can be used to indicate a greater depth of anaesthesia consistent with a reduced cerebral oxygen demand.

INSTITUTION OF INTENSIVE CARE

It is impossible to provide a comprehensive review of all the conditions requiring ICU care and their full treatment regimens in one chapter. The following sections are an overview of the management of some common problems presenting to ICU.

The Respiratory System

Respiratory failure is one of the commonest reasons for admission to the ICU (Table 45.3). It may be the primary reason for admission or a feature of a non-respiratory pathological process, e.g. adult respiratory distress syndrome (ARDS) in sepsis. Respiratory failure may encompass hypoxaemia with a normal/low PaCO2 (type 1) or a combination of hypoxaemia and high PaCO2 (type 2).

TABLE 45.3

Causes of Respiratory Failure

Reduced central drive Brainstem injury/CVA
Drug effects, e.g. opioids
Metabolic encephalopathy
Airway obstruction Tumour
Infection
Sleep apnoea
Foreign body
Lung pathology Asthma
COPD
Pneumonia
Fibrosis
ALI/ARDS
Lung contusion
Neuromuscular defects Spinal cord lesion
Phrenic nerve disruption
Myasthenia gravis
Guillain–Barré syndrome
Critical illness polyneuropathy
Musculoskeletal Trauma
Severe scoliosis

Assessment of the Patient with Respiratory Failure

Clinical assessment is often the most rapid way to evaluate the patient with respiratory failure (Table 45.4):

TABLE 45.4

Signs of Impending Respiratory Arrest

Marked tachypnoea, or hypoventilation, patient exhausted

Use of accessory muscles

Cyanosis and desaturation, especially if on supplemental oxygen

Tachycardia or bradycardia if peri-arrest

Sweaty, peripherally cool/clammy

Mental changes, confusion and leading to coma in extreme conditions

A full history including previous functional status, and physical examination are mandatory. Serial arterial blood gases are required to determine the extent of the respiratory failure and response to any therapy. The chest X-ray and other available investigations such as peak flow will aid evaluation of the patient’s condition.

Management of Respiratory Failure

Management is directed at correcting hypoxia/ hypercarbia and reversing the underlying condition if possible. Simple manoeuvres such as supplying supplemental oxygen should be instituted initially. Give oxygen via facemask, preferably humidified. Higher concentrations of oxygen can be achieved with a reservoir system and a fixed performance device (e.g. Venturi) may be preferable in titrating oxygen concentrations in those COPD patients who rely on hypoxia to drive their ventilation. The effect of oxygen therapy should be assessed by pulse oximetry and arterial blood gas analysis after around 30 min.

Other therapies may be useful such as bronchodilators, steroids, diuretics and physiotherapy in the first instance depending on the mechanism of respiratory failure. Many patients may be dehydrated due to poor fluid intake and increased losses and will require IV fluids. If there is no improvement over time, additional respiratory support may be necessary (Table 45.5). Options include:

Mechanical Ventilation

The usual indication for mechanical ventilation is in patients with potentially reversible pathology who are unable to maintain adequate oxygenation or who develop hypercapnia. In some cases, blood gases may be normal but are predicted to deteriorate because the patient is becoming exhausted.

Tracheal Intubation: To enable mechanical ventilation to be carried out effectively, a cuffed tube must be placed in the trachea either via the mouth or nose, or directly through a tracheostomy stoma. In the emergency situation, an orotracheal tube is usually inserted. If the patient is conscious, anaesthesia should be induced carefully with an appropriate dose of an i.v. anaesthetic induction agent and neuromuscular blocker. The full range of adjuncts for difficult intubation should be available.

The critically ill patient is often exquisitely sensitive to i.v. anaesthetic drugs, and cardiovascular collapse may occur; consequently, full resuscitation equipment must be immediately available. I.v. fluid resuscitation and vasoactive drug infusions are often required.

If the patient is unconscious, a neuromuscular blocker alone may be necessary (but not obligatory) to facilitate the passage of the tube; however, an i.v. anaesthetic induction agent and neuromuscular blocker should always be used in patients with severe head injury to prevent an increase in intracranial pressure (ICP) during laryngoscopy and tracheal intubation.

Many patients are hypoxaemic, and it is essential that 100% oxygen is administered before tracheal intubation.

image After neuromuscular blockade has been produced, the tube should be inserted by the route which is associated with the least delay.

image If the patient is unconscious and the victim of blunt trauma, when cervical spine injury is a possibility, the cervical spine should be immobilized during intubation using manual in-line immobilization.

image Cricoid pressure should be applied to minimize the risk of aspirating gastric contents.

image A sterile, disposable plastic tube with a low-pressure cuff should be used. The tube should be inserted such that the top of the cuff lies not more than 3 cm below the vocal cords.

image The head should be placed in a neutral or slightly flexed position (on one pillow) after tracheal intubation and a chest X-ray taken to ensure that the tip of the tube lies at least 5 cm above the carina.

Bronchial intubation is a common complication during mechanical ventilation as the tracheal tube may migrate down the trachea when the patient is moved during normal nursing procedures. Intubation of the right main bronchus cannot be detected reliably by observation of chest movements or by auscultation of the chest because of the exaggerated transmission of breath sounds during IPPV, although absent or asynchronous chest movement may occur when pulmonary collapse has taken place. Bronchial intubation is one of the causes of a sudden decrease in compliance, and restlessness and coughing often occur if the end of the tube irritates the carina. If this is suspected, the tube should be withdrawn gradually by up to 5 cm while lung compliance and chest expansion are observed carefully. The position of the tube should always be confirmed by a chest radiograph.

When the upper airway or larynx is obstructed and conventional tracheal intubation is not possible (e.g. occasional cases of epiglottitis or laryngeal trauma), the emergency airway of choice is cricothyroidotomy.

Tracheostomy is increasingly performed percutaneously on the ICU and is most frequently an elective decision. Indications include:

The recently completed Tracman study confirmed no clear benefit from early compared with delayed performance of tracheostomy.

Sedation and Analgesia: Once tracheal intubation has been performed, some amount of sedative drugs will be required to tolerate the tube and facilitate effective mechanical ventilation. The balance between providing adequate sedation to permit patient co-operation with organ system support and oversedation, which leads to a number of detrimental effects (Table 45.6) is often difficult. The aims of sedation include patient comfort and analgesia, minimizing anxiety, and to allow a calm co-operative patient who is able to sleep when undisturbed and able to tolerate appropriate organ support. Patients must not be paralysed and awake but the efficiency of supportive care will be reduced in the patient who is agitated and distressed. Clearly the patient’s needs for sedation will alter with changes in clinical condition and requirements for care, so regular review and sedation scoring are helpful (Table 45.7).

TABLE 45.6

Problems and Potential Consequences of Excessive Sedation in ICU

Problem Potential consequence
Accumulation with prolonged infusion Delayed weaning from supportive care
Detrimental effect on cardiovascular system Increased requirement for vasoactive drugs
Detrimental effect on pulmonary function Increased VQ mismatch
Tolerance Withdrawal on stopping sedation
No REM sleep Sleep deprivation and ICU psychosis
Reduced intestinal motility Impairment of enteral feeding
Potential effects on immune/endocrine function Drugs such as opioids may have a role in immunomodulation and risk of infection
Adverse effects of specific drugs e.g. propofol infusion syndrome, with cardiovascular collapse

An Overview of Modes of Ventilation

Different manufacturers used different terms for basically similar modes of ventilation which often cause confusion for the inexperienced.

Pressure Support Ventilation (PSV)/Assisted Spontaneous Breathing (ASB): Breathing through a ventilator can be difficult because respiratory muscles may be weak and ventilator circuits and tracheal tubes provide significant resistance to breathing. During PSV the ventilator senses a spontaneous breath and augments it by addition of positive pressure. This reduces the patient’s work of breathing and increases the tidal volume. Pressure support is usually set at 15–20 cmH2O in the first instance and can be reduced as the patient’s condition improves. It is best not to remove pressure support completely, however, because of the internal resistance of the ventilator and its connections. SIMV and PSV require a method of detecting the patient’s own respiratory effort, in order to trigger the appropriate ventilator response. This is achieved by flow sensors detecting small changes in gas flow within the circuit.

Problems Associated with Mechanical Ventilation

Once the patient’s trachea is intubated and lungs ventilated they are crucially dependent on technology to avoid hypoxaemia and hypercarbia. Other important aspects of care include; humidification of gases, regular physiotherapy and tracheal toilet and continuous monitoring of SpO2, end-tidal CO2, inspired O2 concentration, minute volume, and peak airway pressure.

Other constant risks include: tracheal tube dislodgement and difficult re-intubation, laryngeal/tracheal damage with prolonged intubation, ventilator associated pneumonia (see below), needs for sedation, and the haemodynamic effects of positive pressure ventilation and PEEP.

Ventilator associated lung injury (VALI) encompasses a number of components including barotrauma where high pressures are applied to the airway, especially if lung compliance is reduced. This may result in clinically obvious damage like pneumothorax, pneumomediastinum, pneumoperitoneum and subcutaneous emphysema. Volume trauma may occur if excessive tidal volumes are applied and the clinical manifestations are similar to barotrauma. In addition there is considerable experimental evidence for less clinically obvious damage to the lung microstructure even with lower tidal volume positive pressure ventilation, with release of cytokines and other markers of inflammation. There is some evidence that such trauma to the lungs may cause systemic inflammation and have a role in the development of lung damage and multi-organ failure.

Problem Solving in Ventilated Patients

The first priorities are to exclude and, if necessary, correct hypoxaemia or hypercapnia and to detect any adverse effects or complications of ventilation. When a problem arises, consider whether the underlying issue is related to the ventilator (by manually ‘bagging’ the patient, the ventilator can effectively be excluded), an equipment issue, e.g. function/position/blockage of the tracheal tube or is the problem related to the patient’s pathophysiology? Is there progression of the lung problem, e.g. ARDS or development of a new problem, e.g. pneumothorax or bronchospasm? When the problem has been identified, correct management will rectify the situation and is often directed at changes in ventilatory settings and sedation.

Other Aspects of Ventilation

In view of the above problems, interest is increasing around other forms of ventilation and adjuncts that improve oxygenation and CO2 clearance. Examples include high frequency oscillation, use of the prone position, nitric oxide and extracorporeal membrane oxygenation.

Nitric Oxide: Nitric oxide (NO) is an ultra-short-acting pulmonary vasodilator. When added to the respiratory gases (5–20 parts per million), it is delivered preferentially to the recruited alveoli and results in pulmonary vasodilation in areas of well ventilated lung. Blood is diverted away from poorly ventilated areas and ventilation–perfusion mismatch is reduced. It is rapidly inactivated by haemoglobin and so vasodilator effects are limited to the pulmonary circulation.

NO at high concentrations (> 100 ppm) is highly reactive and toxic, and the delivery system used must conform to rigid safety standards. The dose used should be the lowest which is effective in achieving a 20% improvement in PaO2:FiO2 ratio. The concentration of methaemoglobin in the blood and the inspired nitrogen dioxide concentration must be measured. NO therapy is expensive and potentially dangerous. It improves oxygenation in the short term in about 50% of patients but the effect is often transient and no outcome benefits have been shown in clinical trials.

Extracorporeal Membrane Oxygenation: Extracorporeal membrane oxygenation (ECMO) is a possible final option if other conventional techniques of providing ventilatory support have failed. Partial cardiopulmonary venovenous bypass is initiated using heparin-bonded vascular catheters, and extracorporeal oxygenation and carbon dioxide removal are achieved using a membrane oxygenator. A low-volume, low-pressure, low-frequency regimen of ventilation is continued to allow the lungs to recover. Results of a recent trial (CESAR) appear favourable in selected patients but the trial design has been subject to criticism and in the UK the availability of ECMO in adults is limited to very few centres, so the additional risks, benefits and timing of transfer of the severely hypoxaemic patient must be considered. Smaller more portable lung assist devices are under evaluation and may be available for use in the future.

Weaning from Mechanical Ventilation

Weaning is the process by which the patient’s dependence on mechanical ventilation is gradually reduced to the point where spontaneous breathing sufficient to meet metabolic needs is sustained. Because of the adverse effects of mechanical ventilation, weaning should be undertaken at the earliest opportunity and the decision to commence weaning is based largely on clinical judgement.

Ideally, before weaning, the condition requiring mechanical ventilation should have resolved and a patient should:

Weaning is a dynamic process and will involve reduction in level of ventilatory support. Pressure support ventilation (PSV) and synchronized intermittent mandatory ventilation (SIMV) are the most commonly used ventilatory modes and these techniques are forms of partial ventilatory support. The degree of support should be gradually weaned so that the patient contributes increasingly to the work of breathing. Introduction of ventilator independence can be rapid, e.g. a T-piece trial. This involves allowing the patient to breath spontaneously through a T-piece circuit, ideally for 30 minutes up to a maximum of 2 hours. If successful the patient can be extubated, and if not a repeat trial can be performed on a daily basis. A gradual form of weaning is to allow a short period of spontaneous breathing without ventilatory assistance (e.g. initially 1 to 5 minutes) with close observation and monitoring of the patient. The duration and frequency of these trials is increased as the patient’s condition improves.

It may take from a few hours to several weeks before total independence from ventilatory support is achieved. Weaning may also be facilitated by the use of a tracheostomy tube, which has the advantage of reducing dead space and allowing sedation to be discontinued, as they are much better tolerated than a translaryngeal tube. Patients with a tracheostomy and CPAP or partial ventilatory support may be suitable to be stepped down from an ICU to a suitable location (e.g. HDU).

Outcomes from Lung Injury Requiring Prolonged IPPV

While no specific intervention has been shown to provide a clear benefit in the treatment of ALI and ARDS, there appears to be a trend towards increasing survival rates over the past few years. The mortality from ARDS varies widely in the literature and between countries. In the UK mortality approximates to 35–40%, but recognition that lower tidal volume ventilation and avoidance of VALI, as well as more general measures such as bundling of care, restrictive transfusion protocols, early antibiotic administration and nutritional support may all play a part in enhancing survival. Of those that survive, significant functional impairment often persists (severe disease and duration of mechanical ventilation are predictors of persistent abnormal lung function). Reduced exercise capacity, inability to return to work and health-related quality of life significantly below normal are common problems in survivors.

Cardiovascular System

Shock

Many intensive care patients will require support of the cardiovascular system at some time. Failure of the cardiovascular system to deliver an adequate supply of oxygenated blood to organs and tissues results in shock, which if unchecked will result in organ failure and death. Shock often accompanies conditions such as sepsis, multiple trauma and pneumonia and so is often found in ICU patients.

Common mechanisms of tissue underperfusion include: hypovolaemia (e.g. haemorrhage and burns), septic shock, cardiogenic shock, e.g. myocardial infarction and other rarer causes, e.g. anaphylaxis, neurogenic shock and adrenocortical insufficiency. There may be many elements contributing to shock in an individual patient and common features include hypotension, tachycardia, oliguria, increased serum lactate and metabolic acidosis. As initial compensatory mechanisms fail, multiple organ dysfunction ensues, and renal failure and ARDS are common. Hepatic, gastrointestinal, pancreatic impairment and disseminated intravascular coagulation may occur.

Management should be directed at:

Basic Applied Cardiovascular Physiology

Monitoring the cardiovascular system plays a key role in optimization and support and allows guidance towards provision of the all important balance between oxygen delivery and oxygen consumption.

Oxygen delivery can be calculated from the multiple of cardiac output and arterial oxygen content. Arterial oxygen content is determined by arterial oxygen saturation and haemoglobin concentration. Oxygen consumption is the total amount of oxygen consumed by the tissues. The difference between the amount of oxygen carried to the tissues (arterial oxygen delivery) and the amount of oxygen returned to the heart (venous oxygen delivery) indicates the total amount of oxygen consumed by the tissues. Mixed venous oxygen saturation reflects the amount of oxygen returning to the pulmonary capillaries, since it was not used by the tissues to support metabolic function. The pulmonary artery is the site where SvO2 values should be measured. It is important to sample only at this site to allow for adequate mixing of blood from the superior and inferior vena cavae and coronary sinus. Controversies exist as to whether SVC venous oxygen saturation can be used as a surrogate for SvO2 and although it mainly reflects oxygen supply and demand from the head and neck and upper extremities, it correlates reasonably well with the SvO2, without the need for pulmonary artery catheterization.

If the SvO2 is in the normal range (60–80%), then the clinician may assume that there is adequate tissue perfusion. If the SvO2 falls below 60%, a decrease in oxygen delivery and/or an increase in oxygen consumption has occurred. If the SvO2 is elevated above 80%, an increase in oxygen supply and/or a decrease in demand has occurred. An increase in oxygen delivery can be caused by an increased FiO2, Hb, or CO. A decrease in oxygen consumption can be seen in hypothermic states or in patients who are anaesthetized, mechanically ventilated or paralysed. In sepsis, oxygen uptake into the tissues may be decreased.

The volume of oxygen carried by 1 g of haemoglobin is 1.34 mL.

O2 Delivery:

image

O2 Consumption:

image

Therefore, it can be seen that sufficient oxygen delivery can be achieved with good oxygen saturation, haemoglobin concentration 80–100 g L–1 and an adequate cardiac output.

Cardiac output is the product of heart rate and stroke volume. Cardiac index is the cardiac output referenced to the patient’s body surface area. In health there is little fluctuation of cardiac output within the normal range of heart rate (60–160 beats per min.). However the critically ill, especially those with pre-existing heart disease and the elderly, tolerate extremes of heart rate much less well.

At low heart rates, cardiac output falls as a function of reduced heart rate, despite the maintenance of stroke volume.

Tachycardia results in reduced available time for the ventricles to fill and a subsequent fall in stroke volume. With an increase in heart rate, myocardial consumption also increases and this, coupled with reduced diastolic coronary artery perfusion, can lead to significant myocardial ischaemia.

Stroke volume is the amount of blood ejected with each heartbeat and is determined by preload, contractility and afterload.

Preload is the pressure that stretches the cardiomyocytes of the right or left ventricle before contraction. It reflects venous return or the extent of ventricular filling and depends on venous tone, circulating volume and the extent of ventricular relaxation. According to the Frank–Starling law of the heart, the force of myocardial contraction is proportional to the degree of ventricular filling, up to a point when over-stretch of the ventricle may result in a fall in stroke volume and heart failure will subsequently develop.

Afterload is the tension developed in the wall of the ventricle during ejection, i.e. the pressure required to eject blood from the left ventricle. The term afterload is sometimes confused with systemic vascular resistance, which is the overall resistance to flow in the systemic circulation. Afterload is determined by the degree of vasomotor tone, the elasticity of the arterial tree and the presence of valvular stenosis or arterial disease. Afterload is usually high in compensated cardiogenic shock or heart failure, and low in sepsis and high spinal cord injury.

Contractility is the intrinsic force generated by the myocardium, independent of preload and afterload.

Optimization of the Cardiovascular Status

The key aim in improving a patient’s haemodynamic status is optimal cardiac output and oxygen delivery to allow adequate organ perfusion. The precise management of shock is beyond the scope of this chapter but a rational approach includes ensuring optimal filling status initially (a dynamic form of monitoring may be best – see above). If blood pressure, urine output, tissue perfusion and other measures of cardiac output still remain low, positive inotropic or vasopressor drugs may be required. These should be started at low doses and titrated to effect. There is little evidence base to recommend one drug regimen over another and adverse effects can arise with all agents so caution should be exercised.

If the predominant problem is thought to be loss of systemic vascular resistance due to sepsis or other causes then it is logical to start with a vasoconstrictor to increase arterial pressure. Common agents include noradrenaline and phenylephrine, which both act on α1 receptors. Vasopressin is often given as second line to help restore vascular reactivity and tone. If cardiac contractility is thought to be a problem then a positive inotrope is used. The vasodilatation produced by some agents may be beneficial in the presence of a high systemic vascular resistance which is seen in cardiogenic shock.

Examples of positive inotropes can be found in Table 45.8 and further details are found in Chapter 8. Initiation of these drugs requires central venous access, although low dose phenylephrine can be infused through a peripheral cannula.

TABLE 45.8

Positive Inotropic Drugs Commonly Used in ICU

Drug Mode of Action
Dobutamine Increases contractility, and produces peripheral vasodilatation.
Dopexamine Vasodilator at low doses, with reflex tachycardia. Positive inotropic effects seen at higher doses.
Dopamine Vasodilatation at low doses via dopamine receptors. At higher doses, inotropic and vasoconstrictor effects appear.
Adrenaline Positive inotropic and vasoconstrictor effects.
Milrinone, Enoximone Positive inotropic and vasodilator effects by inhibition of phosphodiesterase enzymes.
Levosimendan Positive inotrope which increases myocardial response to calcium.

Cardiac rhythm disturbances are common in ICU patients. Ensure that general resuscitation measures are adequate and treat any electrolyte disturbances (especially of potassium and magnesium). Specific treatment may be required, e.g. amiodarone or digoxin for supraventricular tachycardia (see Ch 8). Other cardiovascular conditions to consider include myocardial ischaemia, cardiac failure and cardiogenic shock.

Gastrointestinal System

The gastroinestinal tract is important in the pathophysiology of critical illness. Not only is it a common site for surgical intervention and a frequent source of intra-abdominal sepsis, the gut is a large ‘third space’ for fluid loss within the lumen of the gut and may also act as a bed for altered blood flow (AV shunting) during shock states. It can become a reservoir for bacteria and endotoxins which may translocate into the portal, lymphatic and systemic circulations, producing the systemic inflammatory response syndrome, sepsis and multiorgan failure, particularly during periods of altered blood flow.

Micro-organisms from the gut can also colonize and infect the respiratory tract, and the gastrointestinal tract itself can be a site for secondary nosocomial infections, e.g. clostridium difficile colitis. The maintenance of gastrointestinal integrity and function is therefore of major importance during critical illness and adequate splanchnic blood flow is thought to be crucial. Early resuscitation in shock states is essential and both volume resuscitation and vasopressors should be used early to aid perfusion pressure. In those patients who are adequately resuscitated, early enteral nutrition may also be of value in helping to preserve mucosal integrity and gastrointestinal function.

Nutrition

It is important to provide adequate nutrition during critical illness, especially as many patients are likely to be already nutritionally deficient from pre-existing illness. When providing nutritional support, estimation of energy and nitrogen requirements are made to attenuate the negative effects of the catabolic phase. However, it is generally accepted that underfeeding is better than overfeeding in terms of mortality, but failure to provide at least 25% of calculated requirements results in greater risk of infection and death.

Vitamins, minerals and trace elements are essential for health. Water and fat soluble vitamins are provided in commercially available preparations while folic acid and vitamin B12 need to be prescribed independently. Trace elements and minerals such as calcium, magnesium and iron can also be added according to need.

Glutamine, arginine, fish oils, selenium and a variety of anti-oxidants have been the focus of research into immuno-nutrition. Currently there is no clear evidence for an improved outcome (many of the studies involved administration of a cocktail of combined substrates) and some substances may only be of benefit in specific patient sub-groups, with associated higher mortality in alternative groups of patients.

It is usually accepted practice to initiate enteral feeding early, although in the resuscitative phase of critical illness, nutrients may not be utilized efficiently. Enteral feeding should be considered before the parenteral route, but can be associated with significant complications, e.g. under-nutrition and high gastric aspirates. Prokinetic drugs (metoclopramide, erythromycin) and the use of a head-up tilt will promote gastric emptying. Diarrhoea can be a problem and the use of pre- and probiotics may help normalize gut flora. There is a risk of aspiration with enteral feeding and recently there has been increased use of post-pyloric feeding; there is no strong evidence that this reduces aspiration.

Fluid Balance

Ensuring adequate fluid balance is a fundamental requirement in treating the critically ill patient. Normal approximate intake in a 70 kg man is 1500 mL from liquid, 750 mL in food and 250 mL from metabolism. In health, output matches input, with insensible losses accounting for approximately 500 mL. In addition to providing adequate water, electrolytes should be replaced: normal daily sodium and potassium requirements are 50–100 mmol per day and 40–80 mmol per day, respectively. A typical maintenance regime might be based on a balanced salt solution, e.g. Hartmann’s, as longer term administration of 0.9% saline can result in hyperchloraemic acidosis.

Fluid balance is almost invariably disturbed in the critically ill patient. Common causes include- widespread capillary leak associated with sepsis and inflammatory conditions leading to peripheral and pulmonary oedema, gastrointestinal dysfunction, fluid sequestration and diarrhoea. Fluid losses occur from burns, fistulae and wounds while increased insensible losses are associated with pyrexia and poor humidification of inspired ventilator gases. High urinary output states such as diabetes insipidus will also result in water loss. Therefore fluid and electrolyte replacement should be dictated by the underlying clinical condition, the overall fluid balance and the serum biochemistry.

Colloids are often preferred to crystalloids when rapid resuscitation, rather than maintenance is required, as a greater proportion remains in the intravascular space following infusion. The SAFE study showed no difference in 28-day outcome of patients admitted to ICU and who were given either albumin or 0.9% saline for fluid resuscitation. Albumin is now used less for volume expansion compared to the relatively cheaper synthetic colloids. However, colloids are associated with an increased incidence of adverse reactions and interference with renal function and coagulation. Blood and blood products should be used in cases of haemorrhage and coagulopathy, guided by local policy and senior advice.

Renal Dysfunction

Renal dysfunction is common in ICU and the cause is often multifactorial. Pre-existing renal disease may be worsened by the patient’s new pathology, and some nephrotoxic drugs are still used in ICU. This section will deal predominantly with new onset renal dysfunction.

Acute kidney injury is defined as an abrupt (within 48 hours) reduction in kidney function, with the diagnosis made on the specific changes from baseline in patients who have achieved an optimal state of hydration (Table 45.9).

TABLE 45.9

Diagnosis of Acute Kidney Injury

AKI Stage Serum Creatinine Criteria Urine Output Criteria
1 Increase in serum creatinine
≥ 0.3 mg dL–1 or
Increase to ≥ 150–200% from baseline		 < 0.5 mL kg–1 h–1 for > 6 h
2 Increase in serum creatinine
> 200–300% from baseline		 < 0.5 mL kg–1 h–1 for > 12 h
3 Increase in serum creatinine to
> 300% from baseline (or serum creatinine ≥ 4 mg dL–1) with an acute increase ≥ 0.5 mg dL–1,
or receiving renal replacement therapy		 < 0.3 mL kg–1 h–1 for 24 h
Or anuria for 12 h

This classification takes into account the significance of even small increases in serum creatinine, given the recognized associated adverse outcomes. When managing a patient with acute kidney injury, focus the history and examination to distinguish potential causes (Table 45.10). These are classically distinguished as prerenal, renal and postrenal causes, although in many patients the cause of acute kidney injury is multifactorial. A sudden cessation of urine output should be assumed to be caused by obstruction until proved otherwise. Ensure the patient is adequately hydrated.

In most cases of AKI the primary cause is prerenal, but up to 10% of cases will have other significant pathologies. Serial U & Es are essential, while urine tests can be helpful (unless the patient has received diuretics) in distinguishing pre-renal from renal failure (Table 45.11).

Other investigations may be needed as determined by the clinical scenario: creatinine kinase/urinary myoglobin, vasculitic screen, and imaging, e.g. CT or renal ultrasound.

In the case of oliguria (urine output < 0.5 mL kg–1 h–1 for at least 2 consecutive hours), consider a fluid challenge of 500 mL colloid. As renal filtration is pressure dependent, renal perfusion pressure should be maintained. If circulating volume is adequate, consider the early use of vasopressors or inotropes to maintain mean arterial pressure > 65 mmHg. If the cause of oliguria remains unclear and there is no response, consider whether any prescribed nephrotoxic drugs need to be stopped. Look for and treat sources of sepsis. Consider loop diuretics if the patient remains oliguric. If cardiac output, mean arterial pressure and renal perfusion pressure have been restored with fluids and drugs and there remains no response to diuretics, renal replacement therapy is likely to be required.

Renal Replacement Therapy (RRT)

Continuous renal replacement therapy is used in intensive care units because the gradual correction of biochemical abnormalities and removal of fluid results in greater haemodynamic stability, compared to intermittent haemodialysis (Table 45.12).

TABLE 45.12

Indications for Renal Replacement Therapy

Classical Indications Alternative Indications
Volume overload Endotoxic shock
Hyperkalaemia (K+ > 6.5) Severe dysnatraemia (Na+ < 115 or > 165 mmol L–1)
Metabolic acidosis (pH < 7.1) Plasmapheresis
Symptomatic uraemia (encephalopathy, pericarditis, bleeding)
Dialysable toxins (lithium, aspirin, methanol, ethylene glycol, theophylline)

Continuous Venovenous Haemofiltration (CVVHF)

The simplest form of continuous renal replacement is continuous venovenous haemofiltration. As the patient’s blood passes through a filter, plasma water, electrolytes and small molecular weight molecules pass through down a pressure gradient. This filtrate is discarded and replaced by a balanced electrolyte solution. Typically 200–500 mL h–1 of filtrate are removed and replaced. Overall negative fluid balance can be achieved by replacing less fluid than is removed. As no diasylate is used, solute movement is entirely dependent on convective transport, which is a slower removal process, so clearance of small molecules and solutes is inefficient. This can require large volumes of filtrate to be removed and replaced in order to achieve acceptable creatinine clearance.

Continuous Venovenous Haemodialysis (CVVHD)

Continuous haemodialysis depends on diffusive solute clearance occurring because of the countercurrent flow of dialysate fluid through the haemofilter. Fluids, electrolytes and small molecules can move in both directions across the filter, depending on hydrostatic pressure, ionic binding and osmotic gradients. Overall creatinine clearance is greatly improved compared with haemofiltration alone. In CVVHD, provided the volume of dialysis fluid passing out from the system matches the volume of dialysis fluid passing in, there is no net gain or loss of fluid to the patient. By allowing more dialysate fluid to pass out of the filter than passes in, fluid can be effectively removed from the patient, with removal rates of up to 200 mL per hour possible.

Vascular Access for Renal Replacement Therapy

Renal replacement therapies require dedicated vascular access (using a 10–14 Fr gauge catheter). Veno-venous RRT has replaced arteriovenous RRT, as the latter has greater vascular morbidity and requires an adequate arterial pressure to drive flow. For veno-venous access, a single large vein is cannulated percutaneously with a double-lumen catheter using the Seldinger technique. All catheters have a lumen that functions as the ‘arterial’ outflow limb of the circuit and a second lumen which functions as the ‘venous’ inflow limb of the circuit. The ‘arterial’ port removes blood from holes in the side of the catheter and blood is returned down the ‘venous’ lumen through a single hole at the catheter tip to minimize recirculation of haemofiltered blood. When not in use, these catheters are at risk of clotting off, and so it is often necessary to fill the deadspace (labelled on catheter) with heparin 1000 units mL–1.

Similarly as blood is passing through an extracorporeal circuit, some form of anticoagulation is required (unless the patient has severe coagulopathy) and either heparin or prostacyclin infusions are run directly into the dialysis circuit. Citrate has also been used as a form of anticoagulation.

Table 45.13

Interest has recently centered upon the role of CVVHF in sepsis. Many patients with AKI have multi-organ dysfunction and most mediators involved in the inflammatory response are water soluble middle-sized molecular weight compounds, such as tumour necrosis factor (TNF), interleukins (IL-1, IL-6, IL-8), platelet activating factor (PAF) and complement. The highly porous synthetic membranes used for convective filtration in CVVHF lend themselves to elimination of such compounds through filtration and adsorption. However, high volume haemofiltration (HVHF), producing ultrafiltration volumes of more than 75 litre day–1, may be required to produce significant reductions in plasma mediator concentrations because of their very high generation rate. Recent outcome studies have not supported this approach.

Outcomes After Kidney Injury

Acute kidney injury has three potential outcomes: return to baseline function, the development of chronic kidney disease, or persistent renal failure. Most cases of AKI occurring in ICU return to baseline function over time (acute tubular necrosis pattern, may take up to 6 weeks). The re-establishment of a spontaneous urine output is generally followed by a polyuric phase which gradually settles. However, a proportion of patients may develop chronic kidney disease in previously normal kidneys (e.g. acute cortical necrosis pattern, most commonly in pregnancy). Patients with pre-existing renal disease may have accelerated disease progression and increased risk for end stage disease. The latter two groups of patients will therefore benefit from early referral to renal physicians for longer term management.

Neurological System

Despite the wide range of pathologies that require patients to be admitted to the ICU for specialized neurological support, some specific treatment regimens are common to them all. Recognition of the primary problem and any secondary pathologies (e.g. a secondary brain haemorrhage) is important, as is the prevention of secondary injury due to brain swelling or poor perfusion.

Irrespective of the primary cause of neurological damage, secondary injury may be caused by hypoxaemia, hypotension, hypercapnia, seizures, hyperglycaemia and other metabolic disturbance. In order to prevent this, measures need to be taken and will include securing the airway and instituting mechanical ventilation. These are the main principles underlying neuro-critical care. Ventilatory variables should be set to achieve a PaCO2 of 4–5 kPa. Aggressive hyperventilation needs to be avoided as hypocapnia induces cerebral vasoconstriction and may promote cerebral ischaemia in the context of brain injury. The inspired oxygen concentration needs to be adjusted to sustain a PaO2 in excess of 12 kPa and appropriate steps taken to maintain blood pressure within the normal range. Ideally mean arterial pressure should be maintained above 70 mmHg as even isolated periods of systolic pressures below 90 mmHg have been shown to be associated with worse outcome in the case of traumatic brain injury. Intravenous administration of glucose should be avoided as hyperglycaemia increases cerebral metabolic rate and i.v. insulin should be infused if the blood glucose concentration exceeds 11 mmol L–1.

The plasma osmolality and serum sodium concentration should be monitored carefully because hypo-osmolality of the plasma creates an osmotic gradient across the blood–brain barrier which can provoke cerebral oedema. Hyperthermia (even mild) should be avoided as this increases cerebral metabolism and worsens outcomes. However the benefits of induced hypothermia are unclear as it affects other systems. For example, hypothermia worsens coagulopathy and could be detrimental in the case of cerebral haemorrhage. Currently induced hypothermia has only been shown to be of benefit after out-of-hospital cardiac arrest, where the primary rhythm was ventricular fibrillation.

Patients with severe head injury (GCS < 8) and/or focal signs (which may not necessarily require surgical correction) should be referred to a regional neurosurgical centre, as should patients who require ventilation and ICP monitoring. Discussion and review of CT scans should be undertaken with the neurosurgeons before transfer. Transfer should be in accordance with national guidelines and will include:

In patients with severe head injury and an abnormal admission CT scan, it may be appropriate to monitor cerebral perfusion pressure (CPP) by direct measurement of ICP and mean arterial pressure. ICP should be maintained within the normal range if possible; sudden increases may occur in patients who are restless or hypertensive, and adequate sedation and analgesia are usually important components of therapy. Deep sedation with neuromuscular blockade may be necessary to minimize cerebral metabolism and therapy can be guided using the EEG to attain burst suppression.

CPP can be manipulated with fluid loading and the use of vasopressor agents. However, high arterial pressure should be avoided, because many patients with brain injury have impaired cerebral autoregulation and a high CPP may result in increased cerebral oedema. Hypotension does need to be treated, however, as critical CPP, when ischaemia is likely to occur, is in the order of 30–40 mmHg.

Other useful measures to consider when managing the patient with acute neurological injury include nursing in a head up position to improve venous drainage. Increasing serum osmolality to 300–310 mOsm L–1 using mannitol or hypertonic saline judiciously will reduce brain tissue water and result in a fall in ICP. In addition it is important to control clinical and subclinical seizures as these have a detrimental effect on cerebral metabolism. At all times therapy should be adjusted to maximize oxygen delivery, minimize oxygen consumption, preserve cerebral blood flow and normalize ICP.

OTHER ASPECTS OF INTENSIVE CARE

Venous Thromboembolism Prophylaxis

An estimated 25 000 people in the UK die from preventable hospital-acquired venous thromboembolism (VTE) every year. Therefore it is a considerable cause of mortality and, in non-fatal cases, morbidity. The critical care population is at higher risk than general medical patients for a number of reasons including: severe physiological upset, maximal inflammatory response, the presence of intravascular catheter devices, injuries specifically implicated in VTE, e.g. pelvic and long bone injuries, and often long periods of immobility. Similarly these patients are also at increased risk from anticoagulation therapy, due to disease process/concurrent interventions and treatment, so pharmacological prophylaxis with low molecular weight heparins can potentially be problematic.

Low-molecular-weight heparins are associated with a lower incidence of haemorrhage and heparin-induced thrombocytopaenia than unfractionated heparin. In addition their use does not require monitoring of activated partial prothrombin time (APTT). Unless contraindicated, mechanical means (such as anti-embolic stockings) of VTE prophylaxis should also be given to all patients.

Where both mechanical and pharmacological prophylaxis are contraindicated and the patient is at high risk, consider the requirement of an inferior venal caval filter. There should be a daily review of the risk of venous thromboembolism, risk of bleeding and therefore thromboprophylaxis. Early mobilization and physiotherapy where possible, and avoiding dehydration can also help reduce the risk of VTE.

ICU-Acquired Muscle Weakness

Neuromuscular abnormalities resulting in skeletal muscle weakness are a common occurrence in the intensive care unit. Some degree of loss of muscle mass is likely in all cases of immobility and critical illness. However, more severe problems are commonly seen and they can be described into two distinct conditions, namely polyneuropathy and myopathy. However, it is likely that these two entities often coexist, and while the exact incidence remains variable amongst studies, their presence is associated with multiple adverse outcomes, including higher mortality, prolonged duration of mechanical ventilation, and increased length of stay.

The pathogenesis of such nerve and muscle damage is not well defined, but probably involves inflammatory injury of nerve and/or muscle that is potentiated by functional denervation and corticosteroids. The latter is a well identified risk factor for developing acquired muscle weakness. Other risk factors include sepsis, hyperglycaemia, neuromuscular blockade and increasing severity of illness. The clinical diagnosis of ICU-acquired neuromuscular disorders is suspected in the presence of unexplained weakness in patients recovering from critical illness. Weakness can be so severe as to be confused with coma. Other metabolic, pharmacologic, and central-nervous-system causes of weakness must be ruled out before establishing the diagnosis. Electrophysiological testing is useful primarily to exclude other (possibly treatable) causes of severe weakness, e.g. Guillain–Barré syndrome or cervical spine problems.

So far the only intervention recognized to reduce the incidence of ICU acquired muscle weakness is intensive insulin therapy and standard measures that reduce the severity and duration of the critical illness episode (e.g. early recognition and treatment of sepsis). Physical rehabilitation may accelerate recovery and the National Institute for Health and Care Excellence has published guidelines recognizing the value of rehabilitation during and post critical care, however more research is required for an improved understanding of this illness.

Healthcare-Associated Infection (HAI)

Unfortunately HAI is common, especially amongst ICU patients where risk factors such as immunocompromise, tracheal intubation, the presence of intravascular and urinary catheters, antimicrobial therapy, stress ulcer prophylaxis and protracted length of stay are frequent. Catheter-related blood stream infections, ventilator-associated pneumonia, Clostridium difficile diarrhoea and emergence of antibiotic-resistant bacteria such as methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant enterococcus (VRE) remain important causes of ICU mortality, morbidity and increased financial burden. Routine surveillance of HAI rates is essential to identify problematic pathogens and to develop initiatives to reduce their incidence.

Preventative measures are multifactorial and start with good standards of hospital environmental cleanliness. The EPIC study recognized poor hand hygiene as being a major factor in nosocomial infection and great effort has gone into publicizing good hand hygiene at a national level. Protective garments should be worn with all patient contact, however gloves are not a substitute for hand washing.

Catheter-Related Bloodstream Infection (CRBSI)

CRBSI is common in the ICU and results from venous and arterial catheters becoming coated in plasma proteins following insertion. Bacteria are then able to migrate from the skin and catheter hubs to become embedded in this protein sheath, with both external and endoluminal colonization occurring. There is a direct relationship between the number of organisms colonizing the catheter and the risk of CRBSI and presence of thrombus also increases this risk. Mortality from CRBSI may be as high as 25% and diagnosis is made from a positive blood culture with the same organism grown from the access device.

To reduce rates, the need for invasive catheters should always be considered in the first instance. Consider the site of insertion: the subclavian vein has the least risk of catheter-related bloodstream infection compared to the internal jugular and femoral veins, respectively. Strict aseptic technique should be adhered to on insertion and during all handling of catheters. If the device is to be used for parenteral nutrition, ensure that there is a dedicated line or lumen for this. If there is a suspicion of CRBSI, the catheter should be removed and antibiotic therapy tailored to the culture result. Matching Michigan is a quality improvement project based on a model developed in the United States. It introduced data definitions (infection rates per 1000 catheter days) as well as technical and non-technical interventions in order to reduce catheter-related bloodstream infection and a similar project is underway across the UK.

Antibiotic Therapy

Appropriate antibiotic use is imperative, and local policies as well as advice from the microbiologist are important sources of information. If appropriate empirical therapy is started early, clinical outcomes from serious infection are improved (as per the Surviving Sepsis campaign). De-escalation when a causative pathogen is identified reduces inappropriate use and minimizes superinfection. Rotation of antibiotics has been used but conflicting evidence has suggested that there may be promotion of resistance amongst Gram-negative organisms. Selective decontamination of the digestive tract (SDD) is a technique designed to eradicate aerobic, potentially pathogenic bacteria colonizing the oropharynx and upper gastrointestinal tract, thus eliminating an important risk factor for nosocomial pneumonia. It has not been widely adopted in the UK because of its inconsistent effects on mortality and concerns about the potential for selecting antibiotic-resistant pathogens.

Ventilator-Associated Pneumonia (VAP)

VAP is a common nosocomial infection occurring in ICU patients receiving mechanical ventilation for > 48 hours. There is no gold standard for diagnosis, so exact incidence remains difficult to estimate but mortality is in the order of 30%. Aerobic Gram-negative bacilli colonize the oropharynx and upper GI tract (augmented by the use of H2-receptor antagonists) and these pathogens gain access to the lungs with movement aided by the positive pressure of mechanical ventilation. Clinical suspicion should arise with standard diagnostic features of pneumonia but this is non-specific. Quantitative culture of bronchio-alveolar lavage specimens should aid diagnosis. Treatment is timely administration of appropriate antibiotics and preventative measures include scrupulous hand washing, good oral hygiene, nursing the patient semi-recumbent, ensuring adequate tracheal cuff inflation, improved cuff design, supraglottic suction, the rational use of H2-receptor antagonists, avoiding the need for re-intubation where possible and potentially SDD.

Psychological Problems on the Intensive Care Unit

Longer stay patients on the ICU can suffer significant psychological morbidity. A combination of the underlying pathology, sedative and analgesic drugs, an environment of loud noise, bright lights, and frequent nursing input can all lead to sensory overload which may result in anxiety, depression, delirium and hallucinations during treatment. Research into the longer term consequences of surviving critical illness has suggested that for a significant number of patients there may not only be continuing physical debilitation, but also a risk of subsequent depression, post traumatic stress disorder and a potential loss of cognitive function. Family dynamics may become altered as can financial security, so it is important to identify patients at risk of physical and non-physical morbidity and work towards short and medium term agreed rehabilitation goals in an attempt to optimize recovery.

Delirium in ICU

Delirium is often under diagnosed, but is associated with increased length of hospital stay and is an independent predictor of increased mortality at 6 months. It is often described as hyperactive, hypoactive or a mixture of both. A validated tool such as the Confusion Assessment Method for the Intensive Care Unit (CAM-ICU) can be used to detect delirium. Preventative measures include avoidance of pharmacological precipitants where possible (although this may be impossible in practice) and employing non-pharmacological interventions such as clear communication, provision of clocks, calendars, diaries and the patient’s own familiar objects. In addition, consistent nursing care, controlling excess noise and creating a day/night cycle are also helpful. Allowing self-care where possible and ensuring that the patient has their own glasses, dentures or personal items can often be as important as treating any organic cause. If preventative measures fail and no organic cause can be found, treatment with haloperidol and other drugs may be helpful.

Care Bundles

There is an increasing interest in the development of ‘care bundles’ for specific ICU illnesses. They consist of a number, usually up to 5 or so, of evidence-based practices each of which has been shown to improve outcome and is easily achievable. When performed collectively, reliably and continuously these bundles confer a greater probability of survival. The most familiar bundles are the Surviving Sepsis Campaign resuscitation (6 hours) and management (24 hours) bundles and ventilator care bundles. The ventilator care bundle comprises the following components to reduce acute lung injury and ARDS:

image low tidal volumes (6 mL per kg predicted body weight)

image capped plateau airway pressure (30 cmH2O)

image sedation holds and use of sedation scores. The practice of interrupting continuous sedative infusions on a daily basis to allow intermittent decreased sedation, has been shown to reduce length of ICU stay

image permissive hypercapnia (accepting a PaCO2 above normal to allow pressure limitation and low plateau airway pressures)

image semi-recumbent positioning (head up by 45° unless contraindicated) during ventilation to reduce the incidence of ventilator-induced pneumonia

image lung recruitment by PEEP to prevent alveolar collapse at end-expiration

image avoidance of neuromuscular blocking drugs may reduce the incidence of skeletal muscle weakness associated with critical illness

image protocol-driven weaning

Ventilator associated pneumonia rates have been shown to be reduced by combining sedation holds, semi-recumbent nursing, peptic ulcer prophylaxis, DVT prophylaxis and daily oral hygiene with chlorhexidine. Good nursing care should not be underestimated and is an important contributor to good overall outcome.

ETHICAL ISSUES IN ICU

As in all medical practice, four ethical principles can be applied to the ICU patient.

Autonomy relates to the patient’s individual dignity and is about respect for the individual and their ability to make decisions with regard to their own health and future. To do this they must be able to understand and believe the information given.

Beneficence is the concept that any action that is performed on the patient should be in that patient’s best interest, i.e. doing the greatest good whilst balancing the risks and benefits. The corollary of that is that any action carried out on a patient must not harm that patient, which is the concept of non-maleficence. The fourth principle is the notion of justice. This relates to fairness, equitable use of resources and equal access to care. Individuals should be similarly treated. When a resource is limited, there is potential for an individual’s treatment to affect the wellbeing of someone else.

There are inherent problems with achieving all of these ideals in the ICU situation. For a patient to have the capacity to consent to a treatment, they must be able to understand information relevant to that treatment, retain that information, use or weigh up that information as part of the process of making a decision and finally they must be able to communicate their decision. Thus the majority of patients at some point during their ICU admission will lack capacity. It is important to be able to defend decisions regarding treatment or withholding of treatment so there must be robust evidence that a patient’s lack of capacity has undergone assessment. It is prudent to discuss complicated matters with consultant colleagues so that a consensus of opinion can be formalized before difficult treatment decisions are made. With the patient who lacks capacity, management is directed towards the patient’s best interests and although there should be documented evidence of involvement of the patient’s family and others close to them, the next of kin does not have a decisive role and cannot formally consent on behalf of a patient who lacks capacity.

OUTCOME AFTER INTENSIVE CARE

Attempts to predict outcome after discharge from critical care has led to the development of a number of scoring systems, which generally involve collection of large quantities of data, stratifying this data to produce a risk score and using this to predict survival for a patient population. However there are flaws with this approach including problems of diagnostic categorization: the initial hospital diagnosis may bear little relation to the subsequent, often multiple pathologies in the individual ICU patient. While scoring systems are helpful in predicting population outcomes, their application to individual cases is limited. Patients may survive discharge from the ICU, but mortality remains high on the wards and at home, so that 6-month or 1-year outcomes of mortality and morbidity may prove better end points than the traditional 28-day mortality.

Assessments of functional disability, quality of life and return to work among patients who have survived an admission to the ICU are more difficult to quantify than death, but the small numbers of studies which have been undertaken suggest that mortality is significantly higher than would be expected in matched individuals for several years. In addition, a significant proportion of patients report impaired quality of life and that many remain unable to work for prolonged periods after discharge. However, the majority of patients who survive can return to a reasonable quality of life.

There are a number of scoring systems in use:

Some patients with, for example, diabetic keto-acidosis may score highly and have a perceived high risk of death, but they generally get better quickly. Lead-time bias results from the stabilization of patients in the referring hospital before transfer. This artificially lowers the score for the patient arriving at the referral centre. Finally the Glasgow Coma Scale component may be difficult to interpret, as clearly there is a difference in GCS 3 from head injury compared to GCS 3 from drug induced sedation.

The importance of national collaborative audit and research in improving the practice of critical care is well recognized and the Intensive Care National Audit and Research Centre for England and Wales (ICNARC) collects demographic data, diagnostic criteria, physiological scoring and outcome for the majority of patients admitted to ICU. The case mix programme for April 2008 to April 2009 noted almost 90 000 admissions across 180 general ICUs in the UK. In this dataset, mortality in the intensive care unit was 17%, while acute hospital mortality was almost 26%.

DEATH IN THE ICU

Death is common and is a fundamental part of ICU care. Unfortunately, despite maximal support and care, some patients succumb to the overwhelming nature of the underlying disease process. Few deaths are directly attributable to an unexpected primary cardiorespiratory arrest, once the patient is fully supported on the ICU, hence ‘do not resuscitate’ (DNR) orders are less relevant to critical care than care on the general ward.

Futility and withdrawal

Approximately 70% of deaths occur on the ICU following withdrawal of support, where continued treatment would be futile; however, legally, the cause of death remains the underlying pathological process. This typically follows a variable period of continued deterioration or a failure to improve, despite maximal appropriate supportive therapy.

A principle of justice in the treatment of intensive care patients is based on the fact that all patients have an equal right to all treatments. Yet some patients with extensive comorbidities or very advanced disease have very little prospect of responding to such treatment. Therefore, to offer them such treatment is futile and unlikely to be in their best interests. Equally, it would be misuse of scarce resource which would be then unavailable to another patient.

There is no legal distinction between the withdrawal of life-sustaining treatment or limiting or withholding treatment. It is important to note that withdrawal of treatment does not equate with withdrawal of all of the basic care given by nurses and doctors including symptom relief. There is a lack of consistency regarding withdrawal, as timing, the actual treatments withdrawn and the manner of withdrawal may vary considerably between intensive care units. In the UK, relatives do not have legal rights of decision making but it is important not to exclude them from honest and timely discussions when withdrawal is being considered.

The process of withdrawal centres upon either setting limits to levels of supportive therapy or a reduction of such interventions, in anticipation that the patient is likely to deteriorate or die without such support. Once the decision is made and an agreement with the family and admitting team has been obtained, support is reduced along the following lines:

The General Medical Council has a guideline relating to withdrawal of treatment and resolution of potential conflicts that may arise when the decision to withdraw is made.

Dependent on the speed of decline, patients may die on the ICU, or be discharged to ward-based care. Occasionally patients may improve despite all odds and clinicians should be prepared to revisit such clinical decisions over time.

Once a patient has died, confirmation of death is required. Although in the UK there is no actual legal definition of death, it should be identified as the irreversible loss of the capacity for consciousness, combined with the irreversible loss of the capacity to breathe. (See a code of practice for the diagnosis and confirmation of death: www.aomrc.org.uk.)

A death certificate may be issued by a doctor who has provided care during the last illness and who has seen the deceased within 14 days of death. Deaths must be reported to the coroner in the following instances:

Depending on the circumstance, a post mortem may be necessary.

Brainstem Death

In patients with overwhelming brain injury, brainstem death testing allows futile treatments to be withdrawn. Clinical features of brainstem death will include profoundly reduced conscious level, with loss of cranial nerve reflexes. As the brainstem is compressed systemic features may include hypertension and bradycardia (Cushing’s reflex), followed by hypotension and vasodilation. Hypothalamic and pituitary function is lost (diabetes insipidus) and reduced thyroid hormone synthesis occurs. Hypothermia is common due to a loss of thermoregulation.

Preconditions for brainstem death testing include:

The tests are undertaken by two medical practitioners, one of whom is a consultant and both of whom have been registered with the General Medical Council for more than 5 years. Two sets of tests are performed and time of death is recorded when the first test indicates brainstem death.

image Pupils must be fixed and not responsive to light (cranial nerves II, III)

image There must be no corneal reflex (cranial nerves V, VII)

image Vestibulo-ocular reflexes are absent, i.e. no eye movement occur following injection of ice cold saline into the auditory meatus (cranial nerves, III, IV, VI, VIII)

image No facial movement will occur in response to supra-orbital pressure (cranial nerves V, VII)

image No gag reflex to posterior pharyngeal wall stimulation (cranial nerve IX)

image No cough or other reflex in response to bronchial stimulation with a suction catheter passed down the tracheal tube (cranial nerve X)

image No respiratory movements will occur when disconnected from the ventilator, hypoxia is prevented with pre-oxygenation and oxygen insufflation via a tracheal catheter and PaCO2 should be > 6.65 kPa.

Spinal reflexes may be present or exaggerated.

ORGAN DONATION

Patients who fulfil the criteria for brainstem death should be considered for organ donation. If suitable on medical grounds and permission is given by the patient (by previous expressions of interest) or relatives, then so-called beating heart donation can take place. After careful planning, the patient is taken to theatres and organs removed before or at the time of circulatory arrest.

At the time of writing, nearly 8000 patients are registered and waiting for a transplant in the UK and demand continues to outstrip supply. With this in mind, moves have been made towards increasing the numbers of non-heart beating organ donors (patient pronounced dead on the basis of loss of cardiac function before organ retrieval).

Whether organ retrieval is from heart beating or non-heart beating donation, appropriate consent must be obtained and early liaison with the transplant coordinator is crucial in determining suitability. There will be a donor management protocol that should be followed to ensure optimal organ viability. The whole process takes time and major coordination between the various teams involved.

Other tissues, e.g. corneas, skin, bone and heart valves, can be removed later after death if appropriate.

DISCHARGE FROM INTENSIVE CARE

For those patients that survive, discharge from ICU is appropriate when their condition has improved so that they no longer warrant intensive care support. Careful discussion with the relatives and admitting teams should be undertaken with clear documentation of decisions made in relation to re-escalation of treatment, readmission to intensive care, whether or not to attempt resuscitation and other ongoing management.

Those patients whose levels of care are to be reduced need to be sufficiently fit for discharge so that their underlying disease process is stable and/or improving. Consideration needs to be made regarding where such patients are to be discharged to. Frequently, discharge is to a high dependency unit or if the patient is fit enough, back to a general ward, with outreach review. If the patient has been transferred from another hospital, ideally they should be returned to the referring hospital as soon as possible. Discharges should be made during daytime hours, as discharges made outside these times are more likely to experience deterioration and readmission.

Follow-Up Clinics

Follow-up clinics are an important aspect of continued treatment of a patient’s physical and emotional wellbeing, as well as a means of service evaluation and an opportunity for patients to reflect and give feedback on their experience. Following periods of critical illness, patients typically experience impaired physical and mental functioning as a result of the underlying disease processes or complications occurring on the ICU. Commonly seen problems include:

In the UK, recommendations have been made to advocate the use of follow-up clinics but its provision as yet remains inconsistent, and cost effectiveness may place restraints on its continued development.

FUTURE DEVELOPMENTS

Few major therapeutic developments have been made with regard to ICU care over the last few years. Published trials which initially showed promise have later been repeated and have not translated well to broad use in the critical care setting. This may partly be due to the heterogeneous nature of the disease and the population but also flaws in study design.

Future focus may well be directed toward better identification of patient populations through genetics and biomarkers, which will aid research into novel therapeutic strategies. Whilst there is already recognition that restoration of haemodynamic variables to normal values is not necessary, better use of functional technology and monitoring tools will help guide resuscitation. There probably will be greater emphasis on bundles of care and perfection of weaning and sedation regimes in addition to computer-led advances.

Demand for critical care resources is likely to continue to grow in the face of an ageing population and ongoing improvement in medical management of cardiorespiratory, cancer and other degenerative diseases. It is likely that some sort of rationing may be used when outcomes in terms of quality life years is likely to be poor. A public and legally accepted recognition of the limitations of what can and should be offered is needed.

Intensive care medicine is an exciting and developing specialty and focused training should continue to aim to attract young clinicians from a variety of primary specialties.

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