Oxford Handbook of Critical Care - part 7 pdf

Fat estimati on mal absorpti on is rarel y necessary in the ICU patient If i schaemic or inflammatory bowel di sease suspected, perform a supine abdominal X-ray and inspect for dil atedl

Haemodynamic management

Pre-renal failure is reversible before it becomes establ ished Careful fluid management to ensure an adequate

ci rculating volume and any necessary i notrope or vasopressor support may establi sh a diuresi s If oli guria persi sts

after pre-renal factors have been corrected, the use of di ureti cs (furosemi de, manni tol ) may establi sh a diuresis

Metabolic management

Hyperkalaemi a may be l ife-threatening (>6.5mmol /l or ECG changes) and may be prevented by potassium restriction,

early dialysis or haemo(dia)fi ltration Hypocal caemia and hyponatraemia are best treated wi th di alysis and/or

haemo(dia)fil trati on, al though calci um suppl ementation may be used Hyponatraemia is usual ly due to water excess

although sal t-l osing nephropathi es (acute tubul ar necrosis, other renal tubular di sorders) may requi re sodium

chl oride suppl ements Hyperphosphataemi a may be treated wi th di alysis, fil tration or alumini um hydroxide orall y

Metabolic acidosi s (not due to ti ssue hypoperfusion) may be corrected wi th dialysis, fi ltration or 1.26% sodium

bicarbonate infusion

Nephrotoxins and crystal nephropathies

Al l nephrotoxi c agents should be wi thheld if possi ble All necessary drugs should have thei r dosage modi fi ed

according to the GFR In some cases uri nary excreti on of nephrotoxi ns and crystal s may be encouraged by urinary

alkali ni sation to maintain their solubil ity wi th an induced diuresis (rhabdomyolysis, acidic crystals) Dialysis may

also be useful

Glomerular disease

Immunosuppressi ve therapy may be useful after di agnosi s has been confi rmed Di alysis is often requi red for the more

severe forms of gl omerul onephriti s despite steroid responsi veness

Urgent treatment of hyperkalaemia

10–20ml calcium chloride 10% by slow intravenous injection

100ml 8.4% sodium bicarbonate i ntravenousl y

Glucose (50g) and i nsuli n (10–20IU) i ntravenously wi th careful blood glucose monitoring and urgenthaemodi alysi s

Renal replacement therapy

Continuous haemofi ltrati on forms the mainstay of replacement therapy i n cri ti cal ly ill pati ents who often cannot

tol erate haemodial ysi s due to haemodynamic instabil ity Peri toneal dial ysi s i s not commonly used today Acute renal

fai lure i n the criti cal ly il l usuall y recovers wi thin 1–6 weeks; permanent renal fail ure is rare

General indications for dialysis or haemo(dia)filtration

Flui d excess (e.g pul monary oedema)Hyperkalaemia (>6.0mmol /l)

Metabol ic acidosis (pH <7.2) due to renal fail ureClearance of dialysabl e nephrotoxi ns and other drugsCreati nine risi ng >100µmol/l/day

Creati nine >300–600µmol/lUrea ri si ng >16–20mmol /l /day

To create space for nutri ti on or drugs

See also:

Haemo(dia)fil trati on (1), p62; Haemo(dia)fi ltration (2), p64; Peritoneal di alysis, p66; Crystalloids, p176; Coll oids,

p180; Diuretics, p212; Dopamine, p214; Basi c resuscitation, p270; Fl uid chall enge, p274; Oli guria, p330; Acute renal

fai lure—diagnosis, p332; Hyperkal aemia, p420; Hyponatraemi a, p418; Hypocal caemia, p428; Metabol ic aci dosis, p434

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 > Gas trointestinal Disor der s

Gastrointestinal Disorders

P.340

Vomiting/gastric stasis

Whi le vomiti ng per se is relatively rare in the ICU patient, l arge volume gastri c aspi rates are commonpl ace and

probably represent the major reason for fai lure of enteral nutriti on

Ileus

Il eus affects the stomach more frequently than the rest of the gastroi ntestinal tract Abdominal surgery, drugs

(parti cularly opi ates), gut dysfunction as a component of multi -organ dysfunction, hypoperfusion and prol onged

starvati on may all contribute to gastric il eus Earl y and continued use of the bowel for feeding appears to mai ntain

forward propulsive acti on Management consists of treating the cause where possible, the use of moti li ty sti mul ants

such as metoclopramide or erythromycin and, i n resistant cases, bypassi ng the stomach with a

nasoduodenal /nasojejunal tube or a jejunostomy

Upper bowel obstruction

Rel ati vel y unusual ; apart from primary surgi cal causes such as neopl asm or adhesi ons, the predominant cause in the

ICU is gastric outlet obstructi on Thi s may be rel ated to l ong-standing pepti c ulcer disease or may occur i n the short

term from pyloric and/or duodenal swell ing consequent to gastri ti s or duodeni tis Thi s can be diagnosed

endoscopi cal ly and treated by bowel rest plus an H2 antagonist, proton pump i nhi bi tor or sucralfate

Gastric irritation

Drugs or chemi cal s—either accidental or adverse reaction (e.g steroids, aspiri n), intenti onal (e.g al cohol, bl each) or

therapeutic (e.g ipecacuanaha syrup) may i nduce vomiti ng Treatment, where appropriate, may comprise (i) removal

of the cause, (i i) di lution wi th copious amounts of fl uid (i ii) neutrali sation wi th al kal i and/or H2 antagonist or proton

pump i nhi bi tor and (i v) admini stration of anti-emetic (e.g metocl oprami de)

Neurological

Stimulation of the emeti c centre may follow any neurol ogi cal event (e.g trauma, CVA), drug therapy (e.g

chemotherapy), pai n and metabol ic di sturbances Management i s by treating the cause where possibl e and by

judici ous use of anti -emeti cs, initial ly metocl oprami de or prochl orperazi ne Consi der ondansetron or grani setron i f

these are unsuccessful

See also:

Enteral nutrition, p80; Electrolytes

, p146; Opioid analgesics, p234; Anti -emeti cs, p224; Gut moti lity agents, p226; Bowel perforati on and obstruction,

p348; Electrol yte management, p414; Poisoni ng—general pri nci pl es

Diarrhoea

The definiti on of diarrhoea in the ICU patient i s problemati c as the amount of stool passed dail y i s difficult to

measure Frequency and consi stency may also vary signi ficantly Loose/watery and frequent (≥ 4 × day) stool wil l

often require i nvesti gation and/or treatment

Commoner ICU causes

Infection—Clostridium difficile, gastroenteri tis (e.g Salmonella, Shigella), rarer tropical causes (e.g cholera,

dysentry, gi ardiasis, tropical sprue)

Drugs, e.g antibi oti cs, l axatives

Gastrointestinal—feed (e.g lactose intolerance), coel iac di sease, other malabsorpti on syndromes, i nfl ammatorybowel disease, diverti culitis, pelvic abscess, bowel obstructi on with overflow Enteral feed is often impli catedbut rarel y causati ve

For bloody di arrhoea consider i nfection, i schaemic or inflammatory bowel di sease

Diagnosis

Rectal examinati on to rul e out impaction wi th overfl ow Consi der si gmoidoscopy if col itis or C difficile suspected

(pseudomembrane seen)

Stool sent to l aboratory for MC & S, C difficile toxin.

Fat estimati on (mal absorpti on) is rarel y necessary in the ICU patient

If i schaemic or inflammatory bowel di sease suspected, perform a supine abdominal X-ray and inspect for dil atedloops of bowel (NB toxi c megacol on), thickened wal ls (increased separation between loops) and ‘thumbprinting’

(suggesti ve of mucosal oedema) Fluid levels seen on erect or lateral abdominal X-ray may be seen i n diarrhoea

or paralytic il eus and do not necessari ly indicate obstruction Diarrhoea is often but not always bloody

If abscess suspected, perform ultrasonography or CT scan

Failure to open bowels

Commoner ICU causes

Prol onged il eus/decreased gut moti li ty (e.g opi ates, post-surgery)Lack of enteral nutri tion

Bowel obstructi on—thi s i s a relatively uncommon secondary event and i s mainly seen post-operatively, ei therafter a curative procedure or with devel opment of adhesi ons

Mall ory–Weiss l ower oesophageal tearNeoplasms

Pathophysiology

Peptic ul ceration is related to protecti ve barrier l oss leadi ng to aci d or bil iary damage of the underl ying mucosa and

submucosa Barrier l oss occurs secondary to criti cal i llness, alcohol , drugs, e.g non-steroi dal s, poi sons including

corrosives Di rect damage, especial ly at the lower oesophagus, may occur from feeding tubes Mucosal damage

(‘stress ul cers’) may al so occur as a consequence of tissue hypoperfusion Gastri c hypersecreti on is uncommon in

criti cal ly il l pati ents; indeed, gastri c acid content and secretion i s often reduced

Prophylaxis

Smal l-bore feedi ng tubesNasogastric enteral nutrition (nasojejunal and parenteral feedi ng has al so been shown to reduce the incidence of

P.346

stress ul cer bl eeding)Adequate tissue perfusion (flow and pressure)The rol e of prophyl actic drug therapy i ncl udi ng H2 antagonists, proton pump inhibi tors and sucralfate iscontroversial Evi dence suggests that enteral nutriti on alone is as effective and there are clai ms that loss of theaci d envi ronment i n the stomach predi sposes the patient to nosocomi al infection Patients at highest risk arethose requiring prolonged mechani cal venti lation or wi th a concurrent coagulopathy

Treatment of major haemorrhage

Flui d resuscitati on with coll oid and blood wi th bl ood products as appropri ate to correct any coagulopathy

Maintai n haemogl obi n between 7–10g/dl and have adequate cross-matched bl ood avail abl e should further largehaemorrhages occur

If possible, di sconti nue any on-going anti coagul ati on, e.g hepari n

Urgent di agnostic fibreopti c endoscopy Local i njecti on of epinephri ne or a sclerosant into (or thermal sealing of)

a bl eeding pepti c ulcer base may halt further bl eeding Likewise, banding or sclerosant i njecti on may arrestbleedi ng varices

If oesophageal vari ces are known or hi ghly suspected, consider vasopressi n or terlipressi n ± a Sengstaken-typetube for severe haemorrhage, ei ther as a bridge to endoscopy or i f banding/injecti on i s unsuccessful Rememberthat sources of bl eedi ng other than vari ces may be present, e.g pepti c ulcer

For peptic ul ceration and general ised i nfl ammati on commence an H2 antagoni st or proton pump inhibi tor Giveintravenousl y to ensure effect Enteral antaci d may also be beneficial

Surgery i s rarely necessary but should be consi dered i f bleedi ng continues, e.g >6–10 uni t transfusi onrequirement Inform a surgeon promptl y of any patient with major bl eedi ng

See also:

Endotracheal i ntubation, p36; Sengstaken-type tube, p72; Upper gastroi ntestinal endoscopy, p74; Coagulation

monitori ng, p156; Coll oi ds, p180; Blood transfusi on, p182; H2 blockers and proton pump inhibitors, p218; Sucral fate,

p220; Antaci ds, p222; Coagul ants and antifi brinolytics, p254; Basic resusci tation, p270; Fluid challenge, p274;

Vomiting/gastric stasi s, p338; Bl eeding varices, p346; Bleedi ng disorders, p396; Systemic infl ammation/multiorgan

fai lure, p484

Bleeding varices

Varices develop foll owi ng a prol onged peri od of portal hypertensi on, usual ly rel ated to l iver cirrhosis Approxi matel y

one third wi ll bl eed They are commonly found in the l ower oesophagus but, occasional ly, in the stomach or

duodenum Torrenti al haemorrhage may occur Approxi mately 50% of patients di e within 6 weeks of presentati on of

their fi rst bl eed; each subsequent bleed carries a 30% mortali ty

Management

If airway and/or breathing are compromised, perform endotracheal intubati on and insti tute mechani calventil ati on This facili tates Sengstaken-type tube placement and endoscopy but may be associated with severehypotensi on secondary to covert hypovolaemi a If possible, ensure adequate intravascular fi ll ing before

Endotracheal i ntubation, p36; Sengstaken-type tube, p72; Upper gastroi ntestinal endoscopy, p74; Coagulation

monitori ng, p156; Coll oi ds, p180; Blood transfusi on, p182; Basic resusci tation, p270; Flui d challenge, p274; Upper

gastrointestinal haemorrhage, p344; Acute l iver fai lure, p360; Chronic liver fai lure, p364

Bowel perforation and obstruction

Patients with bowel perforation or obstructi on may be admitted to the ICU after surgery, for pre-operative

resuscitati on and cardi orespi ratory opti misati on, or for conservati ve management Although rarely occurri ng de novo

in the ICU pati ent, these conditi ons may be difficult to diagnose because of sedation ± muscle relaxati on Consi der

when there i s:

Abdomi nal pain, tenderness, peritoni smAbdomi nal di stensi on

Agi tationIncreased nasogastric aspirates, vomiti ngIncreasing metabol ic aci dosis

Signs of hypovol aemia or sepsis

A firm di agnosis is often not made unti l laparotomy al though supi ne and either erect or l ateral abdominal X-ray may

reveal ei ther free gas i n the peritoneum (perforati on) or di lated bowel l oops with multipl e flui d l evels (obstruction)

Ultrasound i s usuall y unhelpful though faecal flui d may occasi onally be aspirated from the peri toneum fol lowing

perforati on

It may be di ffi cul t to distingui sh bowel obstructi on from a paral yti c i leus as (i) bowel sounds may be present or

absent in ei ther and (ii ) X-ray appearances may be simi lar

Management

Correct fl ui d and electrolyte abnormali ti es Resuscitati on should be prompt and aggressive and usuall y consists

of coll oi d repl acement plus bl ood to mai ntain Hb >7g/dl Inotropes or vasopressors may be required to restore

an adequate circul ati on, parti cul arly fol lowing perforation Earl y cardiac output moni toring should be considered

if the ci rculatory status remains unstabl e or vasoactive drugs are required

1

The surgeon should be informed early A conservative approach may be adopted, e.g with upper smal l bowelperforati on; however, surgery i s usuall y required for large bowel perforati on Small or large bowel obstructionmay someti mes be managed conservati vel y as spontaneous resolution may occur, e.g adhesions Promptexpl orati on should be encouraged i f the patient shows signs of systemi c toxi ci ty

Parenteral nutrition, p82; Fai lure to open bowels, p342; Abdominal sepsi s, p350; Pancreatiti s, p354; Metabol ic

aci dosis, p434; Systemic inflammation/multiorgan fail ure, p484; Post-operative i ntensi ve care, p534

Lower intestinal bleeding and colitis

Causes of lower gastrointestinal bleeding

Bowel i schaemia/infarcti onInfl ammatory bowel disease (ulcerative coli ti s, Crohn's disease)

Infection, e.g Shigella, Campylobacter, amoebic dysentry

Upper gastrointestinal source, e.g peptic ul cerationAngiodysplasia

Neoplasm

Al though relatively rare, massive l ower gastroi ntestinal haemorrhage can be l ife-threatening

Ischaemic/infarcted bowel

Can occur following prol onged hypoperfusion or, occasi onally, secondary to a mesenteric embol us It usual ly presents

with severe abdomi nal pain, bl oody diarrhoea and si gns of systemic toxicity incl udi ng a rapi dly increasi ng metaboli c

aci dosis Plasma phosphate levels may also be el evated X-ray appearances of thickened, oedematous bowel loops

(‘thumb printi ng’) wi th an increased distance between bowel loops are suggesti ve Treatment i s by restoration of

ti ssue perfusi on, bl ood transfusion to maintain haemoglobin >7g/dl and, if cli ni cal features fail to settle promptl y,

laparotomy with a view to bowel excision

Inflammatory bowel disease

Presents with weight loss, abdomi nal pain and di arrhoea which usuall y contains blood Compli cations of ul cerative

col itis include perforati on and toxic megacolon while compl icati ons of Crohn's disease i ncl ude fi stulae, abscesses and

perforati ons

Management i nvol ves:

Flui d and electrol yte replacement

Usuall y presents as fresh bleedi ng per rectum and thi s may be considerable It i s due to an arteri ovenous

mal formation and commoner i n the elderl y Locali sation and embolisati on by angiography may be curative during

active bl eeding, Surgery may be required i f bleedi ng fail s to settle on conservative management and, occasional ly,

‘bl ind’ laparoscopic embol isati on of a mesenteric vessel However, l ocalisati on of the lesion may be difficult at

laparotomy, necessitati ng extensi ve bowel resection

See also:

Col loi ds, p180; Bl ood transfusion, p182; Coagul ants and antifibrinolytics, p254; Basi c resusci tation, p270; Fluid

chall enge, p274; Bowel perforation and obstructi on, p348; Bl eeding di sorders, p396

Abdominal sepsis

Thi s i s a common but difficul t to di agnose condi ti on in intensive care patients A proporti on of such pati ents are

admitted fol lowing laparotomy but others may develop abdominal sepsis de novo or as a secondary complicati on

fol lowing abdominal surgery, i n particular after bowel resecti on Sepsi s may either be local ised to an organ, e.g

cholecystitis, or the peri toneal cavity (abscess); al ternatively, there may be a generalised peritoni tis Non-bowel

Diarrhoea (i f pelvi c sepsis)

Diagnosis

Ultrasound

CT scanLaparotomyGal lium white cell scans are occasi onal ly useful for i denti ficati on of abscesses

Samples should be taken for mi crobiological anal ysis from blood, uri ne, stool , abdominal drain fluid and vaginal

discharge i f present A sampl e of pus i s preferred to a swab Hyperamylasaemia may suggest pancreati ti s though

amylase l evels can al so be elevated with other intra-abdominal pathologi es

Treatment

Antibi oti c therapy provi di ng Gram negative and anaerobic cover (e.g 2nd or 3rd generation cephalosporin,qui nol one or carbapenem, plus metroni dazol e ± ami noglycosi de) Treatment can be amended dependi ng oncul ture results and pati ent response

Ultrasoni c or CT-guided drainage of pus

Laparotomy wi th removal of pus, peritoneal lavage, etc

A negative l aparotomy shoul d be viewed as a useful means of excluding i ntra-abdominal sepsi s rather than an

unnecessary procedure Laparotomy shoul d be encouraged if the pati ent deteriorates and a high suspi ci on of

abdomi nal pathology persists

Cholecystitis, wi th or without (acal culous) gal lstones, may present with signs of i nfecti on There is a characteristic

ultrasound appearance of an enl arged organ with a thickened, oedematous wall surrounded by fluid Treatment i s

often conservative wi th antibi oti cs (as above) and percutaneous, ul trasound-gui ded drai nage vi a a pi gtail catheter

Cholecystectomy is rarel y necessary in the acute si tuati on unl ess the gall bl adder has perforated, though some

authorities argue that thi s i s the treatment of choice for acalculous chol ecystiti s

See also:

Parenteral nutrition, p82; Bacteriology, p158; Coll oids, p180; Inotropes, p196; Vasopressors, p200; Antimi crobials,

p260; Basic resuscitati on, p270; Flui d chal lenge, p274; Bowel perforation and obstruction, p348; Pancreatitis, p354;

Infection—di agnosis, p480; Infection—treatment, p482; Systemi c i nflammati on/mul ti organ fai lure, p484; Sepsis and

septi c shock treatment, p550; Pain, p532; Post-operative i ntensi ve care, p534

Pancreatitis

Inflammation of the pancreas and surroundi ng retroperi toneal tissues The appearance of the pancreas may range

from mildly oedematous to haemorrhagi c and necrotising A pseudocyst may devel op which can become infected and

the bi le duct may be obstructed causing bi li ary obstruction and jaundice Though mortality i s quoted at 5–10%, this

is much higher (approx 40%) i n those wi th severe pancreatitis requiring i ntensi ve care

Causes

AlcoholGal lstonesMiscel laneous, e.g i schaemia, trauma, viral, hyperlipidaemi aPart of the multipl e organ fail ure syndrome

Diagnosis

Non-specific features include central, severe abdominal pain, pyrexia, haemodynami c i nstabi li ty, vomiting, i leus

Discol ourati on around the umbi li cus (Cull en's sign) or flanks (Grey Turner's sign) is rarel y seen

Plasma enzymes—elevated l evel s of amyl ase (usually >1000IU/ml) and pancreatic li pase are suggestive butnon-specific Level s may be normal , even in severe pancreatitis

Ultrasound

CT scanLaparotomy

Complications

Mul ti-organ dysfuncti on syndromeInfection/abscess formati on

Hypocal caemiaDiabetes mel litusBleedi ng

Gal lstone obstruction shoul d be rel ieved either endoscopically or surgi cally

Hypocal caemia, i f symptomati c, should be treated by intermittent slow IV injection (or, occasionall y, infusi on) of10% cal ci um chl ori de

Hypergl ycaemi a should be controll ed by a conti nuous insul in infusi on

No specifi c treatment is routi nel y used

The rol e and extent of surgery remains controversial ; Some advocate percutaneous drai nage of infected and/ornecrotic debris whil e surgery frequently consists of regular (often dai ly) laparotomy with debri dement of necrotictissue and peri toneal lavage Pseudocysts may resolve or require drai nage ei ther percutaneously or into thebowel

Ranson's signs of severity in acute pancreatitis

On hospital admission:

Age >55 years ol dBlood glucose >11mmol/lSerum lactate dehydrogenase (LDH) >300U/lSerum aspartate ami notransferase (AST) >250U/lWhi te blood count >16×109/l

Pancreatitis severe if more than 2 criteria met within 48h of admission

Imrie scoring system

Whi te bl ood count >15 × 109/l

Bl ood gl ucose >10mmol /l

Bl ood urea nitrogen >16mmol /l

Pancreatitis severe if more than 2 criteria met within 48h of admission

APACHE II scoring system

Pancreatitis severe if APACHE II score>8

See also:

Venti latory support—indicati ons, p4; Enteral nutri tion, p80; Parenteral nutrition, p82; Basic resuscitati on, p270; Flui d

chall enge, p274; Respiratory fail ure, p282; Acute respiratory distress syndrome (1), p292; Acute respiratory di stress

syndrome (2), p294; Hypotension, p312; Oli guria, p330; Abdomi nal sepsi s, p350; Metaboli c aci dosis, p434; Systemic

inflammation/multi organ fai lure, p484; Sepsis and septi c shock—treatment, p486; Pai n, p532

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 > Hepatic Disor ders

Hepatic Disorders

Jaundice

Jaundi ce is a cli nical diagnosis of yellow pigmentati on of scl era and skin resul ti ng from a rai sed pl asma bil irubin It i s

usuall y visibl e when the pl asma bil irubin exceeds 30–40µmol /l

Commoner causes seen in the ICU

Pre-hepati c—i ntravascular haemolysis (e.g drugs, malaria, haemolytic uraemic syndrome), Gilbert's syndrome

Hepatocell ul ar—cri ti cal il lness, viral (hepati ti s A, B, C, Epstein–Barr), alcohol , drugs (e.g paracetamol,hal othane), toxoplasmosis, l eptospirosi s

Chol estati c—cri ti cal il lness, i ntrahepatic causes (e.g drugs such as chl orpromazine, erythromycin and isoni azi d,pri mary bili ary ci rrhosis), extrahepatic causes (e.g bi li ary obstruction by gallstones, neopl asm, pancreatitis)

Diagnosis

Uri nal ysi s—unconjugated bil irubi n does not appear i n the urine

Measurement of conjugated and unconjugated bili rubin—conjugated bil irubi n predomi nates in cholestaticjaundice, unconjugated bi li rubin in pre-hepatic jaundi ce, and a mi xed pi cture is often seen i n hepatocell ularjaundice

Plasma alkali ne phosphatase is usual ly markedl y elevated i n obstructi ve jaundi ce whil e prothrombin times,aspartate transami nase and alanine aminotransferase are el evated in hepatocellular jaundice

Ultrasound or CT scan wil l diagnose extrahepatic bi liary obstruction

An antihi stamine and topical calamine l oti on may provi de symptomatic rel ief for pruritus if troubl esome

Chol estyrami ne 4g tds PO may be hel pful in obstructi ve jaundi ce

4

Li ver function tests, p152; Acute li ver failure, p360; Chronic li ver fail ure, p364; Haemol ysi s, p404; Infection

control—general princi ples, p476; Infection—diagnosis, p480; Infection—treatment, p482; Systemi c

inflammation/multi organ fai lure, p484; HELLP syndrome, p540

Acute liver failure

Thi s condition resul ts from massive necrosi s of li ver cell s l eading to severe l iver dysfuncti on and encephalopathy

Survi val rates for l iver fail ure wi th Grade 3 or 4 hepatic encephalopathy vary from 10–40% on medical therapy alone,

to 60–80% wi th orthotopi c l iver transplantation

Major causes

AlcoholDrugs, parti cul arly paracetamol overdoseViral hepati ti s, particul arl y hepatitis B, hepati ti s CPoisons, e.g carbon tetrachloride

Acute decompensati on of chroni c disease, e.g fol lowing i nfecti on

Adequate moni toring should be instituted i f cardiorespiratory instabil ity i s present

Mechani cal venti lation may be necessary if the ai rway i s unprotected or respiratory fai lure develops Lung shuntsare frequentl y present, causing hypoxaemia

Infection is commonpl ace and is frequently ei ther Gram positive or fungal Cli nical si gns are often absent

Samples of bl ood, sputum, urine, wound sites, drain fl uid, i ntravascular catheter sites and ascites should be sentfor regul ar microbiol ogi cal surveil lance Systemi c anti microbial therapy, wi th or without sel ective gut

decontaminati on, has been shown to reduce the i nfection rate Fungal i nfecti ons are al so wel l recognised SomeLiver Uni ts give prophyl actic antifungal therapy

Hypoglycaemia is a common occurrence It shoul d be frequently monitored and treated wi th ei ther enteral (orparenteral) nutrition, or a 10–20% glucose infusion to maintain normoglycaemia

Renal fail ure occurs in 30–70% of cases and may necessi tate renal repl acement therapy The i ncidence may bereduced by careful mai ntenance of intravascular volume Vasopressi n/terl ipressin has also been used

successfully for hepatorenal syndrome

Upper gastrointestinal bleedi ng i s more common due to the associated coagul opathy Prophylactic H2 bl ockers orproton pump i nhi bi tors may be of benefit

N-acetylcysteine and/or epoprostenol improves O2 consumpti on Though tissue hypoxi a may be reduced by thesedrugs, parti cul arly when vasopressor drugs are needed, outcome benefit remai ns unproved

Corticosteroids, prostaglandi n E and charcoal haemoperfusion have not been shown to have any outcome benefit

See also:

Venti latory support—indicati ons, p4; Li ver function tests, p152; Coagul ation monitori ng, p156; Hepati c

encephalopathy, p362; Paracetamol poi soning, p456

Hepatic encephalopathy

Grading

Stuporose but rousabl e, very confused, agitated3.

Coma, unresponsi ve to pai nful stimuli4

The ri sk of cerebral oedema is far higher at Grades 3 and 4 (50–85%) and i s the leadi ng cause of death Suggestive

si gns include systemic hypertension, progressi ve heart rate slowing and i ncreasing muscl e rigidi ty These occur at

intracranial pressures >30mmHg

Management

Correct/avoid potential aggravati ng factors, e.g gut haemorrhage, over-sedation, hypoxia, hypoglycaemia,infection, electrolyte i mbalance

Consider earl y i ntracranial pressure (ICP) monitori ng CT and clinical features correl ate poorl y with ICP though

no control led studies have yet been performed to show outcome benefi t from ICP monitori ng whi ch carri es itsown compli cation rate (bl eeding, i nfection)

Maintai n patient i n slight head-up posi tion (20–30°)

Regular l actulose, e.g 20–30ml qds PO, to achieve 2–3 bowel moti ons/day

Dietary restri cti on of protei n i s now not encouraged as this promotes endogenous protei n util isati on

Hyperventi lation to achi eve a PaCO2 of 3.5–4kPa is often attempted but is frequentl y unsuccessful in achievingimprovement It may al so compromise cerebral blood flow

Mannitol (0.5–1mg/kg over 20–30min) if serum osmol ali ty <320mOsmol/kg and either a rai sed ICP or clinicalsigns of cerebral oedema persi st If severe renal dysfunction i s present, use renal replacement therapy i nconjuncti on with manni tol

Sodium benzoate (2g tds PO) may be considered i f the patient i s severel y hyperammonaemi c

If no response to above, consider barbiturate admini stration, e.g thiopental infusi on at 1–5mg/kg/h, i deall ywith ICP moni toring

If sti ll no response, consi der urgent l iver transplantation

Exerci se caution with concomitant drug usage

Identification of patients unlikely to survive without transplantation

Prothrombin time >100s

Or any three of the following:

Age <10 or >40 yearsAetiol ogy is hepatiti s C, halothane, or other drug reacti onDurati on of jaundice pre-encephalopathy >2 days

Prothrombin time >50sSerum bil irubi n >225µmol /l

If paracetamol-i nduced:

pH <7.3 or prothrombin ti me >100s and creatini ne >200µmol/l plus Grade 3 or 4 encephalopathy

As onl y 50–85% of patients identi fied as requiring transplantati on wil l survive long enough to recei ve one, the

Regional Liver Uni t should be informed soon after diagnosis of all possi bl e candi dates

See also:

Venti latory support—indicati ons, p4; Intracrani al pressure monitoring, p134; Li ver function tests, p152; Coagul ati on

monitori ng, p156; Sedati ves, p238; Jaundice, p358; Chronic li ver failure, p364; Paracetamol poi soning, p456

Chronic liver failure

Patients admitted to intensive care with chroni c l iver fail ure may develop speci fic associated probl ems:

Acute decompensati on—thi s may be secondary to infection, sedation, hypovolaemia, hypotension, diuretics,gastrointestinal haemorrhage, excess di etary protei n and electrol yte imbal ance

Infection—the pati ent may transmi t i nfecti on, e.g hepati tis A, B or C and, by bei ng immunosuppressed, is al somore prone to acqui ri ng infections such as TB and fungi

Drug metabol ism—as many drugs are all or part-metaboli sed by the li ver and/or excreted i nto the bil e, the drugaction may be prolonged or slowed dependi ng on whether the metabol ites are active or not Inparticul ar,

sedati ves may have a greatly prolonged duration of acti on

Portal hypertension—results i n asci tes, vari ces and splenomegaly Ascites may produce diaphragmati c spl intingand is at ri sk of becoming i nfected Drainage may incur a considerabl e protein loss Vari ces may bl eed whilespl enomegaly may resul t i n thrombocytopenia Renal fail ure is al so recognised due to high i ntra-abdominalpressure

Bleedi ng—an increased ri sk is present due to decreased production of cl otting factors (II, VII, IX, X), varices andspl enomegaly rel ated thrombocytopenia

Alcohol—the most frequent cause of ci rrhosis in the western world; acute wi thdrawal may lead to deli ri umtremens wi th severe agitati on, hal lucinati ons, sei zures and cardi ovascular di sturbances

2° hyperal dosteronism—resul ts in ol iguri a, sal t and water retenti on

Increased tendency to jaundi ce, especial ly during critical ill ness

Management

AscitesTake speci mens for microbiol ogi cal analysis (i ncluding TB), protei n and cytology If WBC > 250 per highpower fi el d, give Gram negati ve antibi otic cover

If present in large quantity, (i) decrease sodium and water intake, (ii ) commence spironolactone PO (orpotassi um canrenoate IV) ± furosemi de Paracentesi s ± colloid replacement, or asci tic reinfusion (i funinfected/non-pancreatitic in ori gi n) may be considered, particul arl y i f diaphragmatic spli nti ng occurs

1

Coagulopathy:

Vitamin K 10mg/day slow IV bolus for 2–3 days

Fresh frozen plasma, pl atelets as necessary

Li ver function tests, p152; Sedati ves, p238; Jaundice, p358; Acute liver fai lure, p360

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 > Neu rological Disor der s

Neurological Disorders

Acute weakness

Severe acute weakness may requi re urgent i ntubation and mechanical venti lation if the FVC <1l or gas exchange

deteri orates acutely

if paralysis is compl ete Pati ents with myasthenia gravis wi ll al so respond

Gui llain–Barré syndrome—a l umbar puncture shoul d be performed to confirm raised CSF protei n with normalcel ls If these features are not found but suspicion i s strong, nerve conducti on studi es may demonstratesegmental demyel inati on with sl ow conducti on veloci ties

Myasthenia gravi s—fati gueabl e weakness or ptosis suggests myastheni a gravis; response to IV edrophonium

P.370

(Tensil on test) and a strongly positive acetyl choli ne receptor antibody titre confi rm thi s diagnosis A myastheni csyndrome associ ated wi th mal ignancy (Eaton–Lambert syndrome) involves pel vic and thigh muscles

predomi nantl y, tending to spare the ocul ar muscl es

Other diagnoses are made largel y on the basis of cli ni cal suspi ci on and speci fic speci ali sed tests

General management

FVC should be monitored 2–4-hrl y and intubation and mechanical ventilati on should fol low if FVC <1l Otherindices of respiratory functi on are less sensitive In particular, arteri al bl ood gases may be mai ntained up to thepoi nt of respiratory arrest

Weak respi ratory muscles lead to progressi ve basal atelectasis and sputum retenti on Chest infecti on i s asignificant ri sk; regul ar chest physiotherapy with intermittent positi ve pressure breathing are required forprevention where mechanical ventil ation is not necessary

Pati ents who are immobile are at risk of venous stasis and deep venous thrombosi s Prophylaxis withsubcutaneous hepari n is reasonabl e Immobi le patients also require attenti on to posture to prevent pressuresores and contractures

Weak bulbar muscles may compromise swall owi ng with consequent malnutri ti on or pul monary aspirati on Enteralnutritional support via a nasogastri c tube i s necessary

In cases with coexi stent autonomic neuropathy enteral nutrition may be i mpossi ble, necessi tating parenteralnutritional support These patients may al so suffer arrhythmias and hypotension requiring appropri ate support

Causes of severe weakness

Common in ICU

Metabolic myopathi es

Prolonged effects of muscle relaxants

Cri ti cal il lness neuropathy or myopathy

Gui ll ain–Barré syndrome

Famili al periodic paral ysi s

Mul ti ple sclerosi s

Lead poisoni ng

Organophosphorus poi soning

See also:

Venti latory support—indicati ons, p4; IPPV—assessment of weani ng, p18; Enteral nutrition, p80; Parenteral nutriti on,

p82; Pulmonary functi on tests, p94; Electrolytes

, p146; Calcium, magnesi um and phosphate, p148; Muscle rel axants, p240; Respi ratory fail ure, p282; Guill ai n–Barré

syndrome, p384; Myastheni a gravis, p386; ICU neuromuscul ar di sorders, p388

Agitation/confusion

In the ICU, agi tation and/or confusi on are predominantly rel ated to sepsis, cerebral hypoperfusi on drugs or drug

withdrawal ‘ICU psychosis’, with l oss of day–ni ght rhythm and inabil ity to sleep, is a common occurrence i n the

patient recovering from severe il lness