Tim Crozier
12.1 Introduction: what is intensive care?
Intensive care is a relatively new specialty, which has evolved at a considerable pace over the past 30 years. Intensive care medicine involves the care of critically ill patients within a dedicated ward of the hospital, with the ability to continuously monitor and support the various organ systems while allowing the patient to recover. The intensive care unit (ICU) is staffed by dedicated intensive care specialist doctors (intensivists) and specialist intensive care nursing staff. There are medical staff present within the unit at all times and most patients are nursed at a 1:1 ratio of nurses to patients. Other staff such as physiotherapists, dietitians, speech therapists and pharmacists all play an important role within the unit.
Surgical patients within the ICU are looked after by the ICU staff but are also cared for by their primary surgeon or surgical team. Further subspecialty medical or surgical input is sought on a case by case basis. This collaborative approach allows discussion about the patient’s status and facilitates a joint approach to decision making. Good communication between the treating parties is of paramount importance.
12.2 Patient selection
Most ICU patients are admitted directly from the operating suite or recovery room. This may be a planned event but may also occur as a result of an unexpected complication, such as anaphylaxis or major haemorrhage. Some patients may develop problems on the postoperative ward and require ICU admission some days after their original operation.
Post elective surgery
Postoperative ICU admission after elective surgery is most commonly a planned event, with the surgeon, anaesthetist, intensivist and patient all expecting a postoperative ICU stay. This may be because of the nature of the surgery (such as coronary artery bypass grafting) or because of a severe coexistent medical problem that may complicate what would otherwise be a relatively routine operation and anaesthetic. In this case, preoperative consultation with the patient’s primary medical specialist(s) is important. Optimisation of the patient’s medical problems is always desirable if time permits. In certain circumstances surgery may be best deferred or even not offered if the patient is felt to be at extremely high risk. Very occasionally, patients are admitted to the ICU preoperatively for line insertion and haemodynamic/respiratory/renal or metabolic optimisation.
Post emergency surgery
Certain presentations, such as severe trauma, often necessitate time-critical surgery. In these instances ICU care may be instigated without a full knowledge of the patient’s prior functional state, comorbidities or previously expressed wishes. Every effort should be made to access this information as soon as possible to aid in ongoing decision making.
Unplanned admission from the surgical ward
Postoperative deterioration on the surgical ward is not an uncommon problem and patients may require admission to the ICU. Many hospitals nowadays have a rapid response or medical emergency (MET) team to intervene early in the patient’s course and either avert an ICU admission or facilitate rapid transfer to the ICU or operating theatre. This response service may be activated by any member of the medical or nursing staff and calling criteria are based on a set of physiological variables including pulse rate, respiratory rate, blood pressure and conscious state.
Scoring systems
There have been a number of scoring systems developed to quantify how ‘sick’ a patient is on admission to the ICU and to predict patient outcomes. Examples of such scoring systems are the acute physiology and chronic health evaluation score (APACHE) and the simplified acute physiology score (SOFA). Although very useful, none of these systems are yet accurate enough to predict outcome for individualpatients.
12.3 Throughput and efficiency
In Australia, demand for ICU beds is increasing and as such it should be treated as a limited resource. It is also very expensive. It is therefore important that where possible patients are smoothly transitioned through ICU and then to the surgical ward when their condition allows. Some patients, however, end up requiring a prolonged period of ICU support.
12.4 ICU versus high dependency unit care
A high dependency unit (HDU) is a geographical space, usually of four beds or more, where higher acuity patients who do not require ICU-level supports can be cared for. In Australia and New Zealand HDUs commonly coexist within the physical confines of the ICU. HDU patients are typically less unwell than ICU patients but are at high risk for complications. HDU patients are commonly nursed at a 1:2 nursing ratio. Typically, HDU patients may require low-dose vasoactive medications, noninvasive ventilation or simply close nursing care and fluid balance measures. Patients who require invasive ventilation or increased support should be in the ICU.
12.5 Postoperative ICU care
Many patients who are admitted to the ICU postoperatively have no problems; their ICU stay is little more than an extension of their time in the recovery room. However, many patients are extremely unstable in the immediate postoperative period and pose significant challenges to the ICU staff. A further subset of patients initially behave in a stable manner before becoming unstable some hours into their ICU stay. It is therefore extremely important that monitoring and observations of the patient are diligently undertaken and that potential problems are anticipated and averted whenever possible.
Monitoring — an overview
Monitoring is one of the mainstays of intensive care. It allows for early detection and treatment of problems and to observe and titrate any interventions made. Monitoring may be invasive or noninvasive and includes point of care tests such as arterial blood gases (Table 12.1).
Table 12.1 Examples of monitoring by systems
|
Cardiovascular monitoring |
|
|
Noninvasive |
Invasive |
|
ECG monitoring |
Intra-arterial line — invasive blood pressure monitoring |
|
Respiratory monitoring |
|
|
Noninvasive |
Invasive |
|
Thoracic impedance measurement of respiratory rate (RR) |
Venous/arterial blood gas monitoring (also allows metabolic monitoring) |
|
Neurological monitoring |
|
|
Noninvasive |
Invasive |
|
Continuous EEG monitoring |
Measurement of intracranial pressure (ICP) |
Intra-arterial and central venous pressure access
Intra-arterial blood pressure monitoring allows continuous ‘beat to beat’ monitoring of the blood pressure. This is achieved by inserting a catheter into an artery, most commonly using the Seldinger technique of entering a vessel with a needle, inserting a guidewire and then threading the catheter over the guidewire. The catheter is then attached to a pressure transducer and levelled at the phlebostatic axis (the level of the tricuspid valve). Common arterial sites selected are radial (Fig 12.2), femoral and dorsalis pedis. Complications include arterial occlusion, arterial dissection, distal ischaemia and embolisation, infection and bleeding. There are many case reports of limb or digit loss secondary to one of these complications. For this reason, end arteries such as the brachial artery or the femoral artery in young children are less commonly preferred.
Figure 12.1 Swan-Ganz catheter
A: line to inflate the balloon in pulmonary microvasculature; B: line for measuring pulmonary capillary (left atrial) wedge pressure; C: line for measuring right artial pressure; D: thermistor catheter for measuring cardiac output by thermodilution
Figure 12.2 Radial artery cannulation
Central venous cannulation allows for measurement of the central venous pressure and for administration of drugs into the central circulation. Central venous catheters may be single or multilumen and are usually inserted via the Seldinger technique. Common sites (Fig 12.3) include the internal jugular, subclavian and femoral veins. These veins are often localised by ultrasound prior to insertion. The catheters are placed so the distal tip lies in the superior vena cava (SVC) for internal jugular and subclavian catheters. Complications relate to either their insertion (pneumothorax, arterial puncture, haemothorax, haematoma) or presence in a central vein (blood stream infection, venous thrombosis/embolisation, venous perforation etc).
Figure 12.3 Central venous catherisation
A: infraclavicular approach. A short 15-gauge needle is passed below the clavicle near the junction of the middle and lateral thirds and directed towards the suprasternal notch. B: internal jugular approach. The needle is inserted lateral to the sternomastoid muscle about two fingers above the clavicle and directed towards the suprasternal notch.
Nursing care
The bedside nurse plays a vital role in the overall care of the intensive care patient, being responsible for monitoring the patient’s overall status and vital signs, implementing the physician’s therapeutic plan and attaining physiological targets, administering medications and infusions and, often, adjusting and running the various machines attached to the patient, such as the ventilator or haemodialysis machine. Nursing staff are often in the best position to first notice a change in the patient’s condition and then notify the medical staff. Communication between the two groups is absolutely of paramount importance.
In addition to the above, other tasks such as providing patients’ personal care and giving information and reassurance to family members and patients are equally important.
Meticulous nursing care and attention to detail is one of the factors most responsible for a patient’s recovery and smooth transition through the ICU to the ward.
Organ preservation
Preservation of organ systems and support of their functions is one of the cornerstones of ICU management. In any patient, but particularly the critically ill, avoidance of hypoxaemia and hypotension is vital to prevent further, secondary injury to organ systems already damaged by the primary insult. This is achieved by maintenance of oxygen delivery to the tissues (i.e. reversal of shock), optimisation of the patient’s volume state, correction of severe metabolic abnormalities, neuroprotective strategies in central nervous system injury and other directed therapies to assist recovery, such as early antibiotic treatment of infection and surgical drainage of abscesses.
Individual organ system dysfunction and supports will be discussed further later in this chapter, as will sepsis.
Wound healing in the ICU
Intensive care patients often have significantly impaired wound healing, which is due to a multitude of factors. As can be imagined, poor wound healing, wound breakdown and susceptibility to infection can have a major adverse effect on a patient’s recovery from surgery.
Poor wound healing may be due to a number of causes such as:
• poor nutrition — often present in ICU patients and frequently predating their ICU admission
• cigarette smoking
• compromised blood supply — may be secondary to poor cardiac output (CO), vasoconstrictive drugs or surgical factors
• concurrent infection — either associated with the surgical site or at a distant site
• chronic renal or hepatic disease
• poor premorbid state
• medications — prednisolone, immunosuppressants
• critical illness itself
• surgical factors such as the need for continuous irrigation and drainage or laparostomy
• diabetes mellitus/hyperglycaemia.
Intensive care management of these problems includes meticulous nursing care of wounds, optimisation of nutritional and metabolic parameters and aggressive, early (medical and surgical) treatment of infection.
Pain management
Pain is often a significant management issue in the postoperative ICU patient. Uncontrolled or poorly controlled pain, as well as distressing the patient, may manifest as haemodynamic instability, difficulty with breathing and ventilation (mechanical or spontaneous), increased bleeding due to hypertension or extreme agitation. This is turn can lead to a greater length of mechanical ventilation, longer ICU stay and more complications. On the other hand, good analgesia assists with recovery, physiotherapy and mobilisation, as well as improved patient wellbeing.
Provision of pain management in the ICU may be undertaken solely by the intensive care staff but is often run in conjunction with a pain service. This team, often led by anaesthetists, assists and guides with pain management and is able to follow patients through ICU and continue to manage their pain on the surgical ward.
A full rundown of all the modalities of pain management available in the ICU is beyond the scope of this book. However, in broad terms analgesia may be systemic — that is, intravenous or oral medications — or regional (epidural or intrathecal catheters, nerve blocks etc). It is also worth remembering that in the ICU the sedative effects of some agents, such as morphine, may well convey an additional advantage over their purely analgesic effects. This can, however, be a double- edged sword in terms of gaining adequate analgesia while also attempting to wean from mechanical ventilation.
Nutrition
Intensive care patients pose special challenges in terms of the provision of adequate nutrient intake. Critical illness imposes great stresses on the body and critically ill patients are often profoundly catabolic, even with the provision of seemingly adequate feeding. Added to this is the fact that a significant proportion of ICU patients enter the unit with pre-existing nutritional deficiencies as a result of either their acute illness or a more chronic condition. This has a significant impact on their ability to combat critical illness and increases the challenge of providing adequate nutrition.
A number of methods are used to determine the ideal amount of nutrition a patient should receive. One common formula used is the Schofield equation.
Once the amount of energy required is decided upon, nutrition is provided in the ICU by one of two routes: enteral or parenteral. Occasionally, combination therapy is used.
Enteral feeding
Enteral feeding uses the patient’s gastrointestinal tract to provide nutrition and is generally the preferred route in the ICU. This may occur by having the patient eat in the usual manner, but in ICU it usually occurs by administering a prepared feeding formula into the patient via a nasogastric or nasojejunal tube. It may also be administered via a PEG or PEJ (a percutaneous feeding tube into the stomach or small bowel respectively; Fig 12.4). Initially small volumes of food are used, with a gradual escalation to a target volume. Enteral feeding has the advantage of using the patient’s own gastrointestinal tract, is usually relatively noninvasive and confers protective effects on the stomach and intestines. The major drawback is that critically ill patients often have gastrointestinal dysfunction such as gastroparesis or ileus that limits absorption or have had surgery or bowel injury that prohibits the use of the native gut.
Figure 12.4 Percutaneous jejunostomy
Parenteral feeding or total parenteral nutrition (TPN)
Parenteral feeding involves the infusion of a specially formulated solution into a central vein via a dedicated catheter (CVC or Hickman) (Fig 12.5). It is usually only used in situations where enteral feeding is contraindicated. It has the advantage of having guaranteed delivery of nutrients into the body (Fig 12.6) but has a number of drawbacks. First, it is quite invasive because it requires the placement of a dedicated catheter into a central vein, with all the potential complications that this entails (see above). It has also been associated with an increased risk of blood stream infection via this catheter. Other problems include electrolyte and water balance, hyperglycaemia and hyperlipidaemia.
Figure 12.5 Hickman catheter
A: a silicone catheter is inserted into the right atrium via the cephalic vein: B; subcutaneous tunnel; C: a teflon cuff reduces ascending infection and prevents inadvertent removal
Figure 12.6 Parenteral nutrition
A: container for replacement of abnormal losses and drug infusion; B: balance nutrient solution; C: monitoring pump; D: Hickman catheter; E: bag for collection of fistula loss; F: urinary catheter; G: blood collection for routine measurement of Na, K, Cl, PO4, HCO3, glucose, urea, creatinine, albumin and osmolality
12.6 Recovery and discharge from the ICU to the surgical ward
The principle aim of intensive care medicine is to support the patient while they recover from their insult or illness. This may take a few hours or several months depending on the insult or illness involved, the patient’s ability to cope with that insult and any intervening complications. For example, a patient with a severe brain injury or spinal cord injury would be expected to stay longer than a patient who had routine cardiac surgery.
While in the ICU the patient is continuously observed and monitored with a view to reducing their levels of organ support. Whenever possible, improvements in isolated organ function or global state should lead to a reduction in the level of ICU intervention. This may manifest as cessation of inotropic or vasoconstrictor drugs, liberation from the ventilator or the removal of intercostal catheters or intracranial pressure monitoring devices. Some supportive therapies, such as renal replacement therapy, may have to be continued for many weeks or even permanently.
Once the patient has been successfully weaned from ICU-level treatments they can be discharged to a step down unit or regular ward to continue their recovery. It is important to consider both the needs of the patient and the skill mix of the ward staff when sending an intensive care patient to the ward, particularly one who has spent a considerable amount of time in the ICU. For example, a patient with a tracheostomy should be in an environment where both nursing and medical staff are comfortable and experienced in the care of the tracheostomised patient. More and more ICUs now have an outreach service to follow up and assist with the management of these patients on the general ward.
The transition to the surgical ward can be a very anxious time for patients and families, especially if their ICU stay has been prolonged. This is because patients and families often become used to the ICU environment over time and develop trust and relationships with the staff. This process then has to begin again on the surgical ward.
12.7 General management of ICU patients
All patients in the ICU, including surgical patients, require daily attention to general aspects of their care to ensure good outcomes and to minimise complications. These areas include:
• deep venous thrombosis (DVT) prophylaxis
• stress ulcer prophylaxis
• skin and pressure area care
• bowel regime
• head up positioning
• sedation and analgesia monitoring.
12.8 Cardiopulmonary arrest
Cardiopulmonary arrest is not a frequent event in the ICU, probably because the increased level of vigilance and monitoring detects problems before full-blown arrest occurs. However, circulatory and respiratory arrest does occur in the ICU and up to date knowledge and skills are mandatory.
This chapter will not list algorithms for advanced adult life support — these are freely available from the Australian Resuscitation Council (see: www.resus.org.au). It should be remembered though that certain types of problems leading to arrest may be more common in the ICU patient than the general hospital population. These include massive haemorrhage, tension pneumothorax, pacing failure, tamponade or pseudotamponade in the cardiac or thoracic surgical patient, intracranial catastrophe and various others.
12.9 Common problems in the ICU
Intensive care patients often have very diverse diagnoses and manifestations of disease. Many ICU patients are sedated and on positive pressure ventilation and therefore the telltale signs and symptoms found in the ward patient are absent or disguised. A systematic approach to problems is therefore necessary. The following sections each outline a simple clinical approach to common ICU problems in postoperative surgical patients.
Fever
Fever is a common problem in the postoperative period, as discussed elsewhere in this book (e.g. Ch 11). In the ICU, fever is extremely common and may herald a significant underlying event or problem. The most important condition not to be missed is sepsis (discussed later), which can have many manifestations.
The febrile ICU patient should be carefully assessed for evidence of infection. This may be located at an obvious site such as the surgical site, chest or urinary tract, or at an occult site such as acalculous cholecystitis, endocarditis or an epidural abscess. Invasive lines are common sources of infection and should be changed if the suspicion of infection exists. If no obvious infective process is apparent, then other causes of fever need to be considered. These include drugs, DVT and central nervous system problems.
Systemic inflammatory response syndrome (SIRS)
SIRS refers to a systemic inflammatory response to a range of insults. The criteria are outlined in Table 12.2.
Table 12.2 Criteria for SIRS
|
Infection |
Microbial phenomenon characterised by an inflammatory response to the presence of microorganisms or the invasion of normally sterile host tissue by those organisms. |
|
Bacteraemia |
The presence of viable bacteria in the blood. |
|
Inflammatory response |
The systemic inflammatory response to a variety of severe clinical insults. The response is manifested by two or more of the following conditions: (1) temperature >38°C or <36°C; (2) heart rate >90 beats per minute; (3) respiratory rate >20 breaths per minute or PaCO2<32 mmHg; and (4) white blood cell count >12,000/cu mm, <4,000/cu mm or >10% immature (band) forms. |
|
Sepsis |
The systemic response to infection, manifested by two or more of the following conditions as a result of infection: (1) temperature >38°C or 36°C; (2) heart rate >90 beats per minutes; (3) respiratory rate >20 breaths per minute or PaCO2 <32 mmHg; and white blood cell count >12,000/cu mm, <4,000/cu mm or >10% immature (band) forms. |
|
Severe sepsis |
Sepsis associated with organ dysfunction, hypoperfusion or hypotension. Hypoperfusion and perfusion abnormalities may include, but are not limited to, lactic acidosis, oliguria or an acute alteration in mental status. |
|
Septic shock |
Sepsis-induced with hypotension despite adequate fluid resuscitation along with the presence of perfusion abnormalities that may include, but are not limited to, lactic acidosis, oliguria or an acute alteration in mental status. Patients who are receiving inotropic or vasopressor agents may not be hypotensive at the time that perfusion abnormalities are measured. |
|
Sepsis-induced hypotension |
A systolic blood pressure <90 mmHg or a reduction of ≤ 40 mmHg from baseline in the absence of other causes of hypotension. |
|
Multiple organ dysfunction syndrome (MODS) |
Presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention. |
Source: Bone et al 1992 Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine. Chest; 101, 1644–1655
SIRS may be as a result of many insults, but conditions such as pancreatitis, trauma, burns and the postoperative state are common. Hypotension may be a significant feature. Treatment is supportive. Although SIRS occurs as a result of an infective process, the term used for this condition is sepsis.
Sepsis
Sepsis refers to a SIRS state caused by an infectious process such as bacteraemia, pneumonia or faecal peritonitis. The criteria for sepsis, severe sepsis and septic shock are outlined in Table 12.2.
Sepsis is an extremely common reason for admission to the ICU and has a high mortality rate. It has deleterious effects on all organ systems and its manifestations may initially be nonspecific. As a result it may not initially be recognised, as the presentation of tachypnoea or confusion in seeming isolation may initially suggest another diagnosis. Sepsis may occur in the preoperative or postoperative period and requires aggressive resuscitation. Source control is extremely important, with early and aggressive surgical treatment required for peritonitis, abscesses etc. Obstruction of the biliary and renal tracts should be relieved promptly. Antibiotics alone are frequently insufficient treatment and should not replace definitive surgery. Adjunctive therapies include steroids (stress dose hydrocortisone) and, occasionally, vasopressin in refractory shock. Other therapies such as activated protein C are occasionally used.
Common sequelae of severe sepsis in the ICU include renal injury, critical illness neuromyopathy, acute lung injury/acute respiratory distress syndrome (ARDS) and multiple organ dysfunction (MODS). All of these are mentioned below.
ICU patients require ongoing vigilance to detect new episodes of sepsis, as they are a vulnerable group. Reasons for this include invasive lines and tubes, prolonged immobility and poor nutritional state. Prolonged hospital stay and injudicious use of antibiotics increases the risk of atypical or multiresistant organism infections. Close liaison with the hospital infectious disease and microbiology units is now standard practice in large ICUs for anti-infective prescribing.
Hypoxia and hypercarbia
Hypoxia, or low arterial oxygen saturation, is a medical emergency that if left untreated will result in organ damage and death. Hypercarbia refers to the accumulation of carbon dioxide in the blood, which results in haemodynamic changes and acidosis and eventually coma and death. They are both common causes of admission to the ICU and often pose significant ongoing management problems.
Hypoxia may be caused by a variety of mechanisms, but the inherent underlying problem is that of ventilation and perfusion (V/Q) mismatch within the lungs; that is, either not enough oxygen is reaching enough alveoli or not enough blood is flowing to those alveoli that are receiving oxygen. At one extreme of this spectrum is upper airway obstruction, resulting in complete occlusion of the airway and hence no oxygen entry to the lungs. At the other extreme is the absence of pulmonary blood flow because of blood moving from the right side of the heart directly to the left without flowing through the lungs (such as is the case with a ventricular/atrial septal defect with right to left flow) This situation is called a shunt and a similar situation may occur with a massive pulmonary embolus, where blood flow is cut off to the pulmonary circulation. Most conditions causing hypoxia lie somewhere in between these two extremes.
Hypoxia should be treated urgently, with the dual aim of correcting the hypoxia and treating the underlying cause. Supplemental oxygen should be administered and an adequate airway established. Mechanical issues, such as haemothorax or pneumothorax, should be excluded and a chest X-ray obtained. Bronchoconstriction should be treated with appropriate agents, as should pneumonia and pulmonary oedema. Pulmonary embolism should be considered and excluded as indicated. If supplemental oxygen fails to safely correct hypoxia then noninvasive or invasive ventilation may be required. Ventilation should be tailored to best meet the individual patient’s needs and care should be taken to avoid further lung insult through injurious ventilation. Specific ventilation strategies have been shown to be lung protective in certain conditions, including ARDS. Adjunctive agents such as inhaled nitric oxide may be useful, as may positioning in the prone position. Extracorporeal life support may be considered as a last resort. It is important to remember that low cardiac output alone may cause hypoxia. Other rarer causes may be signalled in the correct clinical context, such as fat embolism in the presence of long-bone fractures.
Hypercarbia is due to inadequate ventilation, which may be as a result of a neurological condition such as Guillain-Barré syndrome, raised intracranial pressure, drugs such as opiates or increased dead space as in chronic obstructive pulmonary disease (COPD). It is important to remember that patients who normally manage to ventilate effectively may quickly decompensate if their respiratory drive is decreased after anaesthesia or if their carbon dioxide production is dramatically increased, as in sepsis. A small subset of patients with severe COPD rely on their hypoxia as a stimulus to breathe and overgenerous oxygen supplementation may reduce this, leading to reduced ventilatory drive and potentially lethal hypercarbia (however, this should never result in oxygen being withheld from an acutely hypoxic patient). Hypercarbia may be especially deleterious in cases where intracranial pressure rises should be avoided, for example, after head injury. Treatment should focus on the removal of aggravating factors, such as opiates, and the institution of ventilatory support, which may be invasive or noninvasive.
Hypotension and shock
Hypotension is a medical emergency and a very common cause of ICU admission. Shock is the result of inadequate oxygen delivery to the tissues and is almost invariably accompanied by hypotension, such that the two words are sometimes used interchangeably in the ICU.
Hypotension in the ICU is difficult to define, as the desired mean arterial pressure (MAP) may vary from patient to patient and condition to condition. A commonly used aim is a MAP of 70 or greater. Shock refers to a constellation of signs of inadequate tissue oxygenation, including acidosis, oliguria and organ dysfunction.
Causes of hypotension and shock vary and a variety of grouping classifications have been developed. A simple way of approaching the problem is listed in Table 12.3 with a couple of examples shown.
Table 12.3 Causes of hypotension and shock, by group
|
Hypovolaemia |
Bleeding/fluid losses |
|
Cardiogenic |
Acute myocardial infarction, heart failure, brady/tachyarrythmia |
|
Obstructive |
Cardiac tamponade, pneumothorax, massive pulmonary embolism |
|
Distributive |
Sepsis, anaphylaxis, spinal cord injury |
|
Mixed aetiology |
Some drug overdoses, amniotic fluid embolism, total spinal anaesthesia etc. |
Treatment involves restoration of the circulation with the judicious use of fluids/blood, cardiac pacing, inotropic/chronotropic/antiarrhythmic drugs and vasoconstrictors as indicated. Mechanical assistance with an intra-aortic balloon pump or extracorporeal circuit may be needed in extreme circumstances. An arterial line, central venous pressure monitoring and occasionally a pulmonary artery catheter and echocardiography may be required to guide therapy. Every effort should be made to find and aggressively treat the underlying cause. Occult shock may still be present despite restoration of a safe blood pressure and this should be kept in mind, as ongoing organ damage will occur.
Inotropes and vasopressors
These agents are ubiquitous in the ICU and are central to circulatory management. There are different classifications of agents based on their mechanisms of action and clinical effects and wide variation in their clinical application across the world. Long lists of these agents, their differing receptor affinities and actions are often very confusing and will not be entered into here. Instead a very simple rundown of clinical effects and usage will be provided.
Basically, the purpose of a (positive) inotropic agent is to increase myocardial contractility, therefore increasing stroke volume (SV) and CO. Most positive inotropes increase heart rate (HR) as well, that is, they are positive chronotropes. The net effect is to increase cardiac output and hence oxygen delivery (CO = SV × HR). Many inotropes increase vascular tone and resistance as well (the so-called inoconstrictors), including adrenaline and dopamine. The dual effect on CO and vascular resistance raises blood pressure. Some inotropes reduce vascular tone and resistance (the so-called inodilators), including dobutamine and milrinone. These agents may have a net increase in blood pressure due to elevated CO but may also lead to a reduction in blood pressure secondary to vasodilatory effects, necessitating the addition of a vasoconstrictor agent.
Vasoconstrictors act mainly on the peripheral circulation and, as their name suggests, increase arterial and venous tone, elevating blood pressure. Noradrenaline is the most commonly used vasoconstrictor agent in Australian and New Zealand ICUs. It is classified as a vasoconstrictor although it has some positive inotropic and chronotropic effects. Vasoconstrictors are used in situations where CO is adequate or supranormal but blood pressure is low secondary to vasodilation or vasoplegia, such as occurs in septic shock. Vasopressin is a very potent vasoconstrictor occasionally used in the treatment of refractory vasoplegic shock.
Both inotropes and vasoconstrictors are potentially dangerous drugs and should not be used outside of the ICU/HDU/emergency department or operating theatre environment except in extreme emergencies. Potential problems include hypertensive crises, stroke, malignant arrhythmias, high-output cardiac failure and myocardial infarction. Visceral or digital ischaemia secondary to massive vasoconstrictor doses is often postulated upon but is likely multifactorial.
Hypertension
Hypertension per se is a relatively uncommon cause of ICU admission but is an important problem. High blood pressure in the ICU varies in its definition depending on the underlying problem of the patient. For example, in a patient with an unsecured aneurysm post-subarachnoid haemorrhage the target blood pressure will be much lower than in the same patient after securing of the aneurysm but with significant vasospasm. Another perhaps more common example is the tight control of blood pressure required post carotid artery surgery. Treatment may be via the intravenous or enteral route, depending on the patient’s condition and the need for minute-to-minute titration of the agent used. Commonly used agents include glyceryl trinitrate, sodium nitroprusside and beta-blockers.
A very common cause of hypertension in the ICU patient is undertreated pain in the sedated patient. This should always be excluded, as should the fortunately rare occurrence of inadequate sedation in the presence of muscle relaxation and noxious stimuli. Occasionally, other rare causes of hypertension are diagnosed in the surgical ICU, for example, phaeochromocytoma.
Metabolic and electrolyte disturbances
Metabolic and electrolyte disturbances are present in just about every patient in the ICU and are themselves frequently a cause of ICU admission. Although the list of potential problems is myriad, certain disorders are more common than others. The following is a very simple approach to some of the common problems. (See also Ch 11.11.)
Acid–base disorders
Acid–base disturbance is very common in the ICU and is an involved and complicated topic. In extremely simplistic terms, acidaemia/osis and alkalaemia/osis are defined in the following table Table 12.4.
Table 12.4 Definitions of acidaemia and alkalaemia
|
Acidaemia |
Alkalaemia |
|
pH <7.35 |
pH >7.45 |
|
Respiratory acidosis if CO2 high |
Respiratory alkalosis if CO2 low |
It should be noted that these conditions may coexist. Acidaemia and alkalaemia are important because they can have significant adverse effects on body systems, including cardiac function and oxygen delivery. The presence of mechanical ventilation may confound the assessment and management of respiratory acidosis/alkalosis.
Metabolic acidosis
First, the anion gap should be calculated:
Normal is considered 14–17. A raised anion gap indicates the presence of an unmeasured anion such as lactate. Some causes appear in Table 12.5.
Table 12.5 Causes of metabolic acidosis
|
Normal anion gap |
Raised anion gap |
|
GI bicarbonate loss |
Lactate |
|
Renal bicarbonate loss |
Renal injury |
|
Excess chloride administration |
Ketones |
|
Toxins e.g. aspirin, alcohols |
Metabolic alkalosis
Common causes in the ICU include diuretic administration and large nasogastric losses.
Respiratory acidosis
Respiratory acidosis in the ICU is a complex topic. Patient factors such as chronic obstructive airways disease may manifest as chronic respiratory acidosis, while acute respiratory acidosis secondary to opiates for analgesia may be tolerated very well. Patients receiving mechanical ventilation for ARDS may be deliberately hypoventilated for lung protection, resulting in respiratory acidosis. In contrast, respiratory acidosis is deleterious in patients with intracranial hypertension.
Respiratory alkalosis
Respiratory alkalosis in the ICU is usually the result of inadvertent or deliberate hyperventilation of a patient on a mechanical ventilator. Sepsis is the most common cause of a respiratory alkalosis in the unventilated patient. Occasionally, patients who are spontaneously breathing on a ventilator can hyperventilate and bring their CO2 down to low levels. Care should be taken in the correction of CO2 in these patients, as rapid rises can exacerbate intracranial or pulmonary hypertension.
Other metabolic disorders
Other metabolic disorders seen in the ICU include disorders of glucose homeostasis and the metabolic abnormalities associated with renal and hepatic dysfunction or failure. Rarer problems include congenital metabolic syndromes and cellular metabolic abnormalities such as those seen in cyanide poisoning after smoke inhalation.
Electrolyte disorders
Disease or dysfunction of every organ system is associated with various abnormalities of electrolytes, with the most important problems being those of sodium and water imbalance and potassium homeostasis. Other important electrolyte imbalances commonly found in the critically ill include disorders of calcium, phosphate and magnesium homeostasis.
Electrolyte imbalance in the critically ill may be asymptomatic or may be associated with immediate and life-threatening complications. These include cardiac arrhythmias, seizures and cerebral oedema.
Sodium and water (disorders of tonicity)
Hypo- or hypernatremia is a common problem in the ICU. Although there is a tendency to view these conditions as disorders of sodium balance, they are in fact disorders of water balance.
Hyponatremia
A plasma sodium level below 135 mmol/L is called hyponatremia. Hyponatraemia in the ICU is occasionally caused by hypovolemia, for example, gastrointestinal (GI) losses or diuretics but is more commonly caused by water overload. Common causes for this include the administration of hypotonic fluids such as 5% dextrose, 4% dextrose and 1/5 normal saline or TPN. The syndrome of inappropriate antiduretic hormone secretion (SIADH) is not a common cause of hyponatremia in the ICU. Hyponatremia may be mild or life threatening, with profoundly low sodium levels (e.g. <110–120 mmol/L) sometimes associated with refractory seizures or cerebral oedema.
Treatment is aimed at gradual restoration of a normal plasma sodium concentration. Special attention must be given to ensuring a slow rate of rise of the plasma sodium, ideally <12 mmol/L/day. This is especially important in those patients with chronic hyponatremia, although the most feared complication, central pontine myelinolysis (CPML), can occur in any patient, irrespective of the rate of correction. In patients who are volume depleted, restoration of volume with isotonic crystalloids is appropriate, followed by water restriction. All other patients should be fluid and water restricted and the plasma sodium monitored frequently.
Administration of hypertonic (3 or 20%) saline should only be undertaken under expert supervision. This is occasionally indicated in patients with refractory seizures or other problems such as elevated intracranial pressure.
Hypernatremia
Hypernatremia is usually the result of water depletion. This may be the result of water loss through the GI tract, insensible losses, diuretic administration, osmotic diuresis (e.g. hyperglycaemia, high urea, administration of mannitol) or diabetes insipidus. It may occasionally be the result of the administration of large amounts of hypertonic fluids. Treatment involves correction of metabolic disorders, cessation of offending drugs and the administration of water, often in the form of 5% dextrose. If diabetes insipidus is the cause, administration of desmopressin (ddAVP) is indicated.
Disorders of potassium
Hyper- and hypokalaemia are both very common in the ICU. Hypokalaemia may result in atrial and ventricular dysrhythmias and sudden death, while hyperkalaemia if left untreated will result in a so-called sine wave ECG and asystole. Disorders of potassium, a largely intracellular cation, fall into two main categories. These are problems of total body depletion or overload or problems of potassium distribution between the intra- and extracellular compartments. Table 12.6 shows some causes of potassium imbalance.
Table 12.6 Example causes of potassium imbalance
|
Hypokalaemia |
Hyperkalaemia |
|
Urinary losses e.g. diuretics |
Renal injury |
|
Alkalosis |
Acidosis |
|
Drugs e.g. salbutamol |
Potassium administration |
|
Nasogastric losses/vomiting |
|
|
Anorexia/bulimia (poor diet/vomiting) |
Treatment of hypokalaemia involves careful administration of potassium to achieve a safe target level. Potassium is dangerous if administered too quickly. Treatment of severe life-threatening hyperkalaemia is twofold. First, calcium is given for cardiac membrane stabilisation. Measures are then instituted for lowering serum (extracellular) potassium. These are either interim measures to move potassium to the intracellular compartment (hyperventilation/bicarbonate to reduce acidosis, salbutamol, glucose/insulin) or definitive measures to reduce total body potassium (diuretics, renal replacement therapy, potassium-removing resins such as sodium polystyrene sulfonate).
As severe potassium dysregulation can be immediately life-threatening, surgical patients should be moved to the ICU for monitoring and treatment of such disorders.
Magnesium
Magnesium is an extremely important electrolyte and in the ICU is often closely monitored. Magnesium depletion may lead to ECG changes and arrhythmias, while magnesium administration is used as therapy for several disorders including atrial fibrillation, polymorphic ventricular tachycardia, pre-eclampsia/eclampsia and asthma. Profound hypermagnesaemia leads to loss of deep tendon reflexes, respiratory paralysis and bradyarrythmias/heart block. Magnesium toxicity is treatable with intravenous calcium.
Oliguria/renal dysfunction and renal replacement
Decreased urine output is very common in the ICU. This is partly physiological, as major surgery is a powerful stimulus for antidiuretic hormone (ADH) release. However, the ICU patient is extremely susceptible to renal injury from a variety of mechanisms and close monitoring is vital.
Multiple factors contribute to renal injury/dysfunction in the ICU. Patients with pre-existing renal dysfunction are at extremely high risk. Urological causes are discussed in Chapter 9 but urinary tract obstruction secondary to prostatic hypertrophy, calculi or extrinsic ureteric compression (cancer, haematoma etc.) should always be excluded. Acute abdominal compartment syndrome (where raised intra-abdominal pressure causes renal compression and reduced renal blood flow) should also be ruled out. Other causes are listed in Box 12.1.
Box 12.1
Causes of renal dysfunction/oliguria in the ICU
Sepsis
Acute tubular necrosis secondary to volume depletion/hypotension of any cause
Occult shock
Post-cardiopulmonary bypass
Abdominal compartment syndrome
Nephrotoxic drugs — e.g. gentamicin, nonsteroidal anti-inflammatories, ACE inhibitors
Interstitial nephritis secondary to drugs e.g. penicillins
Renovascular causes: embolic events, renal vein thrombosis
Urinary tract infection
Hepatic failure (hepatorenal syndrome)
IV radiocontrast administration
Primary renal disease or renal manifestations of systemic illness such as systemic lupus erythematosus (SLE) or vasculitis
Treatment of renal dysfunction in the ICU involves meticulous support and optimisation of the CO, blood pressure and volume state, removal of nephrotoxins and aggressive treatment of any underlying aggravating factor such as sepsis. Urinary tract obstruction should be relieved promptly. Dopamine has no role in the prevention or treatment of renal injury in the ICU. Diuretics may be used to increase urine output once the volume state and blood pressure are optimised. N-acetyl-cysteine (NAC) is sometimes used as prophylaxis against radiocontrast induced renal injury.
Despite all of the above measures, artificial renal support is still frequently required in the ICU. All modalities of renal support (peritoneal dialysis, haemodialysis) are used but most commonly continuous renal replacement in the form of continuous veno-venous haemodiafiltration (CVVHDF) is instituted. This involves insertion of a large-bore double-lumen catheter into a central vein and has the advantage of being able to titrate fluid removal carefully while being more haemodynamically stable than traditional haemodialysis, although less efficient at the dialysis itself.
Indications for renal replacement therapy in the ICU include volume overload, oligo-anuria, uraemia and its complications, acidosis and hyperkalaemia. There is increasing interest in using renal replacement therapy as a technique of ‘blood purification’ in sepsis.
Patients with established dialysis-dependent renal injury may need renal replacement for many weeks or months post ICU discharge. A minority remain dialysis-dependent lifelong.
Hepatic and gastrointestinal dysfunction
Hepatic dysfunction occurs in a large number of ICU patients and may be secondary to a number of insults. In addition, many of the population have underlying liver dysfunction secondary to alcoholism, viral hepatitis or other disorders. Fulminant hepatic failure is uncommonly seen in the ICU.
Hepatic dysfunction in the ICU may be due to prolonged hypotension (‘shock liver’), drugs, effects of parenteral nutrition, biliary obstruction and others. These abnormalities are most commonly detected on routine blood testing. Clinical manifestations may be minimal in the sedated and unconscious patient but signs of chronic liver disease should be looked for. Impending liver failure may be heralded by an increase in the lactate level and the development of hypoglycaemia. Hyperammonaemia may be a cause of ongoing encephalopathy and failure to wake. Treatment is supportive, with removal of offending agents if possible. The exception is the case of biliary obstruction, which should always be drained. Artificial liver support devices are not in widespread usage.
Gut dysfunction in the critically ill surgical patient is extremely common, even in those patients who have not had abdominal surgery. It may manifest as prolonged ileus, gastroparesis, failure to absorb enteral nutrition, colonic pseudo-obstruction, volvulus or severe constipation. Common reasons include drugs (opiates, barbiturates), metabolic/electrolyte disturbance and prolonged immobility. Treatment involves correction of metabolic disturbance, decrease in sedation if possible and the use of prokinetics for gastric mobility. Occasionally, surgery, colonoscopic decompression or neostigmine is required.
Abdominal compartment syndrome (see renal dysfunction, above) may cause visceral ischaemia as well as renal compromise. Intra-abdominal pressure may be estimated by measuring intravesical (bladder) pressure via an indwelling catheter. A commonly used pressure limit is 20 mmHg, although this varies. If concern exists, surgical treatment to relieve abdominal pressure is indicated.
Neurological dysfunction
Neurosurgical causes of neurological dysfunction are discussed elsewhere in this book (Chs 2 and 5). Neurological dysfunction in the non-neurosurgical ICU patient is common and may be either central (Box 12.2) or peripheral.
Box 12.2
Central causes of neurological dysfunction
Intracerebral events: ischaemic strokes/intracerebral haemorrhage
Infectious causes: meningoencephalitis/cerebral abscess/epidural abscess
Encephalopathy — multiple causes including: metabolic/electrolyte disturbance, sepsis, drugs (especially sedatives/analgesics/hypnotics), hepatic/renal dysfunction, critical illness itself
Seizures
Peripheral causes
The main cause of ICU-aquired peripheral nerve dysfunction in the critically ill is critical care neuromyopathy. This has various different classifications but clinically the picture is very similar — essentially a primarily motor neuromyopathy affecting all four limbs and respiratory muscles.
Other causes of peripheral nerve/muscle dysfunction in the ICU are uncommon but include drugs such as steroids and some anti-infectives.
Haematological dysfunction and haemorrhage
Haematological dysfunction in the ICU may take several forms:
• inadequate production of cell lines
• increased destruction of cell lines
• coagulation failure.
Bleeding and haemorrhage may be the result of surgical factors or loss/inhibition of normal coagulation mechanisms.
Anaemia is very common in ICU patients and is multifactorial in nature. Frequent blood taking and blood loss from procedures contribute, as do nutritional status and the occasional occult bleed, for example, retroperitoneal or gastrointestinal blood loss. Extracorporeal circuits, such as those required for CVVHDF, may contribute to anaemia, especially if the circuit or filter clots with the resulting loss of blood. Significant haemolysis may occur in the presence of an intra-aortic balloon pump (which may also destroy platelets), mechanical heart valves or as the result of medications. Many drugs suppress bone marrow function, as does severe sepsis, with impairment of all cell lines. Certain drugs, such as beta-lactam antibiotics, may cause neutropenia.
Coagulation failure may be as a result of loss of clotting factors, administration of anticoagulants or underproduction of clotting factors secondary to liver disease or poor nutrition. Cardiopulmonary bypass often leads to platelet dysfunction postoperatively, as does the presence of antiplatelet drugs such as aspirin or clopidogrel. Disseminated intravascular coagulation (DIC) occurs in several settings, including severe sepsis. This life-threatening disorder is associated with widespread microthromboses and consumption of coagulation factors and fibrinogen, with resultant significant bleeding. Heparin-induced thrombotic thrombocytopenia (HITT) may cause significant morbidity and even death.
Treatment is largely supportive. Deleterious drugs should be withdrawn and in the case of HITT, alternate anticoagulation to heparin should be undertaken. DIC treatment involves correction of the underlying disorder and judicious use of fresh frozen plasma and cryoprecipitate. In the actively bleeding patient, treatment should not necessarily wait for the results of blood tests of coagulation. A surgical cause for bleeding should always be excluded. Administration of blood, platelets and clotting factors may be necessary to stop bleeding and it should be remembered that massive transfusion itself can cause a coagulopathy. Administration of desmopressin may help in uraemic platelet dysfunction or post cardiopulmonary bypass. Bleeding is exacerbated by hypothermia, hypocalcaemia and acidosis. In the case of massive nonsurgical haemorrhage despite treatment specialist, haematology input is highly desirable, especially if therapies such as recombinant factor VIIa are considered.
Multiple organ dysfunction syndrome (MODS)
This describes a clinical picture of multiple organ/organ system dysfunction that may be the result of any number of causes. Examples of conditions that may lead to MODS are sepsis, post cardiac arrest, burns and severe and multiple trauma. When the insult leads to frank organ failure, the term multisystem organ failure (MOF) is sometimes used. Although potentially recoverable in many cases, MODS often heralds a bleak prognosis that is related to the number of organ systems failing.
12.10 The dying patient
Despite all the advances in modern intensive care medicine, death is still a common event in the ICU. Sometimes deaths in the ICU are unexpected, but more commonly they are heralded by a sequence of events that make the death of the patient inevitable. This occurs in two main ways: (1) the patient has a relentless deterioration, despite all interventions, that leads to their death (i.e. they become ‘unsupportable’) or (2) the patient reaches a point in their illness where continued support is still technically feasible for a period of time but the realistic possibility of recovery is virtually nil or nil. This latter scenario is often the most difficult for both staff and families to come to terms with.
Good communication and the establishment of rapport between staff and families throughout the patient’s ICU stay is very important. Early establishment of good relations may lessen the difficulties involved in discussions around end-of-life issues.
12.11 Limitation of treatment/not for escalation of care orders
On certain occasions it may be appropriate to place limitations of the type or duration of support offered to a particular patient. This may take the form of not offering a particular therapy, for example, extracorporeal life support or renal replacement therapy, or placing limitations on the duration of a particular therapy.
12.12 Withdrawal of treatment
This is a topic with myriad dilemmas and layers, beyond the scope of this chapter. Although a frequent event in most ICUs, there is often significant variation in the actual process between various units and individuals. Although frequently referred to as withdrawal of treatment, it may well be better referred to as withdrawal of specific intensive care supports or life-prolonging measures. This is because patients continue to receive care of a palliative nature after their ICU supports are removed. Following withdrawal of ICU treatment, patients are either cared for in the ICU until they die or else moved to a ward or palliative care facility.
12.13 Brain death and organ donation
Brain death
Brain death occurs as a result of massive injury to the brain, such that all brain function ceases. The injury may be due to a number of insults, but head trauma and subarachnoid haemorrhage are two causes commonly seen in an ICU. In order to establish a diagnosis of brain death there must be clinical or radiological evidence of such damage and no metabolic, pharmacologic or medical factors that may confound the picture. Australian and New Zealand law states that whole brain death must occur in order to diagnose brain death and not just brainstem death.
The diagnosis can be made in two ways: first, by way of clinical testing; and second, by appropriate neuroimaging demonstrating absence of intracranial blood flow. The latter is usually only undertaken when there is a potential problem with clinical testing, such as massive facial trauma, primary brainstem pathology or the presence of long acting anaesthetic drugs such as barbiturates.
When appropriate, clinical testing is undertaken by appropriately qualified and experienced medical practitioners, following a period of observation. Testing involves confirming the presence of an unresponsive coma, the absence of brain stem reflexes and the absence of any respiratory effort. The patient is legally dead once brain death has been established. If organ donation is considered, testing should be conducted separately by two appropriately qualified and experienced practitioners.
Organ donation
Once brain death has been diagnosed, the question of organ donation may be considered, if appropriate. If the patient’s pre-existing wishes about donation are known then this is very helpful but, in all cases, careful, informative, compassionate and unhurried discussions with the patient’s next of kin are mandatory. If the patient’s family consents, organ donation may then proceed. There is currently much debate about organ donation given the lack of supply of donor organs compared with demand and there is an increased interest in and practice of organ donation following cardiac death.