8.critical illness

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  • 179

    8Clinicalexaminationofthecriticallyillpatient180

    Physiologyofcriticalillness182Oxygen transport 182Cardiovascular component of oxygen delivery: flow 182

    Oxygenation component of oxygen delivery: content 183

    Oxygen consumption 184Relationship between oxygen consumption and delivery 184

    Pathophysiology of the inflammatory response 184

    Monitoring185Monitoring the circulation 185Monitoring respiratory function 187

    Recognitionofcriticalillness188Assessment and initial resuscitation of the critically ill patient 188

    Clinical decision-making and referral to critical care 189

    Criticalillness

    Generalprinciplesofcriticalcaremanagement201Daily clinical management in the ICU 202Sedation and analgesia 202

    Dischargefromintensivecare203Withdrawal of intensive support 203Brainstem death 203

    Outcomeofintensivecare204Scoring systems 204

    G.R. NimmoT. Walsh

    Presentingproblems/Managementofmajororganfailure190Circulatory failure: shock 190Circulatory support 190

    Respiratory failure and acute respiratory distress syndrome 191Respiratory support 193

    Acute kidney injury 197Renal support 197

    Gastrointestinal and hepatic disturbance 198Gastrointestinal and hepatic support 198

    Neurological failure (coma) 198Neurological support 199Neurological complications in intensive care 199

    Sepsis 200Management 201

    Disseminated intravascular coagulation 201

  • CritiCal illness

    180

    RECOGNISING THE CRITICALLY ILL PATIENT

    1

    2

    3Initial assessment and resuscitation

    Referral

    Respiratory signs Respiratory arrest Threatened or obstructed airway Stridor, intercostal recession, paradoxical breathing (seesaw pattern) Respiratory rate < 8 or > 35/min Respiratory distress: use of accessory muscles; unable to speak in complete sentences SpO2 < 90% on high-concentration oxygen Rising PaCO2 > 7 kPa (52.5 mmHg) or > 2 kPa (> 15 mmHg) above normal with acidosis

    Cardiovascular signs Cardiac arrest Pulse rate < 40 or > 140 bpm Systolic blood pressure < 100 mmHg Poor peripheral perfusion Evidence of inadequate oxygen delivery Metabolic acidosis Hyperlactataemia Poor response to volume resuscitation Oliguria < 0.5 mL/kg/hr (check urea, creatinine, K+)

    Neurological signs Threatened or obstructed airway Absent gag or cough reflex Failure to maintain normal PaO2 and PaCO2 Failure to obey commands GCS < 10 Sudden fall in level of consciousness (GCS by > 2 points) Repeated or prolonged seizures

    Re-assessment and further management

    ADVANCED RESPONDER/INTENSIVISTFIRST RESPONDER

    A Airway clearNo: head tilt, chin liftYes: take presenting history

    A Airway compromisedConsider intubation and ventilationGive more oxygen

    B BreathingOxygenation failure: give more oxygen;continuous positive airways pressure(CPAP)Respiratory failure: non-invasiveventilation (NIV); intubation andventilation

    C ShockLarge-bore IV accessVolume resuscitationArterial line insertionCentral line insertionMonitoringVasoactive drugs

    D Reduced GCSA + B + C andIs CT scan required?

    E ExtricateTo ICU or HDU as appropriatePlan safe transport

    F Further investigations and fullexaminationFBC, acute biochemistry, coagulation,cultures, targeted specialistinvestigations

    BreathingDistressed? Yes: oxygenRespiratory rate: oxygen if tachypnoeicAuscultation: nebulised salbutamolif wheezeMonitor SpO2Obtain arterial blood gases andchest X-ray

    CirculationPulse rate, rhythm and volumeBlood pressureECG monitorCheck peripheral perfusionEstablish IV access and ?give fluidObtain immediate bloods* and12-lead ECG

    DisabilityEstablish Glasgow Coma Score (GCS):if reduced, exclude hypoglycaemiaCheck pupils and limbs for focal signs

    B

    C

    D

    EvidenceLook for information to assess severityand establish diagnosisExamination: target initially to systems likelyto give most information, e.g. chest andheart if presentation is with breathlessness

    *ABG, potassium, glucose, haemoglobin, lactate

    E

    CLINICAL EXAMINATION OF THE CRITICALLY ILL PATIENT

  • Clinical examination of the critically ill patient

    181Standard Early Warning System (SEWS) chart. (UO = urine output)

    SEWS KEY

    RESP.RATE

    SpO2

    TEMP

    BLOODPRESSURE

    HEARTRATE

    NEURORESPONSE

    PAIN

    SEWS SCORE

    DATE:

    NAME:

    TIME:

    0 1 2 3

    Inspired O2%Humidifier temp

    SEWS SCOREuses Systolic BP

    36+

    3135

    2130

    9092

    8589

    920

    100/min) Hypotension(systolicBP20/minHeartrate>90/minWhitebloodcount>12109/Lor38.0Cor6.7kPa(50mmHg)RespiratorydistressImpairedconsciouslevel

    Assess circulation

    Heartrate BP:directarterialpressure

    CVP Peripheralperfusion

    Optimise volume status

    Fluidchallenge(s):CVP6mmHgorpoorventricularfunctionsuspected:100mLbolusesandconsidermeasuringcardiacoutputbyPAcatheteroroesophagealDoppler

    Optimise haemoglobin concentration

    TransfuseredcellstomaintainHbat7090g/L(or100g/Lifischaemicheartdisease)

    Septicpatientscanbecomeprofoundlyanaemicwithcrystalloid/colloidresuscitationduetohaemodilution

    Achieve target BP

    Usevasopressor/inotropeoncehypovolaemiaiscorrected

    Achieve adequate CO and DO2

    Inotropicagentiffluidaloneisinadequate

    Other measures

    Establishmonitoring,includinginvasivemeasures,atonce Trendsinhaemodynamics,ABG,H+,basedeficitandlactate

    guidefurthertreatment

    8.7 Immediate management of circulatory collapse

    Drug

    Action

    Vasoconstrictor Inotrope Chronotrope

    Adrenaline (epinephrine)

    ++ ++ +

    Noradrenaline (norepinephrine)

    ++++ + (+)

    Dobutamine * ++++ ++

    *In most patients dobutamine acts as a vasodilator but in some it causes vasoconstriction.

    8.8 Actions of commonly used vasoactive agents

  • CritiCal illness

    8

    192

    Acute or chronic hypercapnia usually results from alveolar hypoventilation. Causes include: central depression of respiratory drive impaired nerve transmission between the central

    nervous system and muscle (especially the diaphragm)

    reduced chest wall movements (including diaphragmatic movements)

    reduced alveolar ventilation due to pathology within the lungs.The primary respiratory conditions causing acute res-

    piratory failure are detailed in Chapter 19. Critically ill patients may have both type 1 and 2 respiratory failure at some point, and the pattern and severity can change rapidly. Close monitoring and review are thus essential in order to decide which form of respiratory support is required, as this may change rapidly as the patient dete-riorates and/or improves. Both the disease causing the illness and its effect on the patients physiology over time must be taken into consideration. A combination of clini-cal examination and investigation helps to determine the most appropriate interventions (Box 8.10). The best method for assessing hypoxaemia is the ratio of the PaO2 (measured by blood gas) to the fractional inspired oxygen delivered (PaO2/FiO2). This PF ratio is lower, the more severe the disease. For example, a patient receiving 60% oxygen with a PaO2 of 10.0 kPa (75.2 mmHg) on blood gas has a PF ratio of 10.0/0.6 = 16.7 kPa (125.6 mmHg).

    Acute lung injury and the acute respiratory distress syndromeA range of conditions (Box 8.11) can result in a diffuse acute inflammatory process in the lungs called acute lung injury (ALI); when severe (as defined by hypox-aemia), this is termed the acute respiratory distress syndrome (ARDS; Box 8.12). Inflammation occurs throughout the lungs, affecting both endothelial and epithelial surfaces. Activated neutrophils are seques-tered into the lungs and capillary permeability is increased, with damage to type I and II alveolar cells.

    Inhalation (direct)

    Aspirationofgastriccontents

    Toxicgases/burninjury

    Pneumonia Bluntchesttrauma Near-drowning

    Blood-borne (indirect)

    Sepsis Necrotictissue(particularly

    bowel) Multipletrauma Pancreatitis Cardiopulmonarybypass Drugs(heroin,barbiturates,

    thiazides)

    Severeburns Majortransfusionreaction Anaphylaxis Fatembolism Carcinomatosis Obstetriccrises(amniotic

    fluidembolus,eclampsia)

    8.11 Conditions predisposing to ARDS

    Respiratory pattern

    Inspiratorystridor:typicallycausedbypartialairwayobstruction

    Tachypnoea:oftenthefirstindicatorofcriticalillness Rapidshallowbreathing:indicatesmoresevererespiratory

    failure Prolongedexpiratoryefforts:indicatesseverebronchospasm

    Conscious level

    Worseningdrowsinessoragitation:indicatesmoresevererespiratoryfailureasaresultofhypoxaemiaand/orhypercapnia

    Pulse oximetry

    Oxygensaturations60%:indicatessevereventilationperfusionmismatchand/orshunt

    Arterial blood gases

    CalculatethePFratio(seetext):lowervaluesindicatemoreseveredisease

    Imaging

    ChestX-ray,CTscanorchestultrasound:informationabouttheunderlyingpathologyandtreatableconditions,e.g.pleuraleffusion

    8.10 How to assess respiratory failure

    Type 1 respiratory failure

    Pneumonia Pulmonaryoedema* Pulmonaryembolism Pulmonaryfibrosis ARDS* Aspiration

    Lungcollapse*,e.g.retainedsecretions

    Asthma Pneumothorax Pulmonarycontusion(blunt

    chesttrauma)

    Type 2 respiratory failure

    Reducedrespiratorydrive*,e.g.drugoverdose,headinjury

    Upperairwayobstruction(oedema,infection,foreignbody)

    Latesevereacuteasthma

    COPD Peripheralneuromuscular

    disease*,e.g.GuillainBarrsyndrome,myastheniagravis

    Flailchestinjury Exhaustion*(includesalltype

    1causes)

    *Secondary complicat