Clinical review                          Downloaded from bmj.com on 1 October 2006ABC of intensive careOrganisation of int...
Downloaded from bmj.com on 1 October 2006                                         Clinical reviewstudy sponsored by the De...
Clinical review                            Downloaded from bmj.com on 1 October 2006important step in this respect. ICNARC...
Clinical review                             Downloaded from bmj.com on 1 October 2006ABC of intensive careCriteria for adm...
Downloaded from bmj.com on 1 October 2006                                        Clinical reviewWhen to admitPatients shou...
Clinical review                           Downloaded from bmj.com on 1 October 2006    Degree of respiratory work—A patien...
Downloaded from bmj.com on 1 October 2006                                          Clinical reviewGuillain-Barré syndrome,...
Clinical review                             Downloaded from bmj.com on 1 October 2006ABC of intensive careOrgan dysfunctio...
Downloaded from bmj.com on 1 October 2006                                                            Clinical review    Th...
Clinical review                           Downloaded from bmj.com on 1 October 2006high mixed venous oxygen saturation, me...
Downloaded from bmj.com on 1 October 2006                                            Clinical reviewfor patients with refr...
Clinical review                          Downloaded from bmj.com on 1 October 2006ABC of intensive careRespiratory support...
Downloaded from bmj.com on 1 October 2006                                              Clinical reviewconfirm the imminent...
Clinical review                           Downloaded from bmj.com on 1 October 2006phase (inverse ratio ventilation) to ma...
Downloaded from bmj.com on 1 October 2006                                              Clinical reviewPhysiotherapyPatient...
Downloaded from bmj.com on 1 October 2006                                                      Clinical reviewABC of inten...
Abc of intensive care
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Abc of intensive care
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Abc of intensive care

  1. 1. Clinical review Downloaded from bmj.com on 1 October 2006ABC of intensive careOrganisation of intensive careDavid Bennett, Julian BionIntensive care dates from the polio epidemic in Copenhagen in1952. Doctors reduced the 90% mortality in patients receivingrespiratory support with the cuirass ventilator to 40% by acombination of manual positive pressure ventilation providedthrough a tracheostomy by medical students and by caring forpatients in a specific area of the hospital instead of acrossdifferent wards. Having an attendant continuously at thebedside improved the quality of care but increased the costsand, in some cases, death was merely delayed. These findings are still relevant to intensive care today, eventhough it has expanded enormously so that almost everyhospital will have some form of intensive care unit. Manyquestions still remain unanswered regarding the relationbetween costs and quality of intensive care, the size and locationof intensive care units, the number of nursing and medical staffand intensive care beds required, and how to direct scarce The origins of intensive care can be traced to the 1952 polio epidemic in Copenhagenresources towards those most likely to benefit.PatientsIntensive care beds are occupied by patients with a wide range ofclinical conditions but all have dysfunction or failure of one ormore organs, particularly respiratory and cardiovascular systems.Patients usually require intensive monitoring, and most needsome form of mechanical or pharmacological support such asmechanical ventilation, renal replacement therapy, or vasoactivedrugs. As patients are admitted from every department in thehospital, staff in intensive care need to have a broad range ofclinical experience and a holistic approach to patient care. The length of patient stay varies widely. Most patients aredischarged within 1-2 days, commonly after postoperativerespiratory and cardiovascular support and monitoring. Somepatients, however, may require support for several weeks ormonths. These patients often have multiple organ dysfunction.Overall mortality in intensive care is 20-30%, with a further 10%dying on the ward after discharge from intensive care. “Experimental” intensive care ward, St George’s Hospital, 1967ProvisionIntensive care comprises 1-2% of total bed numbers in theUnited Kingdom; this compares with proportions as high as20% in the United States. Patients admitted in Britain thereforetend be more severely ill than those in America. The averageintensive care unit in Britain has four to six beds, although unitsin larger hospitals, especially those receiving tertiary referrals,are bigger. Few units have more than 15 beds. Throughputvaries from below 200 to over 1500 patients a year. In additionto general intensive care units, specialty beds are provided forcardiothoracic, neurosurgical, paediatric, and neonatal patientsin regional centres. The frequent shortages of intensive care beds and recentexpansion of high dependency units have led to renewed effortsto define criteria for admission and discharge and standards ofservice provision. Strict categorisation is difficult; an agitated,confused but otherwise stable patient often requires at least as Modern intensive care usually includes comprehensive monitoring andmuch attention as a sedated, mechanically ventilated patient. organ support. Pressure on resources is highFurthermore, underresourced hospitals may have to refuseadmission to those who would otherwise be admitted. A recent1468 BMJ VOLUME 318 29 MAY 1999 www.bmj.com
  2. 2. Downloaded from bmj.com on 1 October 2006 Clinical reviewstudy sponsored by the Department of Health suggested thatpatients refused intensive care have a higher mortality thansimilar patients who do get admitted. Transfer to another hospital is generally reserved for thosepatients requiring mechanical ventilation, renal support, orspecialist treatment not available in the referring hospital.Transfer of such critically ill patients is not undertaken lightly. Itis labour intensive and should be performed by experiencedstaff with specialised equipment. In addition, such transfersremove staff from the referring hospital, often at times whenthey are in short supply.StaffingMedicalEach intensive care unit has several consultants (ranging from Mechanical ventilator, 1969two to seven) with responsibility for clinical care, one of whomwill be the clinical director. There are few full time intensivists inthe United Kingdom. Most consultants will have anaesthetic ormedical sessions in addition to their intensive care commitments.The consultants provide 24 hour non-resident cover. In general, junior doctor staffing levels are lower in Britainthan elsewhere in Europe. Most junior doctors are eitheranaesthetic senior house officers or specialist registrars, whomay provide dedicated cover to the intensive care unit or haveduties in other clinical areas such as obstetrics and emergencytheatre. Increasingly, posts are being incorporated into medicalor surgical rotations. Larger units often also have a more seniorregistrar on a longer attachment. These are training posts forthose intending to become fully accredited intensivists. Suchtraining schemes are a relatively recent innovation in Britain. The medical staff will typically perform a morning wardround and a less formal round in the afternoon. The on callteam does a further round in the evening.NursingThe general policy in the United Kingdom is to allocate onenurse to each intensive care patient at all times with two orthree shifts a day. One nurse may care for two less sick patients,and occasionally a particularly sick patient may require two Mechanical ventilator, 1999nurses. This nurse:patient ratio requires up to seven establishednursing posts for each bed and an average of 30-50 nurses perunit. Elsewhere in Europe the nurse:patient ratio is usually 1:2or 1:3, although the units are larger and have a higher Role of other health careprofessionals in intensive careproportion of low risk patients. Many intensive care nurses will Professional Rolehave completed a specialist training programme and haveextensive experience and expertise. Not surprisingly, nursing Physiotherapists Prevent and treat chest problems, assist mobilisation, and prevent contractures insalaries comprise the largest component of the intensive care immobilised patientsbudget. However, a shortage exists of appropriately qualified Pharmacists Advise on potential drug interactions and sidestaff, which leads to refused admissions, cancellation of major effects, and drug dosing in patients with liver orelective operations, and a heavy and stressful workload for the renal dysfunctionexisting nurses. To ease this problem, healthcare assistants are Dietitians Advise on nutritional requirements and feedsbeing increasingly used to undertake some of the more Microbiologists Advise on treatment and infection controlmundane tasks. Medical physics Maintain equipment, including patient monitors, technicians ventilators, haemofiltration machines, and bloodAudit gas analysersIntensive care audit is highly sophisticated and detailed.Dedicated staff are often required to assist with data collectionwhich includes information on diagnoses, demographics,severity, resource use, and outcome. Methods such as severity Effective audit is essential for evaluating treatments inscoring are being developed to adjust for case mix to enable intensive carecomparisons within and between units. The establishment ofthe Intensive Care National Audit Research Centre (ICNARC)and Scottish Intensive Care Society Audit Group has been anBMJ VOLUME 318 29 MAY 1999 www.bmj.com 1469
  3. 3. Clinical review Downloaded from bmj.com on 1 October 2006important step in this respect. ICNARC has recently developeda national case mix programme, to which many UK intensivecare units subscribe.CostIntensive care is expensive. The cost per bed day is£1000-£1800 with salaries accounting for over 60%, pharmacyfor 10%, and disposables for a further 10%. The currentcontracting process has found it difficult to account for intensivecare, partly because it does not have multidisciplinary specialtystatus and is therefore extremely difficult to isolate from thestructure of the “finished consultant episode.” This has beenpartially resolved by the development of the augmented careperiod (except in Scotland), defined by 12 data items whichinclude information about the duration and intensity of care. Itis intended that this will become part of hospital administrationsystems and improve the process of contracting for intensivecare services. This is essential for budgetary health and thedevelopment of intensive care as an independentmultidisciplinary specialty. In the United Kingdom, in parallelwith many other countries, specialty status is in the process ofbeing officially accorded. The intensive care budget often falls within a directoratesuch as anaesthesia or theatres, although large units may have aseparate budget. Units now have a business manager, who maybe employed specifically for this role or, more commonly, be asenior nurse. This is a daunting task. Severe constraints areoften rigorously applied by the hospital management leading tobed closures and an inability to replace ageing equipment. Blood gas analysers, 1964 and 1999: technological developments haveCaring for relatives and patients improved patient care but added to the costThe intensive care environment can be extremely distressing forboth relatives and conscious patients. The high mortality andmorbidity of patients requires considerable psychological and Key pointsemotional support. This is provided by the medical and nursing x Organisation of intensive care units in the United Kingdom variesstaff often in conjunction with chaplains and professional and widelylay counsellors. Such support is difficult and time consuming x Clinical managements strategies are determined by local need,and requires the involvement of senior staff. facilities, and staff Many relatives and close friends wish to be close to critically x Lack of large scale studies has hampered consensus on treatmentill patients at all times. Visiting times are usually flexible and x Underprovision of intensive care is likely to dominate policymany units have a dedicated visitors’ sitting room with basic decisions in near futureamenities such as a kitchenette, television, and toilet facilities.On site overnight accommodation can often be provided.SummaryFew large scale studies exist of intensive care. This is partlybecause the patient population is heterogeneous and difficult toinvestigate. Although clinical management varies according tolocal need and facilities and the views of medical and nursing David Bennett is professor of intensive care medicine, St George’sstaff, similar philosophies are generally adopted. Hospital Medical School, London and Julian Bion is reader in Underprovision of intensive care is likely to dominate policy intensive care medicine, Queen Elizabeth Medical Centre,decisions in the near future. Intensive care will probably have an Birminghamincreasingly important role as the general population ages andthe expectation for health care and the complexity of surgery The ABC of intensive care is edited by Mervyn Singer, reader inincreases. intensive care medicine, Bloomsbury Institute of Intensive Care Medicine, University College London and Ian Grant, director ofThe picture of the patient with polio was provided by Danske intensive care, Western General Hospital, Edinburgh. The series wasFysioterpeuter (Danish journal of physiotherapy). We thank conceived and planned by the Intensive Care Society’s council andRadiometer UK and St George’s Hospital archivist for help. research subcommittee.BMJ 1999;318:1468-701470 BMJ VOLUME 318 29 MAY 1999 www.bmj.com
  4. 4. Clinical review Downloaded from bmj.com on 1 October 2006ABC of intensive careCriteria for admissionGary Smith, Mick NielsenIntensive care has been defined as “a service for patients withpotentially recoverable conditions who can benefit from moredetailed observation and invasive treatment than can safely beprovided in general wards or high dependency areas.” It isusually reserved for patients with potential or established organfailure. The most commonly supported organ is the lung, butfacilities should also exist for the diagnosis, prevention, andtreatment of other organ dysfunction.Who to admitIntensive care is appropriate for patients requiring or likely torequire advanced respiratory support, patients requiringsupport of two or more organ systems, and patients withchronic impairment of one or more organ systems who alsorequire support for an acute reversible failure of another organ.Early referral is particularly important. If referral is delayeduntil the patient’s life is clearly at risk, the chances of full Ward observation chart showing serious physiologicalrecovery are jeopardised. deteriorationCategories of organ system monitoring and support(Adapted from Guidelines on admission to and discharge from intensive care and high dependency units. London: Department of Health, 1996.)Advanced respiratory support Circulatory supportx Mechanical ventilatory support (excluding mask continuous positive x Need for vasoactive drugs to support arterial pressure or cardiac airway pressure (CPAP) or non-invasive (eg, mask) ventilation) outputx Possibility of a sudden, precipitous deterioration in respiratory x Support for circulatory instability due to hypovolaemia from any function requiring immediate endotracheal intubation and cause which is unresponsive to modest volume replacement mechanical ventilation (including post-surgical or gastrointestinal haemorrhage orBasic respiratory monitoring and support haemorrhage related to a coagulopathy)x Need for more than 50% oxygen x Patients resuscitated after cardiac arrest where intensive or highx Possibility of progressive deterioration to needing advanced dependency care is considered clinically appropriate respiratory support x Intra-aortic balloon pumpingx Need for physiotherapy to clear secretions at least two hourly Neurological monitoring and supportx Patients recently extubated after prolonged intubation and x Central nervous system depression, from whatever cause, sufficient mechanical ventilation to prejudice the airway and protective reflexesx Need for mask continuous positive airway pressure or non-invasive x Invasive neurological monitoring ventilation Renal supportx Patients who are intubated to protect the airway but require no x Need for acute renal replacement therapy (haemodialysis, ventilatory support and who are otherwise stable haemofiltration, or haemodiafiltration) As with any other treatment, the decision to admit a patientto an intensive care unit should be based on the concept ofpotential benefit. Patients who are too well to benefit or thosewith no hope of recovering to an acceptable quality of lifeshould not be admitted. Age by itself should not be a barrier to Factors to be considered when assessing suitability foradmission to intensive care, but doctors should recognise that admission to intensive careincreasing age is associated with diminishing physiological x Diagnosisreserve and an increasing chance of serious coexisting disease. x Severity of illness x AgeIt is important to respect patient autonomy, and patients should x Coexisting diseasenot be admitted to intensive care if they have a stated or written x Physiological reservedesire not to receive intensive care—for example, in an x Prognosisadvanced directive. x Availability of suitable treatment Severity of illness scoring systems such as the acute x Response to treatment to datephysiology and chronic health evaluation (APACHE) and x Recent cardiopulmonary arrest x Anticipated quality of lifesimplified acute physiology score (SAPS) estimate hospital x The patient’s wishesmortality for groups of patients. They cannot be used to predictwhich patients will benefit from intensive care as they are notsufficiently accurate and have not been validated for use beforeadmission.1544 BMJ VOLUME 318 5 JUNE 1999 www.bmj.com
  5. 5. Downloaded from bmj.com on 1 October 2006 Clinical reviewWhen to admitPatients should be admitted to intensive care before theircondition reaches a point from which recovery is impossible. Criteria for calling intensive care staff to adult patientsClear criteria may help to identify those at risk and to trigger a (Adapted from McQuillan et al BMJ 1998;316:1853-8.)call for help from intensive care staff. Early referral improves the x Threatened airwaychances of recovery, reduces the potential for organ dysfunction x All respiratory arrests x Respiratory rate >40 or <8 breaths/min(both extent and number), may reduce length of stay in intensive x Oxygen saturation < 90% on >50% oxygencare and hospital, and may reduce the costs of intensive care. x All cardiac arrestsPatients should be referred by the most senior member of staff x Pulse rate < 40 or > 140 beats/minresponsible for the patient—that is, a consultant. The decision x Systolic blood pressure < 90 mm Hgshould be delegated to trainee doctors only if clear guidelines x Sudden fall in level of consciousness (fall in Glasgow coma scoreexist on admission. Once patients are stabilised they should be > 2 points) x Repeated or prolonged seizurestransferred to the intensive care unit by experienced intensive x Rising arterial carbon dioxide tension with respiratory acidosiscare staff with appropriate transfer equipment. x Any patient giving cause for concernInitial treatmentIn critical illness the need to support the patient’s vital functionsmay, at least initially, take priority over establishing a precise Basic monitoring requirements for seriouslydiagnosis. For example, patients with life threatening shock ill patientsneed immediate treatment rather than diagnosis of the cause as x Heart ratethe principles of management are the same whether shock x Blood pressureresults from a massive myocardial infarction or a x Respiratory rate x Pulse oximetrygastrointestinal bleed. Similarly, although the actual x Hourly urine outputmanagement may differ, the principles of treating other life x Temperaturethreatening organ failures—for example, respiratory failure or x Blood gasescoma—do not depend on precise diagnosis.Respiratory supportAll seriously ill patients without pre-existing lung disease shouldreceive supplementary oxygen at sufficient concentration tomaintain arterial oxygen tension >8 kPa or oxygen saturationof at least 90%. In patients with depressed ventilation (type IIrespiratory failure) oxygen will correct the hypoxaemia but notthe hypercapnia. Care is required when monitoring suchpatients by pulse oximetry as it does not detect hypercapnia. A few patients with severe chronic lung disease aredependent on hypoxic respiratory drive, and oxygen maydepress ventilation. Nevertheless, life threatening hypoxaemiamust be avoided, and if this requires concentrations of oxygenthat exacerbate hypercapnia the patient will probably needmechanical ventilation. Any patient who requires an inspired oxygen concentrationof 50% or more should ideally be managed at least on a highdependency unit. Referral to intensive care should not be basedsolely on the need for endotracheal intubation or mechanical Pulse oximeters give no information about presence or absence of hypercapniaventilation as early and aggressive intervention, high intensitynursing, and careful monitoring may prevent furtherdeterioration. Endotracheal intubation can maintain a patent Tachypnoea •airway and protect it from contamination by foreign material Use of accessory muscles • Seesawing of chest and abdomen •such as regurgitated or vomited gastric contents or blood. Putting Intercostal recession •the patient in the recovery position with the head down helps Ability to speak only short •protect the airway while awaiting the necessary expertise for sentences or single wordsintubation. Similarly, simple adjuncts such as an oropharyngealairway may help to maintain airway patency, although it does notgive the protection of an endotracheal tube. Breathlessness and respiratory difficulty are common inacutely ill patients. Most will not need mechanical ventilation,but those that do require ventilation need to be identified asearly as possible and certainly before they deteriorate to thepoint of respiratory arrest. The results of blood gas analysisalone are rarely sufficient to determine the need for mechanicalventilation. Several other factors have to be taken intoconsideration: Signs of excessive respiratory workBMJ VOLUME 318 5 JUNE 1999 www.bmj.com 1545
  6. 6. Clinical review Downloaded from bmj.com on 1 October 2006 Degree of respiratory work—A patient with normal blood gastensions who is working to the point of exhaustion is more likelyto need ventilating than one with abnormal tensions who is alert,oriented, talking in full sentences, and not working excessively. Likely normal blood gas tensions for that patient—Some patientswith severe chronic lung disease will lead surprisingly normallives with blood gas tensions which would suggest the need forventilation in someone previously fit. Likely course of disease—If imminent improvement is likelyventilation can be deferred, although such patients need closeobservation and frequent blood gas analysis. Adequacy of circulation—A patient with established orthreatened circulatory failure as well as respiratory failureshould be ventilated early in order to gain control of at leastone major determinant of tissue oxygen delivery. Peripheral cyanosis and poor capillary refill indicate failing circulationCirculatory supportShock represents a failure of tissue perfusion. As such, it isprimarily a failure of blood flow and not blood pressure.Nevertheless, an adequate arterial pressure is essential forperfusion of major organs and glomerular filtration, particularly Signs suggestive of failing tissue perfusionin elderly or hypertensive patients, and for sustaining flow x Tachycardiathrough any areas of critical narrowing in the coronary and x Confusion or diminished conscious levelcerebral vessels. A normal blood pressure does not exclude shock x Poor peripheral perfusion (cool, cyanosed extremities, poorsince pressure may be maintained at the expense of flow by capillary refill, poor peripheral pulses)vasoconstriction. Conversely, a high cardiac output (for example, x Poor urine output ( < 0.5 ml/kg/h) x Metabolic acidosisin sepsis) does not preclude regional hypoperfusion associated x Increased blood lactate concentrationwith systemic vasodilatation, hypotension, and maldistribution. Shock may be caused by hypovolaemia (relative or actual),myocardial dysfunction, microcirculatory abnormalities, or acombination of these factors. To identify shock it is important torecognise the signs of failing tissue perfusion. Normal blood pressure does not exclude All shocked patients should receive supplementary oxygen. shockThereafter, the principles of management are to ensure anadequate circulating volume and then, if necessary, to givevasoactive drugs (for example, inotropes, vasopressors,vasodilators) to optimise cardiac output (and hence tissue Neurological considerations in referral to intensive careoxygen delivery) and correct hypotension. Most patients will x Airway obstructionneed intravenous fluid whatever the underlying disease. Central x Absent gag or cough reflexvenous pressure may guide volume replacement and should be x Measurement of intracranial pressure and cerebral perfusionconsidered in patients who fail to improve despite an initial litre pressureof intravenous fluid or sooner in patients with known or x Raised intracranial pressure requiring treatmentsuspected myocardial dysfunction. Any patients needing more x Prolonged or recurrent seizures which are resistant to conventionalthan modest fluid replacement or who require vasoactive drugs anticonvulsantsto support arterial pressure or cardiac output should be x Hypoxaemia x Hypercapnia or hypocapniareferred for high dependency or intensive care.Neurological supportNeurological failure may occur after head injury, poisoning,cerebral vascular accident, infections of the nervous system(meningitis or encephalitis), cardiac arrest, or as a feature ofmetabolic encephalopathy (such as liver failure). The sequelaeof neurological impairment may lead to the patient requiringintensive care. For instance, loss of consciousness may lead toobstruction of airways, loss of protective airway reflexes, anddisordered ventilation that requires intubation or tracheostomyand mechanical ventilation. Neurological disease may also cause prolonged or recurrentseizures or a rise in intracranial pressure. Patients who needpotent anaesthetic drugs such as thiopentone or propofol totreat seizures that are resistant to conventional anticonvulsants,or monitoring of intracranial pressure and cerebral perfusionpressure must be referred to a high dependency or intensivecare unit. Patients with neuromuscular disease (for example, Extradural haematoma1546 BMJ VOLUME 318 5 JUNE 1999 www.bmj.com
  7. 7. Downloaded from bmj.com on 1 October 2006 Clinical reviewGuillain-Barré syndrome, myasthenia gravis) may requireadmission to intensive care for intubation or ventilation becauseof respiratory failure, loss of airway reflexes, or aspiration.Renal supportRenal failure is a common complication of acute illness ortrauma and the need for renal replacement therapy(haemofiltration, haemodialysis, or their variants) may be afactor when considering referral to intensive or highdependency care. The need for renal replacement therapy isdetermined by assessment of urine volume, fluid balance, renalconcentrating power (for example, urine:plasma osmolalityratio and urinary sodium concentration), acid-base balance, andthe rate of rise of plasma urea, creatinine, and potassiumconcentrations. In ill patients hourly recording of urine outputon the ward may give an early indication of a developing renalproblem; prompt treatment, including aggressive circulatoryresuscitation, may prevent this from progressing to established Measurement of urine output is important to detect renal problemsrenal failure. promptlyGary Smith is director of intensive care medicine, Queen AlexandraHospital, Portsmouth, and Mick Nielsen is director of the generalintensive care unit, Southampton General Hospital, Southampton. Indications for considering renal replacement therapyThe ABC of intensive care is edited by Mervyn Singer, reader in x Oliguria ( < 0.5ml/kg/h)intensicve care medicine, Bloomsbury Institute of Intensive Care x Life threatening hyperkalaemia ( > 6 mmol/l) resistant to drugMedicine, University College London and Ian Grant, director of treatmentintensive care, Western General Hospital, Edinburgh. The series was x Rising plasma concentrations of urea or creatinine, or bothconceived and planned by the Intensive Care Society’s council and x Severe metabolic acidosisresearch subcommittee. x Symptoms related to uraemia (for example, pericarditis, encephalopathy)BMJ 1999;318:1544-7 A memorable patient What a rotten job you’ve got He was a large man with gynaecomastia and he was covered in the window he added, “God. What a rotten job you’ve got.” I bruises. The day before his general practitioner had sent him up stared at him as he looked out into the watery sunlight of that to hospital for a full blood count. The phlebotomist he saw had winter day. I had no idea what I had been trying to do and I taken enough blood for a clotting screen and this had revealed wondered at his equanimity. He turned back, “It’s my wife I worry disseminated intravascular coagulation. He had been admitted about. I just don’t know how she’s going to react. She could go to urgently to the ward on which I was house officer. There my pieces and she’s losing her job soon. I feel uneasy about going efforts to obtain more blood were failing as each vein I tried home too. Of course there are these new places—hospices—that ballooned and bled into his skin. I sweated, he contained his might be a thing to consider.” There he faltered. irritation, and finally there were a few more millilitres. Within those few minutes he had taken on board his diagnosis, With some relief I stood near the door, talking in general terms his prognosis, and had begun thinking in practical terms. I about further tests. “What do you think’s the cause of this blood realised then that I was out of my depth and that my training had not clotting then?” he asked. He had been diagnosed 17 years not prepared me to know what to do. After he died I rather before with prostatic cancer and had taken stilboestrol long term, dutifully took some books out of the library on communication but I did not know what, if anything, he had been told about the with the dying, but as a house officer I did not have time to read implications of this new development. His directness caught me them. It was only later interviewing patients with cancer for off guard. “I don’t know. Sometimes it can be, er, an after effect of research that my thoughts turned back to the clear sightedness of the, er, prostate.” He frowned, looking as if he were trying to make sense of me. I made a polite escape. this man. He showed me that some patients can face more than The next day I apologised to my consultant for the small blood we can as doctors and see the truth before us. They can also feel sample. “Don’t worry,” she said as we walked to the patient’s room, sympathy for us as we struggle behind. “his bone marrow is stuffed with malignancy. There’s nothing we Elizabeth Davies, research fellow, London can do. He could bleed suddenly or last several weeks. I’m going to tell him now.” She sat down to tell him that he was dying and I We welcome articles of up to 600 words on topics such as busied myself on the ward. A memorable patient, A paper that changed my practice, My most Afterwards, a ward nurse, wincing in the direction of his room, unfortunate mistake, or any other piece conveying instruction, asked me to write up some pain control for him. Hesitating, I pathos, or humour. If possible the article should be supplied on a went into his room to fetch his drug chart. “I’ll not stay if you disk. Permission is needed from the patient or a relative if an don’t want me to,” I said. “No stay,” he said gratefully, “I’d like to identifiable patient is referred to. We also welcome contributions talk. I’ve been waiting 17 years for this, and I sort of knew when for “Endpieces,” consisting of quotations of up to 80 words (but you said last night. I knew what you wanted to do—to let me down most are considerably shorter) from any source, ancient or gently—I sort of knew anyway. He turned away, and looking out of modern, which have appealed to the reader.BMJ VOLUME 318 5 JUNE 1999 www.bmj.com 1547
  8. 8. Clinical review Downloaded from bmj.com on 1 October 2006ABC of intensive careOrgan dysfunctionTimothy W Evans, Mark SmithiesMost illness and death in patients in intensive care is caused by Understanding the pathogenesis of multiple organ failurethe consequences of sepsis and systemic inflammation. These is the key to reducing the unacceptably high mortalityconditions are responsible for an estimated 100 000 deaths a associated with sepsisyear in the United States alone. The systemic inflammatoryresponse syndrome (SIRS) produces a clinical reaction that isindistinguishable from sepsis in the absence of an infectingorganism.Definitions of systemic inflammatory response syndrome (SIRS), sepsis, septic shock, and multiple organ dysfunctionsyndrome (American College of Chest Physicians, 1992)Systemic inflammatory response syndrome SepsisTwo or more of the following clinical signs of systemic response to Systemic response to infection manifested by two or more of theendothelial inflammation: following:x Temperature > 38°C or < 36°C x Temperature > 38°C or < 36°Cx Heart rate > 90 beats/min x Raised heart rate > 90/minx Tachypnoea (respiratory rate > 20 breaths/min or x Tachypnoea (respiratory rate > 20 breaths/min or hyperventilation hyperventilation (Paco2 < 4.25 kPa)) (Paco2 < 4.25 kPa))x White blood cell count > 12 × 109/l or < 4 × 109/l or the presence x White blood cell count > 12 × 109/l or < 4 × 109/l or the presence of of more than 10% immature neutrophils more than 10% immature neutrophils In the setting (or strong suspicion) of a known cause of endothelial inflammation such as: Septic shockx Infection (bacteria, viruses, fungi, parasites, yeasts, or other Sepsis induced hypotension (systolic blood pressure < 90 mm Hg or a organisms) reduction of >40 mm Hg from baseline) despite adequate fluidx Pancreatitis resuscitationx Ischaemiax Multiple trauma and tissue injuryx Haemorrhagic shock Multiple organ dysfunction syndromex Immune mediated organ injury Presence of altered organ function in an acutely ill patient such thatx Absence of any other known cause for such clinical abnormalities homoeostasis cannot be maintained without interventionPathogenesisSystemic sepsis may complicate an obvious primary infectionsuch as community acquired pneumonia or a rupturedabdominal viscus. Frequently, however, an infective sourcecannot be identified and the type of organism cultured may Bacteraemia Infectionprovide no clue to its anatomical origin. Infections that complicate critical illness may arise from thegastrointestinal tract. This region is particularly sensitive to poor Fungaemia Sepsis parasitaemiaperfusion, which may lead to increased bowel permeability and viraemiatranslocation of organisms and endotoxin from the lumen ofthe gastrointestinal tract into the portal venous and lymphatic Systemiccirculations. The subsequent release of cytokines and other inflammatoryinflammatory mediators by hepatic Kupffer cells and circulating response syndrome Pancreatitismonocytes may then initiate a sequence of events that Otherculminates in the clinical signs of sepsis and multiple organfailure. Trauma BurnsScientific backgroundThe movement of oxygen, the regulation of its distribution Relation between infection, sepsis, and systemic inflammatory response syndromebetween and within tissues, and the monitoring of cellularmetabolism are all important in the clinical management ofcritically ill patients. Patients with sepsis or the systemicinflammatory response syndrome have a haemodynamicdisturbance characterised by a raised cardiac output and Multiple organ failure may result from poor distributionreduced systemic vascular resistance. Although delivery of of blood flow or a failure of cells to use oxygen because ofoxygen may be maintained or even increased by the inflammatory processpharmacological means, most patients have poor peripheraluptake of oxygen.1606 BMJ VOLUME 318 12 JUNE 1999 www.bmj.com
  9. 9. Downloaded from bmj.com on 1 October 2006 Clinical review The cause of this phenomenon remains unclear. However,sepsis and systemic inflammatory response syndrome are Oxygen deliveryassociated with damage to the vascular endothelium, whichnormally produces vasoactive substances that regulate Oxygenation Cardiac of blood outputmicrovascular blood flow to ensure that all organs areadequately oxygenated. The microcirculation may therefore be Inspireddisrupted. In addition, inflammatory mediators may modulate oxygen Lungs Heart Tissues Tissues fail to extract oxygendirectly the intracellular mechanisms that regulate use of or pooroxygen, including mitochondrial function. These two factors Normal distribution Oxygen of blood flow extraction oxygenmean that patients with sepsis or the systemic inflammatory uptake ratios normalresponse syndrome commonly develop multiple organ failure, Oxygento which many succumb. Nevertheless, not all patients at risk of extractiondeveloping sepsis and multiple organ failure do so, and ratios lowindividual susceptibility varies widely. Reduced Each patient’s clinical response to the activation of Signs of oxygen Organ uptakeinflammatory cascades may be determined by abnormalities of failure tissue hypoxiagene transcription and regulation that modulate the release ofvasoactive substances such as nitric oxide, endothelins, and Reduced gastric mucosal pH Metaboliccyclo-oxygenase products (thromboxanes, prostaglandins, etc). acidosisAdditionally, changes in the effectiveness of endogenousdefence systems such as cellular antioxidant protection, repair, Generation of tissue hypoxia. Oxygen delivery is the product of arterialand apoptosis may be relevant in determining outcome. In any oxygen content and cardiac output. In systemic inflammatory response syndrome or sepsis blood flow is poorly distributed or tissues fail to useevent, the clinical result of these perturbations is tissue hypoxia. oxygen. Signs of tissue hypoperfusion are apparent and mixed venous oxygen saturation may be increasedDetection of tissue hypoxia MicrobialThe clinical signs of tissue hypoxia are largely non-specific. Tissue traumaHowever, increased respiratory rate, peripheries that are either Initiating factor Cardiopulmonary bypass Ischaemia-reperfusionwarm and vasodilated or cold and vasoconstricted, poor urine Direct/indirect pulmonary insultoutput, and mental dullness may indicate organ dysfunctionand should prompt a search for reversible causes. The following Pro-inflammatory forcesbiochemical and physiological measurements may be helpful. Host response determined by versus Anti-inflammatory forcesMetabolic acidosis Endothelial integrityA low arterial pH and high blood lactate concentration may be Impact directly or indirectly on Endothelial functionimportant. Anaerobic production of lactate may occur Cell signalling/mitochondrial functionsecondary to global hypoxia (for example, cardiorespiratoryfailure or septic shock) or focal hypoxia (for example, infarcted Tissue oedemabowel) or through non-hypoxic causes (for example, delayed Clinical manifestation Tissue hypoperfusion Cell proliferationlactate clearance, accelerated aerobic glycolysis, or dysfunction Direct effect on cell metabolismof pyruvate dehydrogenase). A wide arterial-mixed venouscarbon dioxide pressure gradient ( > 1 kPa) has been shown to Outcome Survival Major organbe relatively insensitive as a marker of anaerobic tissue dysfunctionmetabolism. syndromeOxygen extraction ratio DeathThe uptake of oxygen by tissues (Vo2) is normally independentof oxygen delivery (Do2). If delivery fails the oxygen extraction Determinants of clinical manifestations of systemic inflammatory responseratio (Vo2:Do2) rises to maintain a constant rate of uptake and syndrome and sepsisfulfil tissue demand. The compensatory mechanisms fail only atvery low oxygen delivery levels (termed Do2Crit), when extractionstarts to fall and become dependent on delivery. However,patients with sepsis or the systemic inflammatory responsesyndrome have a low oxygen extraction ratio, indicating poortissue uptake or use. Changes in oxygen delivery and uptakerelations have been used to identify occult tissue hypoxia andpredict outcome since those who survive septic shock tend toachieve normal oxygen extraction levels. Increasing oxygen delivery in these patients should producea corresponding increase in uptake. However, in practice this isdifficult to ascertain because of problems in measurement andthe need for tissue oxygen demand to remain constant. Recent randomised clinical trials have also indicated thatpatients receiving treatment designed to increase oxygendelivery and uptake may have greater mortality than controls. A Poor peripheral perfusionBMJ VOLUME 318 12 JUNE 1999 www.bmj.com 1607
  10. 10. Clinical review Downloaded from bmj.com on 1 October 2006high mixed venous oxygen saturation, measured through apulmonary artery catheter, indirectly indicates a low oxygenextraction ratio.Gastric mucosal pH (pHi)Gastric mucosal pH can be measured using a tonometer,originally a saline filled balloon placed in the gastric lumen. Ifthe arterial bicarbonate concentration is known, the carbondioxide tension in the saline samples withdrawn from theballoon can be used to calculate the pH. Several studies havefound that a falling or persistently low gastric mucosal pH isassociated with poor prognosis in critically ill patients. However,whether gastric mucosal pH truly provides evidence of gastricmucosal hypoxia remains uncertain. Tonometers are nowbecoming semiautomated and use air instead of saline.Measurement of gastric-arterial carbon dioxide tension or Gastric tonometergastric-end-tidal carbon dioxide tension differences has beensuggested instead of gastric mucosal pH.Injury to individual organsLung injuryAbout 35% of patients with sepsis develop mild to moderateacute lung injury and a quarter have fully developed acuterespiratory distress syndrome. Affected patients have increased Recommended diagnostic criteria for acute lung injury andpulmonary vascular permeability, which leads to alveolar acute respiratory distress syndromeoedema and refractory hypoxaemia. Lung injury rarely occurs Acute respiratoryin isolation. It is usually the pulmonary manifestation of a Criteria Acute lung injury distress syndromepan-endothelial insult with inflammatory vascular dysfunction.The annual incidence of acute respiratory distress syndrome is Onset Acute Acuteabout 6 cases per 100 000 population. Data on incidence and Oxygenation* Pao2/Fio2<300 Pao2/Fio2<200outcome of acute lung injury, which was defined relatively Chest radiograph Bilateral infiltrates Bilateral infiltratesrecently, are sparse. (frontal) Acute lung injury and the acute respiratory distress Pulmonary artery <18 mm Hg or no <18 mm Hg or nosyndrome may have different causes as the acute respiratory wedge pressure clinical evidence of clinical evidence ofdistress syndrome is partly determined by the nature of the raised left atrial pressure raised left atrialunderlying or precipitating condition. Moreover, the pressureprecipitating condition and coexisting multiple organ failure *Oxygenation to be considered regardless of the positive end expiratorydictate outcome. The increased permeability of the alveolar pressure. Pao2 = arterial oxygen tension, Fio2=fraction of inspired oxygen.capillary membrane in these conditions suggests that lowering Adapted from Bernard et al Am J Respir Crit Care Med 1994;149:818-24.filling pressures by aggressive diuresis or early ultrafiltrationmay improve oxygenation. However, any concomitant decreasein cardiac output can result in an overall fall in oxygen deliveryand may prejudice the perfusion of other organs.Cardiovascular injuryMyocardial dysfunction also complicates sepsis and the systemicinflammatory response syndrome. Ventricular dilatation occursin patients with septic shock, and the ejection fraction may bereduced to around 30% despite an overall rise in measuredcardiac output. Patients who die tend to have had lower enddiastolic volumes and less compliant ventricles during diastolethan survivors. Normal volunteers given endotoxin also developleft ventricular dilatation during diastole, suggesting that cardiacfunction is greatly affected in septic shock. The cellular changesbehind ventricular dilatation are unknown. Systemic vascular resistance is also low in sepsis, possiblythrough overexpression of vasodilator substances such as nitricoxide and cyclo-oxygenase products in the vascular smoothmuscle. The consequent loss of vasoregulation may result inpoor distribution of perfusion and tissue hypoxia. Patient receiving multisystem support. Note mechanical ventilation, Optimisation of left ventricular filling pressure, inotropic vasopressor agent infusions, and nitric oxide cylinder for nitric oxidesupport, and vasoconstrictors such as noradrenaline are all inhalationbeneficial in septic shock. In addition, novel pressor agents suchas nitric oxide synthase inhibitors have been advocated recently1608 BMJ VOLUME 318 12 JUNE 1999 www.bmj.com
  11. 11. Downloaded from bmj.com on 1 October 2006 Clinical reviewfor patients with refractory septic shock. Increased knowledgeof the changes in vascular biology that characterise sepsis andthe systemic inflammatory response syndrome may allowtransient genetic manipulation of the expression of vasoactivemediators that control microvascular distribution of blood flow.Renal failureAcute renal failure is a common complication of sepsis and thesystemic inflammatory response syndrome. This may reflectchanges in the distribution of intrarenal blood flow between thecortex and medulla. The ability of patients to maintainintravascular homoeostasis may also be impaired. The early useof haemofiltration to correct fluid imbalance and (possibly)remove circulating inflammatory mediators has been advocated,but the benefits are unproved. It is essential to restorecirculating volume and achieve an adequate blood pressure andcardiac output to prevent and treat acute renal failure.Dysfunction of gastrointestinal tractThe bowel is particularly susceptible to ischaemic insults.Hypoperfusion of the gastrointestinal tract is thought to beimportant in the pathogenesis of multiple organ failure as Benefits of early haemofiltration are unprovedoutlined above. Hepatic dysfunction, possibly resulting fromreduced blood flow relative to metabolic demand, is alsocommon in critically ill patients. Maintaining adequate flow and Key pointsperfusion pressure are the only proved treatments to correct x Organ dysfunction probably arises from abnormalities ofthese deficiencies. Inotropic drugs with dilator properties such microvascular control and cellular metabolismas dopexamine may selectively enhance splanchnic perfusion x Susceptibility to the effects of inflammatory activation may be determined geneticallyand oxygenation. Nevertheless, well controlled trials of x The gastrointestinal tract seems to be the “motor” of sepsisaugmented oxygen transport (possibly guided by gastric x New supportive and therapeutic interventions are emerging astonometry) are needed to establish the role of the understanding of sepsis increasesgastrointestinal tract in multiple organ failure.Timothy W Evans is professor of intensive care medicine, Imperial The ABC of intensive care is edited by Mervyn Singer, reader inCollege School of Medicine, Royal Brompton Hospital, London and intensive care medicine, Bloomsbury Institute of Intensive CareMark Smithies is director of intensive care, University Hospital of Medicine, University College London and Ian Grant, director ofWales, Cardiff. intensive care, Western General Hospital, Edinburgh. The series was conceived and planned by the Intensive Care Society’s council andBMJ 1999;318:1606-9 research subcommittee. An incident which changed my medical life Something to celebrate It happened over three decades ago—1963 to be precise, the year Summoning up my courage, I said “no.” I pointed out that my that I became a doctor. That year the Medical Council of India duties ceased at 7 00 pm and that the night senior house officer decreed that six months of internship were to be completed would be able to take care of it. He glanced at the clock over his before the one year as a house officer, a total of 18 months of half rim glasses and said, “Of course. It’s gone 7 10. I am sorry I preregistration jobs. My first was on a surgical unit. delayed you. Run away, my boy, and enjoy the evening.” A friend and I decided to celebrate passing our qualification by Concealing my delight, I was about to leave the ward when he cooking a special meal in the doctors’ canteen, and by called me again. “Tell me, young doctor. What would have contributing equally to a quarter bottle of rum, priced six rupees, happened if instead of this poor old man it was your father? which was all we could afford. My ward duties were from 7 00 am Would you have sent the blood for the necessary investigations?” to midday and 5 30 to 7 00 pm. I arrived at the ward for the His words and his manner struck me like lightning. I was evening shift. It was quiet and there was little to do. My eyes were speechless. The bottle of rum no longer held any pleasure for me. fixed on the clock; my mind in eager anticipation of the rum. The next thing I knew I was collecting the blood and cycling off I then heard the lift coming up, and from it emerged a trolley to the blood bank. I secured two bottles, returned to see my chief carrying a frail old man of about 65 years. He had been seen in performing the operation. I was third or fourth assistant in the casualty with suspected intestinal obstruction. It was 6 35 pm. I operating theatre. We finished at about 3 00 am the following day took the appropriate history, examined him, clerked him in, and when my chief said, “Well done.” put him on a drip. Then, to my delight, the clock chimed seven. I We enjoyed the rum the next day, when it felt that we really had was about to leave the ward when again I heard the lift coming something to celebrate. up. I was by the ward door with my white coat in my hands when Suresh Pathak, general practitioner, Romford, Essex I saw our professor of surgery walking towards me. He asked me if there had been any new admissions. “Yes, sir,” I replied, and told We welcome articles of up to 600 words on topics such as him about the old man. “Let’s take a look,” he said. I accompanied A memorable patient, A paper that changed my practice, My most him to the bed and presented the case. He was impressed with my unfortunate mistake, or any other piece conveying instruction, presentation and diagnosis, which had been made by the casualty pathos, or humour. If possible the article should be supplied on a officer and not me. He looked at the x ray films. Then he asked, disk. Permission is needed from the patient or relative if an “Have you sent his blood for grouping and cross matching?” identifiable patient is referred to.BMJ VOLUME 318 12 JUNE 1999 www.bmj.com 1609
  12. 12. Clinical review Downloaded from bmj.com on 1 October 2006ABC of intensive careRespiratory supportMaire P Shelly, Peter NightingaleMost patients admitted to intensive care require some form ofrespiratory support. This is usually because of hypoxaemia orventilatory failure, or both. The support offered ranges fromoxygen therapy by face mask, through non-invasive techniquessuch as continuous positive airways pressure, to full ventilatorysupport with endotracheal intubation.Oxygen therapyOxygen is given to treat hypoxaemia. Patients should initially begiven a high concentration. The amount can then be adjustedaccording to the results of pulse oximetry and arterial blood gasanalysis. The dangers of reducing hypoxic drive have beenoveremphasised; hypoxaemia is more dangerous than Oxygen masks and nasal cannulahypercapnia. The theoretical dangers of oxygen toxicity areunimportant if the patient is hypoxaemic. Oxygen is usually given by face mask, although nasal prongsor cannulas may be better tolerated. A fixed performance, highflow, air entrainment mask can provide a known fractionalinspired oxygen concentration (Fio2) within the range 0.24-0.60.The fractional inspired oxygen concentration is not known withthe more common variable performance masks. The maximumconcentration is 0.6 unless a reservoir bag is added to the mask.Non-invasive respiratory supportIf the patient remains hypoxaemic on high flow oxygen(15 l/min) continuous positive airways pressure (CPAP) maybe used. The technique improves oxygenation by recruiting Continuous positive airways pressure requires a tight fitting mask andunderventilated alveoli and so is most successful in clinical appropriate valve and breathing systemsituations where alveoli are readily recruited, such as acutepulmonary oedema and postoperative atelectasis. It is alsohelpful in immunocompromised patients with pneumonia. Asintubation is avoided the risks of nosocomial pneumonia arereduced. The continuous positive airways pressure mask oftenbecomes uncomfortable and gastric distension may occur.Patients must therefore be cooperative, able to protect theirairway, and have the strength to breathe spontaneously andcough effectively. Non-invasive ventilation refers to ventilatory supportwithout tracheal intubation. This can be used as a first step inpatients who require some ventilatory support and who are notprofoundly hypoxaemic. Ventilation through a nasal or facemask may avoid the need for intubation, especially inexacerbations of chronic obstructive airways disease. Some Hayek oscillator provides external negativepatients with chronic ventilatory failure rely on long term pressure ventilationnon-invasive ventilation. It may also have a place duringweaning from conventional ventilation. External negative Indications for intubation and ventilationpressure ventilation, historically provided by an “iron lung,” is x Protect the airway—for example, facial trauma or burns,now provided by a cuirass system. unconscious patient x Treat profound hypoxaemia—for example, pneumonia, cardiogenic pulmonary oedema, acute respiratory distress syndromeVentilatory support x Postoperative care—for example, after cardiothoracic surgery and other major, complicated, or prolonged surgeryEndotracheal intubation and ventilation is the next step in the x Allow removal of secretions—for example, myasthenia gravis,management of respiratory failure. Clinical symptoms and signs Guillain-Barré syndrome x Rest exhausted patients—for example, severe asthmaare generally more useful than arterial blood gas analysis or x Avoid or control hypercapnia—for example, acute brain injury,measurements of peak expiratory flow rate and vital capacity in hepatic coma, chronic obstructive airways diseasedeciding the need for intubation.. However, some findings1674 BMJ VOLUME 318 19 JUNE 1999 www.bmj.com
  13. 13. Downloaded from bmj.com on 1 October 2006 Clinical reviewconfirm the imminent need for ventilation. These include Indicators of respiratory distresshypoxaemia in patients receiving maximum oxygen therapy(Pao2 < 8 kPa, or Sao2 < 90%), hypercapnia with impairment of x Tachypnoea, dyspnoeaconscious level, and a falling vital capacity in patients with x Sweating x Tachycardia and bounding pulseneuromuscular disorders. x Agitation, restlessness, diminished conscious level, unwilling to lie flat x Use of accessory muscles, intercostal recession x Abdominal paradox (abdomen moves inward during inspiration)Management of the airway x Respiratory alternans (thoracic movement then abdominalEndotracheal intubation can be extremely hazardous in movement)critically ill patients with respiratory and often cardiovascular x Cyanosis or pallorfailure. Continuous monitoring, particularly of heart rate andblood pressure, is essential and resuscitation drugs must be Potential problems during intubationimmediately available. x Hypotension Hypotension follows induction of anaesthesia because of the x Reduced intrinsic sympathetic drivedirect cardiovascular effects of the drugs given. x Reduced cardiac outputUnconsciousness also reduces intrinsic sympathetic drive. x Severe hypoxaemiaPositive pressure ventilation reduces venous return to the heart x Regurgitation and aspiration of gastric contentsand reduces cardiac output. x Arrhythmias x Electrolyte disturbances, especially Tracheostomies are usually done electively when intubation hyperkalaemia after suxamethoniumis likely to be prolonged (over 14 days). They may also be donefor the patient’s comfort and to facilitate weaning from theventilator. Tracheostomy is often done as a percutaneousprocedure in intensive care. Complications of tracheostomyinclude misplacement or displacement of the tube, bleeding,infection, failure of the stoma to heal, and tracheal stenosis.However, because patients tolerate a tracheostomy much betterthan an orotracheal tube, sedation can usually be reduced,weaning is more rapid, and the stay in intensive care is reduced.A minitracheostomy may help with tracheal toilet in patientswith copious secretions and poor cough effort.Ventilator strategyThe choice of ventilatory mode and settings such as tidalvolume, respiratory rate, positive end expiratory pressure(PEEP), and the ratio of inspiratory to expiratory time dependson the patient’s illness. In asthma, for example, a prolonged A tracheostomy is more comfortable than an orotracheal tubeexpiratory phase may be required for lung deflation, whereas inpatients with atelectasis or other forms of reduced lung volume Lung protective ventilation strategythe emphasis is towards recruiting alveoli with positive end The strategy aims to maintain alveolar volume byexpiratory pressure or a prolonged inspiratory phase. x Using lung recruitment manoeuvres and positive end expiratory Damage to lungs can be exacerbated by mechanical pressure to maximise and maintain alveolar volumeventilation, possibly because of overdistension of alveoli and the x Avoiding alveolar overdistension by limiting tidal volume or airwayrepeated opening and collapse of distal airways. Some evidence pressure, or bothexists for benefit from a lung protective ventilatory strategyusing positive end expiratory pressure or prolonged inspirationto maintain alveolar volume, and limiting tidal volumes and Volume (ml) 1200peak airway pressures. This may result in increased arterialcarbon dioxide pressure (permissive hypercapnia). Serial 1000measurements of airway pressure and tidal volume allow lung Upper inflection zonecompliance to be optimised. Compliance indicates alveolarrecruitment, and reduces the risks of overdistension. 800Methods of ventilation 600No consensus exists on the best method of ventilation. Involume controlled methods the ventilator delivers a preset tidal 400volume. The inspiratory pressure depends on the resistance andcompliance of the respiratory system. In pressure controlledventilation the delivered pressure is preset. Tidal volume varies 200according to the resistance and compliance of the respiratory Lower inflection zonesystem. Pressure controlled ventilation has become popular for 0severe acute respiratory distress syndrome as part of the lung 0 1 2 3 4protective strategy. As well as limiting peak airway pressure, the Pressure (kPa)distribution of gas may be improved within the lung. Pressurecontrolled ventilation is often used with a long inspiratory Pressure-volume curve showing upper and lower inflection pointsBMJ VOLUME 318 19 JUNE 1999 www.bmj.com 1675
  14. 14. Clinical review Downloaded from bmj.com on 1 October 2006phase (inverse ratio ventilation) to maintain adequate alveolarrecruitment. In high frequency techniques gas is delivered to the airwayby oscillation or jet ventilation. The tidal volumes achieved aresmall but gas exchange still occurs. The role of high frequencytechniques in respiratory support is not yet established. Methods of ventilation that allow the patient to breathespontaneously are thought to be advantageous. Modernventilators have sensitive triggers and flow patterns that canadapt to the patient’s needs, thus reducing the work ofbreathing. In synchronised intermittent mandatory ventilation aset number of breaths are delivered by the ventilator and thepatient can breathe between these breaths. This method is oftenused during weaning, often with pressure support, by which theventilator enhances the volume of each spontaneous breath upto a predetermined positive pressure. Biphasic airway pressureis similar to continuous positive airways pressure ventilation but Biphasic airway pressure improves alveolar ventilationpressure is set at two levels. The ventilator switches between thelevels, thus augmenting alveolar ventilation. Ventilation assessment scale x Tolerates ventilationMonitoring ventilatory therapy x Tolerates ventilation most of the time; some transient desaturationPulse oximetry and measurement of end tidal carbon dioxide or coughing on manoeuvres such as tracheal suction, turning, etcconcentration allow continuous monitoring of oxygenation and x Moderate desaturation on coughing or above manoeuvres that resolves spontaneouslyventilation. End tidal carbon dioxide concentration is roughly x Severe or prolonged desaturation on coughing or aboveequal to arterial carbon dioxide partial pressure in normal manoeuvres that requires interventionsubjects but may differ widely in critically ill patients with x Intolerant of mechanical ventilation, requires manual interventionventilation-perfusion mismatch. Nevertheless, monitoring end x Paralysedtidal carbon dioxide may be useful in neurointensive care, whentransferring critically ill patients, and for confirming trachealintubation. Adequacy of ventilation should be confirmed Preparation for weaning from the ventilatorregularly by arterial blood gas analysis. Tolerance to ventilation Ensurecan be assessed using a simple scale. x Clear airway x Adequate oxygenation x Adequate carbon dioxide clearanceWeaning from the ventilator Control ofSeveral techniques are available for weaning. All are likely to fail x Precipitating illnessunless the patient is well prepared. Clinical assessment is the x Fever and infectionmost important issue in deciding when to wean a patient from x Painthe ventilator. The factors considered are similar to the x Agitation x Depressionindications for respiratory support. The patient should beadequately oxygenated (Pao2 > 8 kPa with fractional inspired Optimisation of x Nutritional stateoxygen < 0.6); be able to maintain normocapnia; be able to x Electrolytes (potassium, phosphate, magnesium)meet the increased work of breathing; and be conscious and Bewareresponsive. Weaning techniques allow the patient to breathe x Excessive carbon dioxide production from overfeedingspontaneously for increasing periods or to gradually reduce the x Sleep deprivationlevel of ventilatory support. Recently weaned patients should x Acute left heart failurecontinue to be closely monitored for secondary deterioration.Patients are extubated after they are weaned from the ventilatorand can breathe unaided. Patients also need to be able toprotect their airway once it is no longer protected by anendotracheal tube. This means they must be alert, able toswallow without aspiration, and able to cough well enough toclear secretions.Other aspects of respiratory supportHumidificationInadequate humidification of inspired gases destroys the ciliatedepithelium lining the upper airway. This stops secretions frombeing cleared from the lungs and increases the risk of infection.Piped medical oxygen and air are completely dry. The upperairway may not be able to supply enough heat and moisture tofully saturate them, especially when much of the upper airway isbypassed by tracheal intubation. Additional humidification is Inadequate humidification of inspired gases causes loss of tracheal andtherefore necessary. bronchial cilia (right), which reduces clearance of secretions from the lungs1676 BMJ VOLUME 318 19 JUNE 1999 www.bmj.com
  15. 15. Downloaded from bmj.com on 1 October 2006 Clinical reviewPhysiotherapyPatients who are intubated cannot clear secretions effectivelybecause of reduced conscious level, poor cough effort, anddiscomfort. Regular chest physiotherapy and tracheal suctionare essential.PositionRegular turning to avoid pressure sores also helps mobilise andclear secretions. Patients who are too unstable to be turnedregularly may benefit from being nursed on special beds thatallow some degree of rotation. Patients with resistant hypoxaemia may benefit from beingturned prone. The improved oxygenation probably results fromnormalisation of pleural pressure gradients within the lung. Physiotherapy is important to help clear secretions in ventilated patientsPharmacological adjunctsInhaled nitric oxide may improve oxygenation by dilatingpulmonary vessels passing alongside ventilated alveoli.Although it is widely used, and often effective in increasingarterial oxygen tension in patients with acute respiratorydistress syndrome, there is no evidence of improved survival.Nitric oxide remains unlicensed for this indication. Steroids have a limited role in the acute management ofventilated patients except for treating the underlyingdisease—for example, asthma. However, there is evidence thatthey improve pulmonary function in the later, fibroproliferative,phase of acute respiratory distress syndrome.SedationVentilated patients generally require sedation to tolerate both Nursing patients in prone position may help resistant hypoxaemiaventilation and the presence of an endotracheal tube. The aimis for the patient to be comfortable at all times. In the past, Indications for analgesia and sedationventilation could be controlled only if the patient was heavilysedated or even paralysed. Sophisticated ventilators now allow x Allow effective ventilation x Relieve distressless sedation but patients still require analgesia for pain and x Reduce oxygen demand x Facilitate sleep x Provide analgesia x Provide amnesiarelief of anxiety and distress. x Reduce anxiety x Reduce depression Patients have individual needs and different indications foranalgesia and sedation. Muscle relaxants are now usedinfrequently. Compassionate care and effective communication Indications for muscle relaxantshelp patients, but drugs are often necessary to keep them x Allow intubation and other procedurescomfortable. x Allow control of ventilation where respiratory drive is very Sedatives, however, have some adverse effects. The parent high—for example, permissive hypercapniadrug or active metabolites may accumulate because of renal x Treat certain diseases—for example, tetanusfailure and have prolonged action. There may also be x Reduce oxygen demand while oxygenation is criticalcirculatory effects—for example, hypotension. Tolerance x Control carbon dioxide pressure and prevent increases insometimes occurs. Patients may develop withdrawal syndromes intracranial pressure—for example, in head injurywhen the drug is stopped, while altered sleep patterns mayproduce sleep deprivation. Some patients develop ileus, which Assessment of sedationmay impair feeding. Because critically ill patients cannot usually say whether they + 3 Agitated and restless + 2 Awake and uncomfortableare comfortable, anxiety, depression, and even pain may be + 1 Aware but calmdifficult to assess. This assessment tends to be subjective and 0 Roused by voicevarious scoring systems are used, most being based on the − 1 Roused by touchpatient’s response to different stimuli. − 2 Roused by painful stimuli − 3 Cannot be roused A Natural sleepConclusion P ParalysedMany patients who would previously have died from respiratory Maire P Shelly is consultant in anaesthesia and intensive care andfailure now survive. Improved understanding and management Peter Nightingale is director of intensive care, Withington Hospital,of acute lung injury will hopefully lead to further improvements Manchester.in survival. Appropriate treatment of hypoxia, and early referral The ABC of intensive care is edited by Mervyn Singer, reader into intensive care before complications arise, will also hopefully intensive care medicine, Bloomsbury Institute of Intensive Careimprove the outcome of critically ill patients. Medicine, University College London and Ian Grant, director ofThe picture of cilia is reproduced with permission from Konrad F, Schiener intensive care, Western General Hospital, Edinburgh. The series wasR, Marx T, Georgieff M. Intensive Care Medicine 1995;21:482-9. conceived and planned by the Intensive Care Society’s council andBMJ 1999;318:1674-7 research subcommittee.BMJ VOLUME 318 19 JUNE 1999 www.bmj.com 1677
  16. 16. Downloaded from bmj.com on 1 October 2006 Clinical reviewABC of intensive careCirculatory supportC J Hinds, D WatsonCirculatory support is required not only for hypotension or Types of shockshock but also to prevent complications in patients at risk of x Cardiogenic shock: caused by “pump failure”—for example acuteorgan failure. Shock can be defined as “acute circulatory failure myocardial infarctionwith inadequate or inappropriately distributed tissue perfusion x Obstructive shock: caused by mechanical impediment to forwardresulting in generalised cellular hypoxia.” It is a life threatening flow—for example, pulmonary embolus, cardiac tamponademedical emergency. x Hypovolaemic shock: caused by loss of circulating volume. These Tissue perfusion may be jeopardised by cardiogenic, losses may be exogenous (haemorrhage, burns) or endogenousobstructive, hypovolaemic, or distributive shock. These factors (through leaks in the microcirculation or into body cavities asoften combine. For example, in sepsis and anaphylaxis, vascular occurs in intestinal obstruction) x Distributive shock: caused by abnormalities of the peripheraldilatation and sequestration in venous capacitance vessels lead circulation—for example, sepsis and anaphylaxisto relative hypovolaemia, which is compounded by truehypovolaemia due to fluid losses through increasedmicrovascular permeability. If abnormalities of tissue perfusion are allowed to persist,the function of vital organs will be impaired. The subsequentreperfusion will exacerbate organ dysfunction and, in severe Pressurised bag of salinecases, may culminate in multiple organ failure. Earlyrecognition of patients who are shocked and immediateprovision of effective circulatory support is therefore essential.Such support is usually best provided in an intensive care unitor high dependency area.Cardiovascular monitoring Disposable pressureBlood pressure transducer Non-compliant Intermittent manometer linePatients with a low cardiac output can sometimes maintain a Continuous flush flush devicereasonable blood pressure by vasoconstriction, while (2-5ml/h)vasodilated patients may be hypotensive despite a high cardiac 100/54output. Blood pressure must always be assessed in relation to 104the patient’s normal value. Percutaneous placement of an 75intra-arterial cannula allows continuous monitoring of bloodpressure and repeated sampling of blood for gas and acid-base Monitoranalysis. This is essential when rapid haemodynamic changesare anticipated—for example, when administering inotropic orvasoactive drugs. Continuous monitoring of blood pressure. A cannula placed percutaneously in an artery is connected to a pressure transducer through a fluid filled non-compliant manometer line incorporating a continuous and intermittentCentral venous pressure flush device. Adapted from Hinds CJ, Watson D. Intensive care: a conciseMeasurement of pressure within a large intrathoracic vein is a textbook. WB Saunders, 1996.simple method of assessing circulating volume and myocardialfunction. However, the absolute value is often unhelpful, except inextreme cases of hypovolaemia, fluid overload, or heart failure. Indications for pulmonary artery catheterisationCorrect interpretation requires assessment of the change in x Shock—unresponsive to simple measures or diagnostic uncertainty.central venous pressure in response to a fluid challenge in To guide administration of fluid, inotropes, and vasopressorsconjunction with alterations in other monitored variables (such as x Haemodynamic instability when diagnosis unclearheart rate, blood pressure, urine flow) and clinical signs (such as x Major trauma—to guide volume replacement and haemodynamic support in severe casesskin colour, peripheral temperature, and perfusion). x Myocardial infarction—haemodynamic instability, unresponsive to initial therapy. To differentiate hypovolaemia from cardiogenicPulmonary artery catheterisation shockCatheterisation of the pulmonary artery with a balloon flotation x Pulmonary oedema—to differentiate cardiogenic from non-cardiogenic oedema. To guide haemodynamic support incatheter allows measurement of the filling pressure of the left cardiac failure and acute respiratory distress syndromeventricle (pulmonary artery occlusion pressure). As with central x Chronic obstructive airways disease—patients with cardiac failure, tovenous pressure, correct interpretation requires assessment of exclude reversible causes of difficulty in weaning from mechanicalchanges in pressure in response to treatment together with ventilationalterations in clinical signs and other monitored variables. Most x High risk surgical patientspatients who require pulmonary artery catheters should have x Cardiac surgery—selected cases onlytheir cardiac output measured (by a thermodilution technique.) x Pulmonary embolism—to assist in diagnosis and assess severity. To guide haemodynamic support Pulmonary artery catheters can help establish the nature of x Pre-eclampsia with hypertension, pulmonary oedema, and oliguriathe haemodynamic problem, optimise cardiac output whileBMJ VOLUME 318 26 JUNE 1999 www.bmj.com 1749

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