Oxford Handbook of Critical Care - part 9 ppt

Uri nal ysis, p166; Toxicology, p162; Sodium bi carbonate, p178; Acute renal fail ure— management, p334;Vomiting/gastric stasi s, p338; Metaboli c acidosi s, p434; Poisoni ng—general pri

P.468

A cherry red appearance of the ski n and mucosae are classi cal but not common

PaO2 wi ll be normal unless there is respiratory depressi on and pul se oxi metry is mi sleadi ng

The hal f l ife of carboxyhaemoglobi n i s 4h when breathing room air and 50mi n when breathing 100% oxygen

Management

Carboxyhaemogl obin levels shoul d be measured by a co-oxi meter and treatment started immedi ately wi thoxygen at the maximum concentration that can be delivered (FIO2 1.0 if ventil ated and 0.6–1.0 i f

sel f-venti lating)

If carboxyhaemoglobin levels >25% or carbon monoxi de poi soning is associated wi th mental di sturbance, theopti mal treatment is hyperbari c oxygen at 3 atmospheres for 30mi n, repeated 6-hrly if level s remain >25%

Death i s likely wi th carboxyhaemoglobin level s >60%

High concentration oxygen treatment should conti nue until carboxyhaemogl obi n l evels <10%

Cli ni cal features include anxiety, agi tation, hyperventi lation, headache, loss of consciousness, dyspnoea, weakness,

dizzi ness and vomi ti ng The skin remai ns pink and hypotensi on may be severe An unexplai ned metaboli c aci dosis is

suggesti ve

Management

High concentration oxygen shoul d be given, but is only truly effective when given at hyperbari c pressures

In mil d cases rapi d, natural detoxificati on reduces cyani de level s by 50% within 1h, al lowing supportive therapyonl y

Sodium thiosulphate (150mg/kg i ntravenousl y foll owed by 30–60mg/kg/h) converts cyanide to thiocyanate andshould be used i f there i s unconsciousness It i s, however, slow-acti ng

Nitrites produce methaemogl obi naemia and may potenti all y worsen cyanide toxi city

Dicobalt edetate (300mg IV) is the speci fi c anti dote to cyani de but i s severel y toxi c (vomi ti ng, urticari a,tachycardia, hypotension, dyspnoea, chest pain) i n the absence of cyani de It i s therefore best avoided unl esscyanide toxicity i s l ikely

Key trial

Weaver LK, et al Hyperbari c oxygen for acute carbon monoxide poi soning N Engl J Med 2002; 347:1057–67

See also:

Oxygen therapy, p2; Ventilatory support—i ndi cations, p4; Blood gas analysis, p100; ECG monitori ng, p108; Bl ood

pressure monitori ng, p110; Toxi col ogy, p162; Basi c resuscitation, p270; Inhal ati on injury, p306; Metaboli c aci dosis,

p434; Poi soning—general pri ncipl es

Household chemicals

Corrosives

Strong acids and alkali s are increasi ngl y avail able in the househol d and i ngestion may lead to shock and bowel

perforati on Gastric el imi nation techniques must be avoi ded si nce aspi ration of corrosives may cause severe lung

damage Earl y surgical repair of perforation may be necessary

Petroleum

Al though not stri ctl y a househol d chemical, access to petroleum i n the home i s easy

Clinical features

Gastrointestinal ingestion and absorption gives clinical features similar to those of alcohol intoxicati on with more

severe central nervous system depressi on

Management

P.470

Gastri c eli minati on techni ques must be avoided since a few drops of petroleum spi lli ng into the lungs can l ead to

a severe pneumoniti s Thi s i s due to the low surface tensi on and vapour pressure of petroleum all owi ng rapidspread through the lungs

Treatment invol ves supporti ve therapy and 250ml l iquid paraffin orall y

Paraquat

Paraquat is widely avail abl e as a selective weedkil ler which is i nactivated on contact with the soi l A dose of 2–3g is

usuall y fatal (equivalent to 80–120g of granules or 10–15ml of i ndustrial l iquid concentrate)

Severe di arrhoea may ensue requiri ng careful fluid management

If paraquat poisoni ng is confi rmed 200–500ml of 30% Ful ler's earth is gi ven 2-hrl y for 24h via a nasogastrictube

A forced diuresis should be started to encourage renal excretion

Pul monary fibrosis is more severe when breathi ng hi gh oxygen concentrations; if oxygen i s required the lowestconcentration possibl e should be given accepting a low PaO2 Liposomal superoxide dismutase and gl utathi oneperoxi dase have been used experi mental ly

See also:

Toxicology, p162; Poi soning—general pri ncipl es, p452

Methanol and ethylene glycol

Methanol

Toxici ty mai nl y arises due to oxi dation of methanol to formi c acid and formaldehyde The oxidative pathway is an

enzymatic process invol ving alcohol dehydrogenase but proceeds at 20% of the rate of ethanol oxidati on

Clinical features

Cli ni cal features of poi soning i ncl ude bl indness (due to concentrati on of methanol in the vi treous humour), severe

metabolic acidosi s, headache, nausea, vomi ting and abdomi nal pain

Management

Metabol ism of methanol is sl ow so treatment wi ll need to be prol onged (several days)

Treatment includes gastric emptyi ng (wi thi n 4h of i ngesti on), sodi um bicarbonate titrated to correct arteri al pHand ethanol to saturate the oxi dative pathway

On presentation 1ml/kg ethanol (50%) i s given oral ly fol lowed by 0.5ml/kg 2-hrly for 5 days

Alternati vel y, metabolism can be blocked by 4-methyl pyrazole (fomepizole) which can be i nfused or injected12-hrl y

If methanol l evels are >1000mg/l haemodialysis is used until levels are <250mg/l

Ethylene glycol

Ethylene glycol i s partial ly metabolised by alcohol dehydrogenase to oxali c acid whi ch is responsi bl e for a severe

metabolic acidosi s, renal fai lure and sei zures

Clinical features

Cli ni cal suspi ci on i s aroused by odourless drunkenness, oxalate crystals in the urine or bl ood and the severe aci dosis

As li ttl e as 50ml can be fatal

Uri nal ysis, p166; Toxicology, p162; Sodium bi carbonate, p178; Acute renal fail ure— management, p334;

Vomiting/gastric stasi s, p338; Metaboli c acidosi s, p434; Poisoni ng—general pri nci ples, p452

Organophosphate poisoning

Organophosphate pesti ci des are the major cause of suicidal poisoni ng in devel opi ng countries and are used as nerve

agents in terrori st attacks (e.g Sari n, Tabun, VX, GF) Their mode of acti on is vi a chol inergi c toxi ci ty

Cholinergic (anticholinesterase) syndrome

Sal ivation, lacri mationVomi ti ng, di arrhoeaBradycardia

BronchospasmMeiosi s

Oxygen therapy, p2; Ventilatory support—i ndi cations, p4; ECG moni toring, p108; Toxi col ogy, p162; Bronchodil ators,

p186; Chronotropes, p206; Bradyarrhythmias, p318; Vomiting/gastric stasi s, p338; Di arrhoea, p340;

Poi soning—general principl es, p452

Ovid: Oxford Handbook of Critical Care

Editors: Singer, Mervyn; Webb, Andrew R.

Title: Oxford Handbook of Critical Care, 2nd Edition

Copyri ght ©1997,2005 M Si nger and A R Webb, 1997, 2005 Publ ished in the United States by Oxford Universi tyPress Inc

> Table of Co ntents > Infection an d Inflammation

Infection and Inflammation

Infection control—general principles

Infection acqui red wi thin the ICU i s a major cause of mortal ity, morbidi ty and increased durati on of stay There are

remarkabl e vari ati ons i n practice for whi ch the lack of a good evi dence base i s chiefly responsi ble Examples i ncl ude

different poli cies with regard to pati ent isolati on, mi crobiological survei llance, handwashing procedures, use of

impregnated vascul ar catheters, the duration of indwel li ng catheters, and frequency of change of di sposables such as

intravenous gi ving sets and fi lters It i s neverthel ess accepted that adequate handwashing before and after patient

contact and strict aseptic technique when performi ng procedures are mandatory

Strict aseptic technique for invasi ve procedures (e.g central venous catheter i nserti on) and clean technique forbasi c procedures, e.g endotracheal suction, changi ng ventil ator circui ts or drug infusi ons

Previous i mmuni sation against hepati tis B, tuberculosisStethoscopes shoul d be cleaned between pati ents

Clear sign-posting of precauti ons to be taken on cubicl e doors

Some patients carry potenti all y contagi ous or infecti ve organi sms and requi re source i sol ati on, e.g tubercul osi s

Immunosuppressed pati ents, e.g when neutropenic fol lowing chemotherapy, are at ri sk of acquiring infecti on

Microbiological surveillance

Pol icies vary; some ICUs routi nel y screen sputum, bronchoalveol ar lavage, blood, uri ne and drain fl uid every 3–7

days whil e others screen only when i ndi cated, e.g deteri orating cardiorespiratory status, pyrexi a, neutrophi lia Send

samples promptl y to the lab for anal ysi s

See also:

Bacteriology, p158; Virology, serology and assays, p160; Anti mi crobials, p260; Acute chest infection (1), p288; Acute

chest infection (2), p290; Infection—di agnosi s, p480; Infecti on—treatment, p482; ICU l ayout, p566

Routine changes of disposables

Care of intravascular catheters

Sites should be covered with transparent semi permeable dressings to all ow observation and prevent secreti onsfrom accumulati ng

Routine changes of intravascular catheters are no l onger recommended As the ri sk of infection does increase

considerably after a week in situ, catheters should be removed as soon as cli nical ly feasible.

Catheters can be changed over a gui dewire i f the site l ooks cl ean but signs suggestive of mi ld to moderateinfection are present el sewhere, (e.g pyrexia or unexplai ned neutrophili a) but wi thout major cardiorespi ratorydisturbance

Catheters shoul d be changed to a fresh site if:

the old si te appears i nfectedthe patient shows signs of severe i nfecti on

a positive growth i s obtained from a blood culture drawn through the catheter or from the ti p of theprevious catheter

Routine changes of disposables

Rebreathing bags and masks Between patients unless soiled Intravenous infusion giving sets 48h

Parenteral nutrition giving sets Daily

Arterial/venous pressure transducer sets 48h

Infection—diagnosis

Infection i s both a common cause of admi ssi on to intensive care and the major secondary compli cation Criticall y i ll

patients are predi sposed to further nosocomi al infections as many of their natural barriers and defence mechani sms

have been lost, al tered or penetrated They are often heavi ly instrumented, sedated and i mmobi le They often

develop i mmune hyporesponsi veness as part of thei r cri ti cal di sease process, notwithstanding any therapeuti c

immune suppression they may have received The hi gh antibi otic load given to these si ck patients encourages

col oni sation by pathogenic organi sms and subsequent devel opment of infections by mul tidrug resi stant and/or

atypical (e.g fungi) organisms

Sepsi s i s defi ned as the systemi c response to an i nsult of proven or hi gh l ikeli hood of i nfecti on Whereas infection

can be appli ed to a l ocalised phenomenon, sepsis initi ates a systemic i nfl ammatory response thereby affecting distant

organs

Diagnosis

Often problemati c in the criti cally il l patient as focal signs may be l acking and/or camoufl aged by concurrentdisease (e.g venti lator-associ ated pneumonia on top of ARDS) Symptoms are often notforthcoming due to thepati ent's mentally incompetent state

In addi ti on, al l of the traditional cl ini cal and biochemical markers of infection are non-speci fic These i ncl udepyrexi a, neutrophi lia and altered sputum Furthermore, the frequent presence of colonising organisms e.g MRSA

on skin, Pseudomonas aeruginosa in the respiratory tract, does not imply concomitant infecti on As a

consequence, many pati ents are over-treated with anti bi oti cs, enhancing the ri sk ofovergrowth ofresistant/atypi cal organisms

Markers of inflammation (C-reactive protein, procalcitoni n) may be useful , though studies have producedconfli cti ng resul ts as to their specificity/sensi tivity i n di agnosing underlyi ng infection

The val ue of routine screeni ng (mi crobi ological survei ll ance) i s not proven, though thi s may hel p to i dentifyinfecting organisms earl ier

For cases of suspected infection, appropri ate sampl es should be taken for analysis incl udi ng blood, sputum,wound swabs, drainage fluid, aspirated pus, catheter ti ps, cerebrospi nal fl ui d, etc These shoul dgeneral ly betaken before new antibi otics are commenced

Consider l ess common causes of infection such as endocardi ti s or osteomyeli tis, particularly if the pati ent fails

to settle after a standard course of therapy

P.482

Differential diagnosis of pyrexia

InfectionNon-infective causes of i nfl ammati on, e.g trauma, surgery, burns, myocardial i nfarction, vascul iti s, hepati ti s,acal culous chol ecysti ti s, pancreati ti s

Adverse drug reactionsExcessive ambient heatingMiscel laneous causes, e.g neoplasm

Definitions

Infection

Microbial phenomenon characterised by an i nfl ammatory response to the presence of mi cro-organisms or the invasi on

of normal ly steri le host tissue by those organi sms

Bacteraemia

The presence of vi abl e bacteri a i n the blood

Sepsis

The systemic response to infecti on Defini ti on as for SIRS but as a result of infection

Sites of infection before and after admission to an ICU

Organ Primary site of infection needing

admission to ICU Secondary site of infection acquired while in ICU

Ameri can Col lege of Chest Physici ans/Society of Cri tical Care Medi ci ne Consensus Conference: defi nitions for sepsi s

and organ failure and guidelines for the use of innovative therapi es in sepsis Crit Care Med 1992; 20:864–74

Appropriate antibi otic therapy after l aboratory speci mens taken—though thi s may not be necessary for mildinfections where the cause has been removed, e.g an infected catheter

Radi ologi cal and/or surgical i nterventi on if indicated

Regular i nput from mi crobi ological ± i nfecti ous di sease speciali sts isrecommended to advise on best opti ons for

empiri c therapy and for possi ble modifi cations based on earl y communi cation of laboratory resul ts (includi ng

antibi otic sensitivity patterns)

Empiric antibi oti c therapy i s guided on the severi ty of il lness of the patient, li kel y site of infection and likely

infecting organism(s), whether the i nfecti on is community-acqui red or nosocomi al (incl udi ng ICU-acqui red), pati ent

immunosuppression, and known anti biotic resi stance patterns of hospi tal and l ocal communi ty organi sms In general ,

criti cal ly il l pati ents should recei ve parenteral anti biotics at appropriate dosage, taking i nto account any impai red

hepati c or renal clearance, or concurrent renal repl acement therapy Broad-spectrum therapy may be initi all y needed,

with refi nement, cessati on or change after 2–3 days depending on cl inical response and organi sms subsequentl y

isolated The durati on of treatment remains highly contenti ous Apart from speci fic condi ti ons such as endocardi tis,

tubercul osi s and meningiti s, where prolonged therapy is probably advisable, i t may be sufficient to stop wi thi n 3–5

days provided the patient has shown adequate signs of recovery Alternatively, patients not responding or

deteri orati ng should be consi dered to be either treatment fail ures or i nappropriately treated (i.e no i nfection was

present i n the first pl ace).As descri bed earli er, commonly accepted markers of i nfecti on are poorl y specifi c in the

intensive care patient Indeed, pyrexia may settle on stoppi ng antibi oti c treatment Cessati on or change of antibi oti c

therapy must be consi dered on indivi dual meri ts according to the patient's condi ti on and any subsequent laboratory

resul ts An advantage of ceasi ng therapy i s the abi li ty to take further speci mens for cul ture i n an anti biotic-free

environment

It may be necessary to remove i ndwell ing pacemakers, tunnell ed vascul ar catheters, prosthetic joints, pl ates,

implants, grafts and stents i f these are the suspected cause of infection Thi s should be done i n consultation wi th

microbiologists and the appropri ate speci al ist as individual ri sk and benefi t needs to be careful ly wei ghed up

Specimen antibiotic regimens (organism unknown)

Sepsis of unknown origin 2nd/3rd generation cephalosporin OR quinolone OR carbapenem OR

piptazobactam

± aminoglycoside (if Gram negative suspected)

± metronidazole (anaerobic cover)

± glycopeptide or linezolid (if MRSA suspected)

Pneumonia—community acquired 2nd/3rd generation cephalosporin + macrolide

Pneumonia—nosocomial 3rd generation cephalosporin OR quinolone OR carbapenem OR

piptazobactam ± aminoglycoside (if Gram negative suspected) + teicoplanin, vancomycin

+ rifampicin or linezolid (if MRSA likely) Skin and soft tissue Flucloxacillin (if MSSA likely)

Glycopeptide or linezolid (if MRSA likely)

Benzyl penicillin or clindamycin (if Streptococcus suspected)

Abdominal 2nd/3rd generation cephalosporin OR quinolone OR carbapenem OR

Nephrourological 2nd/3rd generation cephalosporin OR quinolone OR carbapenem OR

piptazobactam

± aminoglycoside

See also:

Bl ood pressure monitori ng, p110; Bacteriol ogy, p158; Anti microbial s, p260; Acute chest i nfecti on (1), p288; Acute

chest infection (2), p290; Hypotensi on, p312; Abdomi nal sepsi s, p350; Meni ngi ti s, p374; Tetanus, p390; Botul ism,

p392; Neutropenia, p408; Systemic inflammation/multi-organ fail ure, p484; Sepsi s and septic shock—treatment,

p486; HIV related disease, p488; Malari a, p490; Pyrexia (1), p518; Pyrexia (2), p520; Post-operati ve i ntensive care,

p534

Systemic inflammation/multi-organ failure

Exposure to an exogenous insul t can result in an exaggerated, general ised and often i nappropriate i nfl ammatory

response This is described as ‘SIRS’—the systemi c i nfl ammatory response syndrome Stimulation of inflammatory

pathways leads to activation of macrophages, endothelium, neutrophi ls, platelets, coagulation, fibrinolytic and

contact systems wi th rel ease of i nfl ammatory mediators and effectors (e.g cytokines, prostanoids, free oxygen

radicals, proteases, ni tri c oxi de, endotheli n) This resul ts in microvascul ar obstruction and occl usi on, bl ood fl ow

redistri bution, i nterstitial oedema and fibrosis, and cell ul ar mitochondri al dysfuncti on The consequences of this may

be organ dysfuncti on, varyi ng from ‘mil d’ to severe, and affecti ng si ngl e or multipl e organs, resulti ng in

cardi ovascular collapse, gastroi ntestinal fail ure, renal fail ure, hepati c fail ure, encephalopathy, neuropathy,

myopathy, and/or di ssemi nated i ntravascular coagulati on Acute respi ratory di stress syndrome (ARDS) i s the

respi ratory component of this pathophysiol ogical response

Causes include:

InfectionTrauma, burnsPancreati tisInhalation i njuriesMassive bl ood loss/transfusionMiscel laneous i ncl udi ng drug-rel ated (i ncluding overdose), myocardial i nfarction, drowning, hyperthermi a,pul monary embolus

Treatment

Largel y supportive, though the cause shoul d be removed/treated if at all possi ble Treatment includes antibiotics,

drainage of pus, fixation of femoral/ pelvi c fractures and debri dement of necrotic tissue

An important facet of organ support is to minimi se iatrogenic trauma It i s sufficient to maintai n survival with

rel ative homeostasis until recovery takes pl ace rather than attempti ng to achieve normal physiological or biochemical

target values An exampl e of this is permi ssive hypercapnia

Speci fic treatment regi mens remain contentious due to a lack of adequately powered studies showi ng optimal

haemodynamic goals, i notropic/ pressor agents, anti bi oti c regi mens, etc Local poli ci es may favour the use of one or

more of a range of ecl ectic therapies that may offer a reasonabl e theoretical basi s for admini stration, or anecdotal

success, though theseal l remain essential ly unproven Examples include antioxidants, protease i nhi bi tors,

immunonutri tion, plasmapheresis, vasodilators, and i mmunogl obuli ns It is generall y agreed that rapi d resuci tation

and restoration of oxygen deli very, glycaemic control and prompt removal of any treatabl e cause i s desi rable in

preventing the onset of SIRS

Because of non-standardi sation of definiti ons, outcome data are confl icting, though singl e organ ‘fail ure’ carri es an

approximate 20–30% mortality whil e ≥3 organ ‘fai lures’ lasti ng ≥3 days carries a mortal ity i n excess of 50%

Recovery is often complete i n survivors, though recent studi es are revealing l ong term physi cal and psychol ogi cal

sequel ae in a signifi cant proportion of pati ents

Current UCL Hospitals principles of management

Respiratory SaO2>90–95% (may have to settle for lower) Permissive hypercapnia

Cardiovascular Maintain cardiac output/oxygen delivery and blood pressure compatible

with adequate organ perfusion (e.g no metabolic acidosis)

Renal Maintain adequate metabolic and fluid homeostasis by intravascular

filling, diuretics, vasoactive agents, and/or haemo(dia)filtration

Haematological Maintain haemoglobin >7g/dl (unless cardiorespiratory problems),

platelets >20–40 × 109/l, INR <1.5–2.5

Gastrointestinal Stress ulcer prophylaxis (generally by enteral nutrition), pancreatitis,

acalculous cholecystitis Infection Antibiotics, pus drainage, good infection control Nutrition Preferably early and by enteral route

Pressure area/mouth/joint care Frequent turns, low pressure support surfaces, nursing care and physiotherapy Psychological Support to both patient and family

Definitions

Systemic inflammatory response syndrome (SIRS)

Two or more of:

Temperature >38°C or <36°CHeart rate >90bpm

Respiratory rate > 20 breaths/min or PaCO2 <32mmHg (4.3kPa)WBC >12,000 cell s/mm3, <4000/mm3, or >10% immature forms

Sepsis

The systemic response to infecti on Defini ti on as for SIRS but as a result of infection

Severe sepsis

Sepsi s associated wi th organ dysfuncti on, hypoperfusi on or hypotensi on These may include, but are not li mi ted to,

lacti c acidosi s, oli guria or an acute al terati on in mental status

Septic shock

Sepsi s wi th hypotension, despite adequate fluid resuscitati on, pl us presence of perfusion abnormal ities

Multi-organ dysfunction syndrome (MODS)

Presence of altered organ function i n an acutely il l pati ent such that homeostasi s cannot be mai ntained without

intervention Mul tiple organ fai lure (MOF) has not achieved worldwide uniformi ty of defi ni tion

See also:

Venti latory support—indicati ons, p4; Bl ood pressure monitori ng, p110; Bacteriology, p158; Anti microbials, p260;

Acute respi ratory di stress syndrome (1), p292; Acute respiratory distress syndrome (2), p294; Inhalation i njury,

p306; Hypotensi on, p312; Abdomi nal sepsis, p350; Pancreati tis, p354; Infection control —general principl es, p476;

Sepsi s and septic shock—treatment, p486; Multi pl e trauma (1), p500; Mul ti ple trauma (2), p502; Burns—fl uid

management, p510; Burns—general management, p512; Pyrexia (1), p518; Pyrexia (2), p520

Sepsis and septic shock—treatment

Principles of treatment

As for other causes of MODS, outcome in sepsi s i mproves with:

Prompt di agnosi s and treatment of the underlyi ng cause

Specific treatments for severe sepsis/septic shock

Activated protein C signifi cantl y i mproves outcome in patients wi th ≥2 organ dysfunctions if commenced wi thi n48h of onset of severe sepsi s The PROWESS study mainly included patients presenti ng from the community andhad numerous exclusion criteri a, parti cul arl y rel ated to those at increased risk of bl eeding Subsequent studiesrevealed <15% of septi c pati ents presenting to ICUs meet both inclusion and exclusion criteri a

1

‘Low-dose’ hydrocorti sone (50mg qds) given for 7 days improved outcomes if commenced wi thi n 8h of septicshock presentation, though onl y i n the subset with an abnormal cortisol response to synthetic ACTH Our currentpracti ce is to start hydrocortisone after performi ng a Synacthen test and to discontinue thi s therapy if the test isnormal

2

For norepi nephrine (NEPI)-resistant septic shock, i e hi gh-output severe hypotension not responding toadequate flui d l oading and a NEPI dose >0.4µg/kg/min, we consi der careful admi ni strati on of terli pressi n ormethylthi oni nium chlori de Until more data are forthcoming, these agents shoul d be viewed as rescue therapiesrather than a straight alternati ve for NEPI

3

We occasi onal ly use pl asmapheresi s, prostaglandi ns or hi gh-output haemofiltration for resistant cases of septi c

4

P.488

shock, parti cul arl y those with low cardiac outputs We readi ly acknowledge the evi dence base for these therapies

is sli ght and our use is based on anecdotal success

Figure No Caption Available.

Key paper

Del linger RP et al Survivi ng Sepsi s Campaign guideli nes Crit Care Med 2004; 32:858–73

Key trials

Bernard GR, for the PROWESS study group Effi cacy and safety of recombinant human activated protein C for severe

sepsi s N Engl J Med; 344:699–709

Annane D, et al Effect of treatment with l ow doses of hydrocortisone and fl udrocorti sone on mortali ty in patients

with septic shock JAMA 2002; 288:862–71

See also:

Oxygen therapy, p2; Ventilatory support—i ndi cations, p4; Haemo(di a)filtration (1), p62; Haemo(dia)fil tration (2),

p64; Plasma exchange, p68; Enteral nutriti on, p80; Parenteral nutri ti on, p82; Blood gas anal ysis, p100; Blood

pressure monitori ng, p110; Cardiac output—thermodil uti on, p122; Cardiac output—other invasi ve, p124; Cardi ac

output—non-i nvasive (1), p126; Cardi ac output—non-i nvasive (2), p128; Bacteriology, p158; Lactate, p170;

Inotropes, p196; Vasopressors, p200; Anticoagulants, p248; Anti microbial s, p260; Steroi ds, p262; Novel therapies in

sepsi s, p266; Fl ui d chal lenge, p274; Acute chest infection (1), p288; Acute chest infection (2), p290; Acute

respi ratory di stress syndrome (1), p292; Acute respiratory distress syndrome (2), p294; Hypotensi on, p312; Acute

renal fai lure—diagnosis, p332; Acute renal fail ure—management, p334; Abdominal sepsi s, p350; Infection—diagnosis,

p480; Infection—treatment, p482; Pyrexia (1), p518; Pyrexia (2), p520

HIV related disease

Affected patients may present electi vel y after diagnosti c biopsies of brai n or l ung, or where el ective ventilation i s

needed postoperati vel y Other cases present with compl icati ons of HIV related di sease, especial ly pul monary

infection (e.g Pneumocystis carinii, CMV) or sei zures (e.g cerebral lymphoma, cerebral abscess, meni ngi tis) HIV

rel ated diseases are now consi dered to be chroni c manageable condi tions with an often good short term prognosis It

is therefore reasonable that i ntensive care should be offered

Infection control

The protecti on of staff from transmi ssi on of HIV follows basic measures Body fluids shoul d not be handled (wear

gloves) and the face and eyes shoul d be protected where there is a risk of splash contami nation

Needles should be disposed of in appropriate bins without re-sheathing Any fl ui d spil lages should be cl eaned up

immedi ately Robust procedures are adhered to where a pati ent is known HIV posi ti ve; the real ri sk i s in the patient

of unknown HIV status Remember that patients presenti ng with non-HIV related ill ness may be unknown positives It

fol lows that precauti ons shoul d be taken for all patients

Pneumocystis carinii pneumonia

P.490

Thi s i s the commonest respi ratory di sorder affecti ng HIV positive patients The majori ty survive thei r first attackbut prognosi s i s not as good i n those requiri ng mechanical ventil ati on Intensive, early support with CPAP andappropriate chemotherapy may avert the need for venti latory support

Treatment is usual ly started without waiti ng for laboratory confirmation

First line treatment is with high-dose co-tri moxazole or pentamidi ne with adjuvant hi gh-dose steroi ds

Co-trimoxazol e has a faster onset of effect and a broader spectrum of antibacterial activity covering the commonsecondary pathogens Pentami dine i s usuall y used where co-tri moxazole fai ls or where patients cannot takeco-tri moxazol e

Methylpredni sol one is used to suppress peribronchi al fibrosis andal veol ar infil trate It i s usual for there to be anini tial deteri oration on treatment lasting several days

Respiratory support i s provided with CPAP (5–10cmH2O) if hypoxaemi c despite high FIO2 Lower CPAP pressuresshould be used where possibl e as these pati ents are at risk of pneumothorax

Mechani cal venti lation i s reserved for those who have a ri si ng with deteriorating gas exchange and fati guedespite CPAP

CXR changes respond very slowly

Lactic acidosis

Nucleosi de reverse transcriptase i nhi bitors (NRTIs) are frequently used anti -retroviral agents However, an

associ ated mitochondrial i mpairment can cause a severe l actic aci dosis and a high mortali ty Anecdotal use of

L-carnitine is reported to be of benefi t

IV drug abusers

IV drug abusers are at high risk for HIV rel ated disease, though present more commonly for other reasons (e.g drug

withdrawal syndromes, overdose, sepsis, endocarditi s, hepatiti s B or C, rhabdomyolysis)

Drug dosages

Co-trimoxazole 120mg/kg/day in divided doses IV for 10–14 days then PO to complete 21

days Pentamidine 4mg/kg/day IV Methylprednisolone 1g/day for 3 days

See also:

Venti latory support—indicati ons, p4; Endotracheal i ntubation, p36; Continuous posi ti ve airway pressure, p26;

Bacteriology, p158; Virology, serology and assays, p160; Anti mi crobials, p260; Steroi ds, p262; Acute chest infection

(1), p288; Acute chest i nfection (2), p290; Pneumothorax, p300; Infection control—general pri nci ples, p476

Malaria

Mal ari a should be suspected i n any pati ent returni ng from endemic areas with a febri le il lness whi ch may have

cerebral , abdominal, lung or renal features Rarel y, people li ving near ai rports may be bi tten by a transported

Anopheles mosquito There may be considerable delay (weeks to months) between the mosquito bi te and si gns of

infection It is caused by protozoal i nfecti on with the Plasmodium genus The most severe form i s P falciparum which

causes malignant, terti an mal ari a Other forms (P malariae, P vivax, P ovale) rarely cause significant li fe

threateni ng di sease and wil l not be discussed further

Pathophysiology

P falciparum i nvades erythrocytes regardl ess of age High l evels of parasi taemia >5% are considered severe i n

non-immune travell ers The cel ls may haemol yse or be destroyed i n l iver or spl een Anaemia may be severe

Increased vascular permeabi li ty, cytokine release, red cell aggluti nation and i ntravascular coagulation (DIC) may al so

P.492

If >5% parasi taemia, features i ncl ude:

Cerebral malari a, causing coma, deli rium, sei zures or focal deficits

Cough and haemoptysi s or acute respiratory distressBlackwater fever is associated wi th massive i ntravascular haemolysis, jaundice, haemogl obi nuria, coll apse andrenal fai lure

Acute renal dysfuncti on occurs i n a thi rd of adult ICU patientsAcute cardiovascul ar col lapse (‘algid mal ari a’) and metaboli c aci dosisThrombocytopenia, DIC and spontaneous bl eeding

Diagnosis

Plasmodia seen i n RBC in thi ck or thi n smears of peripheral blood The parasitaemi a i ntensity may vary fromhour to hour and may be scanty i n number The smear should be carefully scrutinised and repeated if doubtpersists

Leucocytosis is not a feature of malari aSpl enomegaly is al most i nvariable during the second week of i ll ness

Treatment

Early IV qui nine i nfusi on i s the mai nstay of treatment of severe malaria Level s should be monitored dail y anddosage adjusted as appropriate Compl ications include hypogl ycaemia and tinnitus Artemether should beconsidered i n cases of l ikely qui nine resi stance

Quinine 20mg quinine salt/kg IV over 4h, then 10mg/kg infusion over 4h,

repeated 8-hrly until the patient can swallow, then tablets (10mg quinine salt/kg 8-hrly) to complete 7 days' treatment.

Halve maintenance dose to 5mg salt/kg 8-hrly if continuing parenteral therapy for >48h.

Artemether 3.2mg/kg IM followed by 1.6mg/kg daily

Second line after asexual parasites eliminated

Sulfadoxine 500mg/pyramethamine 25mg

3 tablets once

Doxycycline 200mg then 100mg daily for 7 days

See also:

Haemo(dia)fil trati on (1), p62; Haemo(dia)fi ltration (2), p64; Bl ood transfusion, p182; Fl ui d chal lenge, p274; Ol iguri a,

p330; Acute renal fai lure—diagnosis, p332; Acute renal fai lure—management, p334; General ised seizures, p372;

Jaundi ce, p358; Anaemi a, p400; Haemol ysi s, p404; Platel et disorders, p406; Infecti on—diagnosis, p480;

Infection—treatment, p482; Pyrexia (1), p518;Pyrexia (2), p520

Rheumatic disorders