Oxford Handbook of Critical Care - part 6 ppt

See also: Oxygen therapy, p2; Ventilatory support—i ndi cations, p4; IPPV—compl icati ons of ventil ation, p14; Posi tive end expiratory pressure 1, p22; Positi ve end expiratory pressur

Microatel ectasi s—i nadequate depth of respi ration, nitrogen washout by 100% oxygen with subsequent absorpti on

of oxygen occurring at a rate greater than replenishment

Sputum retention

Excess mucous (sputum) normall y stimulates coughing If cil iary clearance is reduced (e.g smoking, sedatives) or

mucous volume i s excessi ve (e.g asthma, bronchi ectasi s, cystic fi brosi s, chroni c bronchiti s) sputum retenti on may

occur Sputum retention may al so be the resul t of i nadequate coughing (e.g chronic obstructive lung disease, pai n,

neuromuscul ar disease) or i ncreased mucous vi scosi ty (e.g hypovol aemia, inadequate humi di ficati on of inspired

Physiotherapy—postural drai nage, percussi on and vibration hyperinflation, intermittent posi tive pressurebreathing, i ncenti ve spi rometry or manual hyperi nfl ati on

Maintenance of l ung volumes—increased VT CPAP, PEEP, positioning to reduce compression of l ung ti ssue byoedema

Management

Speci fic management depends on the cause and should be correcti ve Al l measures taken for prevention shoul d

conti nue If there is l obar or segmental col lapse with obstructi on of proximal airways, bronchoscopy may be useful to

all ow directed sucti on, forei gn body removal and saline i nstil lation Pati ents with high FIO2 may deteri orate due to

the effects of excessi ve lavage or sucti on reducing mi nute ventilation

See also:

Oxygen therapy, p2; Ventilatory support—i ndi cations, p4; IPPV—compl icati ons of ventil ation, p14; Posi tive end

expiratory pressure (1), p22; Positi ve end expiratory pressure (2), p24; Continuous posi ti ve airway pressure, p26;

Non-invasive respi ratory support, p32; Lung recruitment, p28; Endotracheal i ntubation, p36; Minitracheotomy, p40;

Fibreopti c bronchoscopy, p46; Chest physiotherapy, p48; Bl ood gas anal ysi s, p100; Bronchodi lators, p186; Chroni c

airfl ow l imitation, p286; Acute chest i nfection (1), p288; Acute chest i nfecti on (2), p290; Post-operati ve intensive

care, p534

Chronic airflow limitation

Many pati ents requiring ICU admissi on for a communi ty acquired pneumonia have chroni c respiratory fai lure An

acute exacerbation (which may or may not be infection-related) results in decompensation and symptomati c

deteri orati on Infections resulting i n acute exacerbati ons include viruses, Haemophilus influenzae, Klebsiella and

Staph aureus in addition to Strep pneumoniae, Mycoplasma pneumoniae and Legionella pneumophila Otherwi se,

patients with coi nci dental chronic ai rfl ow limitati on (CAL) are admitted for other reasons or as a prophyl actic

measure i n view of their li mited respi ratory function, e.g for el ective post-operative venti lation

Problems in managing CAL patients on the ICU

Disabi li ty due to chroni c ill healthFati gue, muscle weakness and decreased physi ol ogi cal reserve leading to earl ier need for venti latory support,increased di ffi cul ty in weaning, and greater physical dependency on support therapies

Psychol ogi cal dependency on support therapi esMore prone to pneumothoraces

Usuall y have greater l evels of sputum producti onRight ventri cul ar dysfuncti on (cor pulmonale)

Tri als of non-i nvasive venti latory support ± respiratory sti mul ants such as doxepram have shown considerablesuccess i n avoi ding i ntubation and mechani cal venti lation.

Accept lower target l evels of PaO2Accept hi gher target levels of PaCO2 if patient i s known or suspected to have chronic CO2 retenti on on the basis

of elevated plasma bicarbonate levels on admission to hospital

Weaning the patient with CAL

An early tri al of extubation may be worthwhile before the pati ent becomes ventil ator-dependent

Weaning may be a lengthy procedure Dail y trials of spontaneous breathing may reveal faster-than-anti ci patedprogress

Provide pl entiful encouragement and psychol ogi cal support Setting dail y targets and earl y mobi lisati on may beadvantageous

Do not ti re by prol onged spontaneous breathing Consider gradual ly increasi ng periods of spontaneous breathi nginterspersed by periods of rest Ensure a good ni ght's sl eep

Use patient appearance and l ack of symptoms (e.g tachypnoea, fati gue) rather than specifi c blood gas val ues tojudge the durati on of spontaneous breathing

Early tracheostomy may benefit when di ffi culty in weani ng is expected

The patient may cope better with a tracheostomy mask than CPAP

Additi on of extrinsic PEEP or CPAP may prevent early ai rways closure and thus reduce the work of breathi ng

However, this shoul d be done wi th caution because of the ri sk of increased ai r trappi ng

Consider heart fail ure as a cause of difficulty i n weaning

Acute chest infection (1)

Patients may present to intensive care as a result of an acute chest infection or may devel op infection as a

compli cation of i ntensi ve care management Typical features include fever, cough, purul ent sputum production,

breathlessness, pleuritic pain and bronchial breathi ng Urgent i nvesti gation i ncl udes arteri al gases, CXR, blood count

and cultures of bl ood and sputum In community acquired pneumonia, acute phase antibody titres should be taken

Diagnosis and initial antimicrobial treatment

Basic resuscitation is requi red if there is cardiorespiratory compromise Appropriate treatment of the i nfecti on

depends on CXR and cul ture findings, al though empiric ‘best guess’ anti biotic treatment may be started before cul ture

resul ts are avail abl e Treatment includes physi otherapy and methods to aid sputum clearance

Clear CXR

Acute bronchitis is associated with cough, mucoid sputum and wheeze In previ ously healthy pati ents a vi ral aetiology

is most l ikely and there i s often an upper respi ratory prodrome Symptomati c rel ief is usual ly all that is requi red

Li kel y organisms in acute on chroni c bronchi ti s i ncl ude Strep pneumoniae, H in uenzae or Staph aureus.

Appropri ate antibiotics i ncl ude cefuroxi me or ampici ll in and ucloxacill in Viral pneumonia may be confused by the

presence of bacteria in the sputum but secondary bacterial i nfection is common

Pulmonary cavitation on CXR

Cavitation should alert to the possi bi lity of anaerobic infection (sputum is often foul smel ling) Staph aureus, K.

pneumoniae or tuberculosis are also associated with cavi tation Appropriate antibi oti cs include metronidazol e or

cl indamycin for anaerobi c infection, flucloxaci ll in for Staph aureus and ceftazidime and gentami cin for K.

pneumoniae A foreign body or pul monary infarct should al so be considered where there i s a si ngl e abscess.

Consolidation on CXR

The recent history i s i mportant for deciding the cause of a pneumonia:

Hospital acquired pneumonia—enteric (Gram negati ve) organi sms treated wi th ceftazidi me and gentamicin,

Staph aureus treated wi th ceftazidi me and gentamicin, Staph aureus treated with fl ucl oxacil li n (or

tei coplanin/vancomyci n i f multiresi stant)

Recent aspirati on—anaerobic or Gram negati ve i nfection treated with clindamyci n or cefuroxime andmetroni dazol e

Communi ty acquired pneumonia in a previousl y heal thy individual —Strep pneumoniae (often l obar, acute onset)

or atypical pneumonia (insi dious onset, known community outbreaks, renal fai lure and electrol yte di sturbance inLegionnai re's disease) Appropri ate antibiotic therapy i s cefuroxime and clarithromycin

Pneumonia compli cating i nfl uenza—Staph aureus treated wi th flucloxacil lin Both Staph aureus and H.

influenzae are common in those debili tated by chroni c disease (e.g al coholi sm, di abetes, chroni c airflow

limitation or the elderl y)

Immunosuppressed—opportunistic i nfecti ons (e.g tubercul osi s, Pneumocystis carinii Herpes vi ruses, CMV or

fungi)

Antimicrobial treatment

Gram negative spp.

The following samples are required for laboratory diagnosis:

Sputum (e.g cough specimen, endotracheal tube aspirate, protected brush speci men, bronchoalveol ar lavagespecimen)

Blood cul tures

P.292

P.293

Uri ne for antigen tests (if Legionella, Candida or pneumococcus suspected)

In severe pneumoni a, bli nd antibi oti c therapy should not be withheld whi le awaiti ng resul ts Speci mens should,

however, be taken before starti ng antibi otics

Microbiological yiel d i s usuall y very low, especi all y i f anti biotic therapy has started before sampl ing

Where cul tures are posi tive there i s often multipl e growth Separati ng pathogeni c organi sms from col oni sing

organi sms may be difficult

In hospital acqui red pneumoni a, known nosocomial pathogens are the li kel y source, e.g l ocal Gram negative fl ora,

MRSA

Continuing treatment

Antibiotics shoul d be adjusted accordi ng to sensi tiviti es once avai lable Failure to respond to treatment in 72h shoul d

prompt consi deration of infections more common i n the immunocompromised or other diagnoses

Hospital -acqui red pneumoni a requi res treatment with appropriate anti bi oti cs for 24h after symptoms subside (usual ly

3–5 days) After this peri od cul tures should be repeated (off anti bioti cs if there has been i mprovement) Some ICUs

wil l use longer courses—a recent multi centre study showed no difference in outcome between 8 and 15 days'

treatment

In atypical or pneumococcal pneumoni a, 10–14 days of antibiotic treatment i s usual (though no evi dence base exists

to indicate the opti mal duration of therapy)

Key trial

Chastre J, for the PneumA Trial Group Compari son of 8 vs 15 days of antibiotic therapy for ventil ator-associatedpneumonia in adults: a randomized tri al JAMA 2003; 290:2588–98

Acute respiratory distress syndrome (1)

ARDS i s the respi ratory component of multipl e organ dysfunction It may be predominant in the cl inical picture or be

of lesser cl inical i mportance i n relation to dysfunction of other organ systems

Aetiology

As part of the exaggerated inflammatory response fol lowing a major exogenous insul t which may be either di rect

(e.g chest trauma, i nhalation injury) or distant (e.g peri tonitis, major haemorrhage, burns) Histol ogy reveals

aggregati on and activati on of neutrophi ls and pl atelets, patchy endothel ial and alveolar disruption, intersti ti al

oedema and fi brosi s Classi cal ly, the acute phase i s characterised by i ncreased capill ary permeabi li ty and the

fibroproliferative phase (after 7 days) by a predomi nant fibrotic reacti on However, more recent data woul d suggest

such distincti ons are not so clear-cut; there may be evidence of markers of fibrosis as early as day 1

Definitions

Acute lung injury (ALI)

PaO2/FIO2≤300mmHg (40kPa)Regardl ess of level of PEEPWith bilateral infil trates on CXRWith pulmonary artery wedge pressure <18mmHg

Acute respiratory distress syndrome (ARDS)

As above but PaO2/FIO2≤200mmHg (26.7kPa)

Prognosis

Prognosis depends in part on the underl yi ng i nsult, the presence of other organ dysfuncti ons and the age and chronic

health of the pati ent Predomi nant single-organ ARDS carries a mortal ity of 30–50%; there does appear to have been

some i mprovement over the last decade

Some deterioration on lung functi on testi ng is usuall y detectabl e i n survivors of ARDS, even i n those who are

rel atively asymptomatic Recent studies i ndi cate that a significant proporti on of survivors of ARDS have physi cal

and/or psychological sequel ae at 1 year

Key trials

Bernard GR for the The American–European Consensus Conference on ARDS Definitions, mechanisms, rel evant

outcomes, and clinical tri al coordi nation Am J Respi r Cri t Care Med 1994; 149:818–24

P.295

Herri dge MS, Cheung AM for the Canadi an Cri ti cal Care Tri als Group One-year outcomes i n survivors of the acute

respi ratory di stress syndrome N Engl J Med 2003; 348:683–93

Marshall RP, et al Fibroproli feration occurs earl y i n the acute respiratory di stress syndrome and i mpacts on outcome

Am J Respir Cri t Care Med 2000; 162:1783–8

See also:

Oxygen therapy, p2; Ventilatory support—i ndi cations, p4; IPPV—compl icati ons of ventil ation, p14; Posi tive end

expiratory pressure (1) Positi ve end expiratory pressure (2), p24; Continuous posi ti ve airway pressure, p26; Lung

recruitment, p28; Prone positi oni ng, p30; Extracorporeal respiratory support, p34; Endotracheal i ntubation, p36;

Bl ood gas analysis, p100; Bacteri ology, p158; Virol ogy, serol ogy and assays, p160; Col loi d osmotic pressure, p172;

Col loi ds, p180; Bronchodilators, p186; Nitric oxi de, p190; Surfactant, p192; Antimi crobials, p260; Steroi ds, p262;

Prostagl andi ns, p264; Basic resusci tation, p270; Acute chest infection (1), p288; Acute chest i nfecti on (2), p290;

Acute respi ratory di stress syndrome (2), p294; Inhal ation injury, p306; Infecti on—diagnosis, p480;

Infection—treatment, p482; Systemic inflammation/multi organ fai lure, p484; Sepsi s and septi c shock—treatment,

p486; Mul tiple trauma (1), p500; Multiple trauma (2), p502; Pyrexia (1), p518; Pyrexia (2), p520

Acute respiratory distress syndrome (2)

states Care should be taken not to compromi se the ci rculati on

4

Respiratory management

Maintai n adequate gas exchange with i ncreased FIO2 and, depending on severity, either non-i nvasive respiratorysupport (e.g CPAP, Bi PAP) or posi ti ve pressure ventil ati on Speci fi c modes may be util ised, such as pressurecontrolled i nverse rati o venti lation Whi le general agreement exi sts for mini mising VT (6-7ml/kg) and plateauinspiratory pressures (≤30cmH2O) i f possible, there is no consensus regardi ng the upper desired level of FIO2and PEEP Greater emphasi s i s currently pl aced on higher levels of PEEP (up to 20cm H2O) While the currentEuropean view favours the use of hi gher FIO2 (up to 1.0), a common US approach is to keep the FIO2 ≤0.60 but

to maintai n SaO2 wi th hi gher l evels of PEEP A recent study assessing hi gher l evels of PEEP showed no outcomebenefit

3

Pati ent posi tioning may provide i mprovements i n gas exchange This includes ki netic therapy using specialrotati onal beds, and prone posi ti oni ng with the patient being turned frequentl y through 180° Care has to betaken duri ng prone positioning to prevent tube displacement and shoul der injuries

Ventil ator trauma is ubi quitous Multi pl e pneumothoraces are common and may requi re mul ti ple chest drains

They may be di ffi cult to diagnose by X-ray and, despi te the attendant risks, CT scanni ng may revealundi agnosed pneumothoraces and aid correct si ting of chest drai ns

8

Key trials

Acute Respiratory Di stress Syndrome Network Venti lation wi th lower ti dal volumes compared with traditi onal tidal

vol umes for acute lung i njury and the acute respiratory distress syndrome N Engl J Med 2000; 342:1301–8

Hickl ing KG, et al Low mortal ity rate in adult respi ratory di stress syndrome using l ow-vol ume, pressure-l imi ted

ventil ation wi th permissive hypercapni a: a prospective study Cri t Care Med 1994; 22:1568–78

Meduri GU, et al Effect of prolonged methylprednisolone therapy i n unresol ving acute respiratory distress syndrome:

a randomi zed controll ed trial JAMA 1998; 280:159–65

Gatti noni L, et al for the Prone-Supine Study Group Effect of prone positi oni ng on the survi val of patients wi th acute

respi ratory failure N Engl J Med 2001; 345:568–73

See also:

Oxygen therapy, p2; Ventilatory support—i ndi cations, p4; IPPV—compl icati ons of ventil ation, p14; Posi tive end

expiratory pressure (1) Positi ve end expiratory pressure (2), p24; Continuous posi ti ve airway pressure, p26; Lung

recruitment, p28; Prone positi oni ng, p30; Extracorporeal respiratory support, p34; Endotracheal i ntubation, p36;

Bl ood gas analysis, p100; Bacteri ology, p158; Virol ogy, serol ogy and assays, p160; Col loi d osmotic pressure, p172;

Col loi ds, p180; Bronchodilators, p186; Nitric oxi de, p190; Surfactant, p192; Antimi crobials, p260; Steroi ds, p262;

Basic resuscitation, p270; Acute chest infection (1), p288; Acute chest i nfecti on (2), p290; Acute respi ratory di stress

syndrome (2), p294; Inhalation injury, p306; Infecti on—diagnosi s, p480; Infecti on—treatment, p482; Systemic

inflammation/multi organ fai lure, p484; Sepsis and septi c shock—treatment, p486; Mul ti ple trauma (1), p500; Mul tiple

trauma (2), p502; Pyrexi a (1), p518; Pyrexi a (2), p520

Asthma—general management

Pathophysiology

Acute bronchospasm and mucus pluggi ng, often secondary to an insul t such as i nfecti on The pati ent may progress to

fatigue, respi ratory fai lure and collapse The onset may develop slowly over days, or occur rapi dly wi thi n minutes to

A ‘sil ent’ chest i s also a late sign suggesting severely li mi ted ai rfl ow

Pneumothorax and lung/lobar col lapse

Management of asthma

Asthmati cs must be managed in a well -monitored area If clinical features are severe, they shoul d be admi tted to an

intensive care uni t where rapi d institution of mechanical ventil ati on is available Moni toring shoul d compri se, as a

minimum, pul se oxi metry, conti nuous ECG, regular blood pressure measurement and blood gas analysis If severe, an

intra-arterial cannula ± central venous access should be inserted

High FIO2 (≥0.60) to maintai n SpO2≥95%

Anecdotal success has been reported with subanaesthetic doses of a volati le anaesthetic agent such as

i soflurane which both cal ms/sedates and bronchodi lates

8

Indications for mechanical ventilation

Increasing fati gue and obtundationRespiratory fai lure—rising PaCO2 fal ling PaO2Cardiovascul ar col lapse

P.298

Facilitating endotracheal intubation

Summon senior assi stance Pre-oxygenate wi th 100% O2 Perform rapid sequence induction with suxamethoni um and

etomidate or ketamine ‘Breathing down’ wi th an inhalational anaesthetic (e.g isofl urane) pre- i ntubation should onl y

be attempted by an experi enced cli ni cian To minimse barotrauma, care shoul d be taken to avoid excess air trappi ng,

high airway pressures and high tidal volumes

See also:

Oxygen therapy, p2; Ventilatory support—i ndi cations, p4; Endotracheal intubati on, p36; Pulse oximetry, p90; Bl ood

gas analysis, p100; Bacteri ology, p158; Bronchodi lators, p186; Sedatives, p238; Steroi ds, p262; Dyspnoea, p278;

Asthma—venti latory management, p298; Anaphylactoid reacti ons, p496

Asthma—ventilatory management

Early period

Ini tiall y gi ve low VT (5ml /kg) breaths at low rate (5–10/min) to assess degree of bronchospasm and air trapping

Slowly increase VT (to 7-8ml /kg) ± increase rate, taking care to avoi d significant air trapping and highinspiratory pressures Low rates wi th prolonged I:E rati o (e.g 1:1) may be advantageous Avoid very shortexpi ratory times.Do not strive to achieve normocapni a

3

If significant air trapping remains, consider ventil ator disconnection and forced manual chest compressions every10–15mi n

4

If severe bronchospasm persi sts, consider injecting 1–2ml of 1:10,000 epinephrine down endotracheal tube

Repeat at 5mi n i ntervals as necessary

If mucus pluggi ng consti tutes a major problem, i nstil lation of a mucolytic (N-acetyl cysteine) may be considered

though thi s may induce further bronchospasm Bronchoscopi c removal of pl ugs shoul d only be performed by anexperi enced operator

6

P.300

Assessment of air trapping (intrinsic PEEP, PEEPi)

Measure PEEPi by pressing end-expi ratory hold button of venti lator

No pause between expiratory and inspi ratory sounds

Disconnection of ventilator and timi ng of audibl e expi ratory wheeze

An increasing PaCO2 may respond to reducti ons in mi nute volume which wil l l ower the l evel of i ntrinsic PEEP

space out interval s between β2 agoni st nebuli sers Convert other anti asthmati c drugs to oral medicati on Theophyl line

doses should be adjusted to ensure therapeuti c l evels

See also:

Oxygen therapy, p2; Ventilatory support—i ndi cations, p4; Endotracheal intubati on, p36; Pulse oximetry, p90; Bl ood

gas analysis, p100; Bacteri ology, p158; Bronchodi lators, p186; Sedatives, p238; Steroi ds, p262; Dyspnoea, p278;

Asthma—general management, p296; Anaphyl actoi d reactions, p496

Pneumothorax

Si gni ficant coll ection of air i n the pleural space that may occur spontaneously, foll owi ng trauma (incl udi ng

iatrogeni c), asthma, chroni c lung disease, and is a common sequel of ventil ator trauma

Respiratory fai lure and deteri oration i n gas exchange

Increasing airway pressures and difficulty to venti late

Cardiovascul ar deteri oration with mediasti nal shift (tension)

Diagnosis

CXR—most easi ly seen on erect views where absent l ung marki ngs are seen lateral to a well -defined lung border

However, ventilated patients are often i maged i n a supi ne posi ti on; pneumothorax may be easil y missed as itmay be lyi ng anteri or to normal lung gi ving the misleading appearance of lung markings on the radiograph

Supine pneumothorax shoul d be considered i f the foll owi ng are seen:

Hyperlucent l ung fi eld compared to the contral ateral si deLoss of cl ari ty of the di aphragm outl ine

‘Deep sulcus’ si gn, gi vi ng the appearance of an i nverted diaphragm

A parti cul ar cl ear part of the cardi ac contour

A lateral fil m may hel p Tension pneumothorax results i n marked medi astinal shi ft away from the affectedside

Ultrasound—may be helpful but i s highly operator dependent

CT scan—very sensitive and may be useful in difficult si tuati ons, e.g ARDS, and to direct drainage of

l ocalised pneumothorax

Pneumothorax must be distingui shed from bullae, especi all y with l ong-standi ng emphysema; i nadvertent drai nage of

a bull a may cause a bronchopleural fistula Assistance should be sought from a radi ologist

P.302

drain insertion

Repeated needl e aspi ration may be suffici ent i n spontaneously breathing pati ents without respi ratory fail ure;

however, this is not recommended i f the patient i s ventilated

3

Chest drai n i nsertion This may be done under ultrasound or CT guidance, especi al ly if locali sed due tosurroundi ng lung fibrosis

4

A smal l pneumothorax (<10% hemi thorax) may be l eft undrained but prompt acti on should be insti tuted if

cardi orespi ratory deterioration occurs Patients should not be transferred between hospi tal s, parti cul arl y by plane,

with an undrained pneumothorax Drai ns may be removed i f not swi ngi ng/bubbli ng for several days

Bronchopleural fistula

Denoted by continual drainage of air Usually responds to conservative treatment with continual appli cation of 5kPa

negati ve pressure; this may take weeks to resolve For severe leak and/or compromised ventil ati on, hi gh frequency

jet venti lation and/or a doubl e l umen endobronchi al tube may be considered Surgi cal interventi on i s rarely

necessary

Chest X-ray appearance

Figure No Caption Available.

See also:

IPPV—compli cations of venti lation, p14; Hi gh frequency ventil ation, p20; Chest drai n insertion, p42; Central venous

catheter—insertion, p116; Basi c resusci tation, p270; Respi ratory fai lure, p282; Acute respi ratory di stress syndrome

(1), p292; Acute respiratory distress syndrome (2), p294; Mul tiple trauma (1), p500; Multiple trauma (2), p502

Haemothorax

Usuall y secondary to chest trauma or following a procedure, e.g cardiac surgery, chest drai n i nserti on, central

venous catheter inserti on Spontaneous haemothorax is very rare, even in patients wi th clotti ng di sorders

Clinical features

Stony dul lness

Decreased breath sounds

Hypovol aemia and deteriorati on in gas exchange (i f l arge)

Perforati on of an intercostal vessel duri ng chest drain insertion may cause considerable bl eedi ng into the pl eura If

deep tension sutures around the chest drai n fail to stem bl ood loss, remove the chest drai n and insert a Fol ey

urethral catheter through the hole Inflate the bal loon and apply traction on the catheter to tamponade the bleedi ng

vessel If these measures fail , contact a thoracic surgeon

See also:

Chest drain insertion, p42; Central venous catheter—insertion, p116; Bl ood transfusion, p182; Blood products, p252;

Coagul ants and antifi bri nol ytics, p254; Aprotini n, p256; Pneumothorax, p300; Bl eeding di sorders, p396

Haemoptysis

May range from a few specks of bl ood in expectorated sputum to massive pulmonary haemorrhage

More li kel y to disrupt gas exchange before life-threatening hypovol aemia ensues

May be a presenting feature of a patient admitted to intensive care or may resul t from critical i ll ness and itstreatment

Causes

Massive haemoptysis

Disrupti on of a bronchial artery by acute inflammation or invasion (e.g pulmonary neopl asm, trauma, cavitati ng

TB, bronchiectasis, l ung abscess and aspergi lloma)

Rupture of arteriovenous mal formations and bronchovascular fi stulae

Pul monary infarcti on secondary to prolonged pulmonary artery catheter wedging or pul monary artery rupture

Minor haemoptysis

Intrapulmonary inflammation or infarcti on (e.g pul monary embolus)Endotracheal tube trauma (e.g mucosal erosion, ball oon necrosis, trauma from the tube tip, trauma to atracheostomy stoma, trauma from sucti on catheters)

Tissue breakdown in criticall y i ll patients (e.g tissue hypoperfusi on, coagulopathy, poor nutriti onal state, sepsi sand hypoxaemi a.)

Investigation and assessment

Urgent assessment of cardiorespi ratory function and cardiorespiratory moni toring are required Massi ve haemoptysis

may requi re resuscitati on and urgent i ntubation The diagnosis may be suggested by the history and a CXR may

identi fy a cavi tating l esi on Lower lobe shadowi ng on a CXR may be the resul t of overspi ll of blood from el sewhere i n

the bronchi al tree Early surgical intervention should be prompted by a changing ai r-flui d level, persi stent

opacificati on of a previ ous cavity or a mobil e mass Earl y bronchoscopy may identify the source of haemoptysi s,

although onl y whil e bleeding i s active Blood i n multipl e bronchi al orifi ces may be confusi ng but saline l avage may

leave the source visi bl e Rigi d bronchoscopy is useful i n massive haemoptysis al lowing oxygenati on and wi de bore

sucti on

Management

Basic resuscitati on (hi gh FIO2, endotracheal i ntubation and bloodtransfusion) i s needed for cardi orespi ratorycompromise

Correction of coagulopathy i s a priority

Bronchoscopy al lows direct insti llati on of 1 in 200,000 epi nephri ne if the source of haemorrhage can be found or,

P.306

alternati vel y, endobronchial tamponade with a bal loon catheter

In cases of severe haemorrhage from one l ung a double lumen endotracheal tube may prevent some overspi ll tothe other lung whil e defi ni tive treatment is organi sed

Defi ni tive treatment may include radiol ogi cal bronchi al artery embol isati on, or surgi cal resecti on

Induced hypotension may be useful in bronchial artery haemorrhage

In cases of pulmonary artery haemorrhage, PEEP may be used with mechanical venti lation to reduce pulmonarybleedi ng

See also:

Oxygen therapy, p2; Ventilatory support—i ndi cations, p4; Posi tive end expi ratory pressure (1), p22; Posi ti ve end

expiratory pressure (2), p24; Continuous posi tive airway pressure, p26; Endotracheal i ntubation, p36; Fi breoptic

bronchoscopy, p46; Bl ood transfusion, p182; Blood products, p252; Coagulants and anti fibrinolyti cs, p254; Basi c

resuscitati on, p270; Acute chest infection (1), p288; Acute chest i nfecti on (2), p290; Pul monary embol us, p308;

Bl eedi ng di sorders, p396; Amni oti c flui d embolus, p544

Inhalation injury

Causes include smoke, steam, noxious gases and aspirati on of gastri c contents

Clinical features

Dyspnoea, coughi ngStridor (if upper airway obstruction)Bronchospasm

Signs of lung/l obar coll apse (especi all y with aspiration)Signs of respiratory fai lure

Cherry-red skin col our (carbon monoxi de)Agi tation, coma

ARDS (l ate)

General principles of management

100% O21

Early intubation i f upper airway compromised or threatened

Urgent laryngoscopy shoul d be performed if soot i s present i n the nares, mouth or pharynx

If soot is seen or the larynx appears inflamed, perform early endotracheal i ntubation As the upper airway canobstruct within mi nutes it is advisabl e to i ntubate as a prophylacti c measure rather than as an emergency where

it may prove impossibl e

After intubation, perform urgent bronchoscopy wi th bronchial toil et usi ng warmed 0.9% sal ine to remove asmuch soot as possible

Commence benzylpeni cil li n 1.2g qds IV

Specific treatment for poisons contained within smoke (e.g carbon monoxi de, cyani de)

P.308

Early bronchoscopy and physi otherapy to remove as much particulate and li qui d matter as possi ble

Either cefuroxi me plus metroni dazole, or cli ndamyci n for 3–5 days

Steroi d therapy has no proven benefit

See also:

Oxygen therapy, p2; Ventilatory support—i ndi cations, p4; Endotracheal intubati on, p36; Fi breoptic bronchoscopy,

p46; Blood gas analysis, p100; Antimicrobi als, p260; Ai rway obstructi on, p280; Inhaled poisons, p466; Burns—flui d

management, p510; Burns—general management, p512

Pulmonary embolus

Aetiology

Usuall y arises from a deep vein thrombosis in femoral or pelvic vei ns The risk i ncreases after prolongedimmobi lisati on and wi th pol ycythaemi a or hypervi scosity disorders

Amniotic fluid embolus

Fat embolus after pelvic or long bone trauma

Right heart source, e.g mural thrombus

Clinical features

Pleuri tic-type chest pai n, dyspnoea, ± haemoptysi s

The patient with a major embolus often prefers to li e fl at Dyspnoea improves due to i ncreased venous returnand ri ght heart loadi ng

Deteri oration i n gas exchange—may find a low PaO2 low or hi gh PaCO2 and a metabolic acidosi s However, these.ndi ngs are inconsistent and non-diagnosti c

Cardiovascul ar features, e.g tachycardia, low/hi gh BP and coll apse

CXR: may be normal but a massive embol us may produce fewer vascular markings (pul monary ol igaemi a) i n ahemi thorax ± a bulging pulmonary hilum A wedge-shaped peri pheral pulmonary infarct may be seen after a fewdays following a small er embolus

ECG: acute ri ght ventricular strain, i e S1 Q3T3, tachycardia, ri ght axis deviation, right bundle branch block, Ppul monale

Echocardi ogram: may reveal evidence of pulmonary hypertensi on and acute ri ght ventricular strain

D-di mers—though a rai sed level is non-di agnostic, a normal value carries a high probabi li ty of excl usi on of apul monary embolus

Definitive diagnosis

CT scan wi th contrast—the i nvesti gation of choice for major embolus

Pul monary angiographyVentil ati on–perfusion scan—degree of certainty i s reduced i f area of non-perfused lung corresponds to any CXRabnormali ty

Fat globul es or foetal cell s i n pulmonary artery bl ood may be found in fat and amni oti c flui d embolus,respectively

Management of blood clot embolus

Start anticoagulation with low molecul ar wei ght heparin adjusted for wei ght Consider thrombolysis if there is a major

embolus and cardiovascul ar compromi se, and embol ectomy if the pati ent remai ns moribund Otherwise, at 24–48h