Книга_5230_Библиотеки_им_академика_М_И_Перельмана

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323DIARRHOEA

Inammatory bowel disease(IBD)

$ Ulcerative colitis (% OHCM1 p. 258), Crohn’s disease (% OHCM1 p. 260).

Symptoms

malaise, tiredness, anorexia, and weight loss;

Recurrent diarrhoea ±blood ±mucus associated with abdo pain,

Signs

itemp, iHR ±dB P,

pale, abdo pain ±peritonism, palpable abdo mass, abdo swelling (toxic megacolon), malnourished; stulae ±ssures in Crohn’s (Table0.8).

Extra- intestinal manifestationsMouth ulcers, erythema nodosum,

gangrenosum,

7

conjunctivitis,7 episcleritis,7 iritis,7 acute arthropathy,7

7

pyoderma

sacroiliitis, ankylosing spondylitis, fatty liver, primary sclerosing cholangitis.

Investigations blds

iWCC, iCRP, dalbumin (as a marker of inammation, not

nutrition), dK+ (diarrhoeal losses), dCa2+, diron, dfolate, dvitamin B2 (terminal ileal disease), bld cultures; for colonic inammation— if negative may avoid endoscopy in ruling out infective causes of exacerbation including C.dicile;

Faecal calprotectin

sensitive but non- specic screen

Stool cultures

AXR

Vital

Mucosal

oedema, toxic megacolon >6cm, faecal residue suggests uninvolved mucosa;

Sigmoidoscopy ±colonoscopy

allows biopsy;

CT/ MRI

or if surgery being considered;

Shows characteristic appearances/ ulceration and

If concern of abscess, to map small bowel involvement

Complications

Toxic megacolon, bowel ob-

struction, perforation, malabsorption, stulae, ssures, strictures, malignancy.

Table0.8 Dierentiating betweenulcerative colitis and Crohn’s

Feature Ulcerative colitis (UC) Crohn’s

Symptoms Diarrhoea and PR blood/

GI involvement Colon only, extending

Endoscopy Continuous inamed mucosa

Histology Mucosal and submucosal

mucus prominent

proximally from rectum to variable extent

from rectum proximally

inammation, crypt abscesses, reduced goblet cells

Diarrhoea, abdo pain, and weight loss prominent

Anywhere along GI tract, most commonly terminal ileum

Inamed, thickened mucosa; aphthous ulcers; skip lesions

Inammation extends beyond the submucosa, granulomas present

6

Treatment This depends upon disease severity. Rehydrate and correct elec-

trolyte imbalances; avoid antimotility/ antispasmodic agents. Systemically well patients with mild– moderate UC (<6 stools/ day) should start oral ±rectal mesalazine (eg Pentasa® 2g/ 24h PO). For mesalazine- refractory disease or for Crohn’s, give oral ±rectal steroids (eg prednisolone 40mg/ 24h PO tapering by 5mg/ wk for total of 8wk). More severe disease requires IV steroids (eg hydrocortisone 00mg/ 6h IV). Consider antibiotics until infectious causes ruled out (eg co- amoxiclav .2g/ 8h IV). Monitor the patient closely (daily abdo exam, bloods ±AXR) and involve surgeons early. Elemental diet, immunosuppressive drugs (eg azathioprine), and biological agents (eg iniximab) may also beused.

Surgery This is indicated as an emergency procedure in cases of perforation

or massive haemorrhage. Urgent surgery is performed in UC for toxic megacolon or failure to respond to maximal medical therapy after 5– 7d; delaying beyond this risks poor operative results. Surgery in Crohn’s is never curative and associated with risks of recurrence and complications, but is indicated for limited small bowel disease, obstruction, abscesses, and stulae.

6

See Mwww.ecco- ibd.eu for a range of European guidelines. 7 Related to disease activity.

324 CHAPTER0 Gastroenterology

Constipation

2Worrying features Abdominal pain, distension, nausea/ vomiting,

iHR, dBP, absent/ tinkling bowel sounds, weight loss, PR bleeding.

Think about SeriousBowel obstruction, bowel/ ovarian cancer; Common

Medications, poor diet, paralytic ileus, dehydration, functional disorders;

Other Anal ssure/ stricture, pelvic mass, spinal injury, hypothyroid (Table0.9).

Ask about Abdo pain, nausea, vomiting, date bowels last opened,

normal bowel habit and frequency, stool consistency and colour, blood in stools, pain on opening bowels, straining, bloating, atus, uid intake, weight loss, tenesmus, recent surgery; ♀:periods, discharge; IBD, diverticulosis, hernias, previous surgery, colon cancer, hypothyroidism;

DH(see ‘Medications causing constipation’); SHMobility,diet.

Medications causing constipation Opioids, iron supplements,

non- magnesium antacids, calcium- channel blockers, psychotropic drugs, anticholinergics, chronic laxative use (may lead to the development of a dilated atonic colon).

Obs Temp, HR, BP, uid balance. Look forVolume status (E p. 402), tenderness ±peritonism, disten-

sion, masses, absent/ tinkling bowel sounds, hernias, scars; sures, rectal masses, faecal impaction, melaena/ blood.

Investigations blds FBC, U+E, TFT, Ca

AXR To exclude obstruction; Sigmoidoscopy ±biopsy if sub- acute onset; ColonoscopyIf cancer suspected.

ManagementSee Boxes 0.9– 0..

K Box 0.9 General management ofconstipation

• Conservative Increase uid intake, high- bre diet, review drugs:

consider alternatives without GI side eects; start stool chart— this will often be kept more accurately if you educate patients to complete it themselves

• Medical E p. 204 for detailed st- line laxative prescribing

information; begin treatment with a bulk- forming laxative (egFybogel (eg Movicol

); if necessary add in or switch to an osmotic laxative

); if stools soft but still dicult to pass, add a stimulant laxative (eg senna). Glycerol suppositories or arachis oil enemas will help soften impacted stool, while phosphate enemas should be reserved for when other measuresfail

• Refractory symptoms Newer medications that may be initiated under

specialist advice include prucalopride, linaclotide, and lubiprostone

• Opioid- induced constipation Avoid bulk- forming agents; use osmotic

and/ or stimulant laxatives. Naloxegol or methylnaltrexone bromide may be added for refractory symptoms

• Surgical disimpaction Scooping hard faeces from the rectum is a

seriously unpleasant point of last resort for everyone concerned.

; Stool FIT test (?cancer);

PMH IBS,

PR Anal s-

Table0.9 Common causes ofconstipation

History Examination Investigation

Bowel obstruction

Paralytic ileus Absence of atus,

Bowel cancer Abdo pain, weight

Ano- rectal pathology

Poor diet Anorexia (eg post-

Drugs See ‘Medications causing constipation’

Pain, distension, nausea, vomiting, constipation

recent operation

loss, fresh blood or melaena

Fresh red blood on toilet paper, ±pain

op), low- bre diet

Distension, tenderness, absent/ tinkling bowel sounds

Distended abdomen, absent bowel sounds

PR blood or melaena, mucus/ palpable mass

Perianal tags, may have a tear or tenderness

Cachexia

Dilated loops of bowel on AXR

Distended bowel loops on AXR, dK

dHb, lesion on sigmoidoscopy/ colonoscopy

Proctoscopy or sigmoidoscopy

dHb, dMCV, dCa

Poordiet

$ A surprising number of in- patients fail to achieve adequate nutri-

tion, with major impacts on wound healing, recovery, and physical condition. Try to recognize this and involve dieticians where appropriate, while avoiding prolonged NBM periods where possible. Markers for nutritional adequacy are problematic, but end- of- the- bed assessment is useful. Where constipation is a feature, encourage to aim for regular high- bre meals, with good uid intake and regular physical activity.

K Box 0.0 Hints andtips

• Prescribe prophylactic laxatives for patients at risk of developing

constipation (eg when prescribing opioids, post- op)

• Exclude obstruction before prescribing a laxative

• Lactulose is poorly tolerated by many patients and is associated

with abdominal pain and bloating

• Reassess regularly for resolution of constipation— do not put o

doing a rectal examination

• Consider malignancy in all adult patients presenting with altered

bowelhabit (oer FIT testing).

325CONSTIPATION

I Box 0. Causes ofconstipation covered elsewhere

Anal ssures/ haemorrhoids E p. 317 Bowel obstruction E p. 306 Inammatory bowel disease E p. 323 Polyps E p. 317 Irritable bowel syndrome E p. 322

326 CHAPTER0 Gastroenterology

2Liver failure emergency

2 Airway 2 Breathing 2 Circulation 2 Disability

Check airway is patent; consider manoeuvres/ adjuncts

If no respiratory eort—

If no palpable pulse—

If GCS ≤8—

CALL ANAESTHETIST

CALL ARREST TEAM

$ Altered mental state or coagulopathy in the presence of jaundice.

3Call for

senior help early if patient deteriorating.

Airway

• Look inside the mouth, wide- bore suction if secretions present

Jaw thrust/ head tilt/ chin lift; oro/ nasopharyngeal airway if tolerated.

•

Breathing

• 5L/ min O2 if SOB or sats<94%

Monitor O

•

sats andRR.

Circulation

• Venous access, take bloods:

•

FBC, U+E, LFT, PT/ APTT, CRP, glucose, amylase, Ca2+, Mg2+,

3–

, bld cultures, paracetamol levels, viral serology

IV uids L of 5% glucose over4– 6h

• Start

Monitor HR, ECG,BP.

•

Disability

• Check blood glucose, treat if <3.5mmol/ L (Ep. 336)

Check GCS, pupil reexes, limb tone, plantar responses.

•

Exposure

• Checktemp

• Ask ward sta for a brief history or checknotes:

•

previous liver disease, likely causes (Box0.2)

Examine patient, brief RS, CVS, abdo, and neuroexam:

•

signs of chronic liver disease

ECG, ABG, and urgent portableCXR

•

• Stabilize and treat(Epp. 327–31)

• Call for

•

senior help and arrange transfer to HDU/ ICU

Reassess, starting with A, B, C…

2Box 0.2 Causes ofliver failure

Acute liver failure

Paracetamol overdose, drugs, toxins, alcoholic hepatitis, viral hepatitis, autoimmune hepatitis, ischaemic hepatitis (heart failure and shock), Budd– Chiari

Decompensated chronic liver disease

Alcohol excess, malignancy, GI bleeds, metabolic disturbances, sedatives, portal vein thrombosis, acute illness, surgery, infection (eg spontaneous bacterial peritonitis)

Liver failure

2Worrying features Ascites, hepatic ap, altered mental state, and

jaundice are cardinal features of decompensation in liver disease; also beware active bleeding, renal failure, iHR,dBP.

Think about 2Emergencies Acute liver failure, decompensated chronic

liver disease, hepatic encephalopathy; (E p. 499), alcoholic hepatitis, viral hepatitis (A, B, C, E, CMV, EMV), pregnancy, medications (Box 0.3), toxins (eg poisonous mushrooms), vascular (eg Budd– Chiari), sepsis, Weil’s disease, abscess; medications (Box 0.3), obesity, idiopathic, autoimmune, hepatitis (B±D, C), malignancy, Wilson’s disease, haemochromatosis, α

K Box 0.3 Drug- induced hepatotoxicity

This may result in response to a large number of drugs, ranging from mild elevations in LFTs to fulminant hepatic failure. NSAIDs, ACEi, erythromycin, uconazole, and statins commonly cause hepatocellular injury (ALT >2× upper limit normal with normal/ minimally iALP). Chlorpromazine, oestrogens, ciprooxacin, isoniazid, phenytoin, erythromycin, and co- amoxiclav can all cause cholestasis (iALP, with or without associated hepatocellular damage). Always ask about recreational drugs (eg cocaine, mushrooms) and OTC or herbal medications.

Ask about Tiredness, jaundice (+onset), abdo pain, drowsiness ±con-

fusion, bruising, bleeding (skin, nose, bowel, urine), distension, ankle swelling, vomiting, rashes, recent infections (sore throat), weight loss, hair loss, darkeningskin;

DHSee Box 0.3; FHLiver disease, recent jaundice; SHAlcohol, IVDU, tat-

PMH Previous jaundice, gallstones, blood transfusions;

toos, piercings, foreign travel, sexual activity.

Obs Temp, HR, BP, RR, O Look for Volume status E p. 402; Acute liver failure Drowsiness, confu-

sion, slurred speech, jaundice, apping tremor (asterixis), poor co ordination, bruising, foetor hepaticus (sweet, faecal smelling breath), abdominal tenderness, hepatomegaly, ascites; thema, clubbing, xanthelasma, spider naevi, caput medusa, gynaecomastia, muscle wasting, splenomegaly, genital atrophy, track marks (IVDU), pneumonia/ chronic lung disease, darkenedskin.

Investigations $ These are aimed at establishing the extent and pos-

sible cause of liver damage, and nding a possible cause of any decompensation, especially intercurrent infection.

iron, ferritin, U+E, LFT, hepatitis serology (A, B+C), EBV and CMV serology, caeruloplasmin (if <50yr), autoimmune screen (antimitochondrial, antinuclear, and antismooth muscle antibodies, E p. 621), bld cultures;

Urgent USS abdo

vein thrombosis;

Looking for parenchymal mass(es), dilated ducts, or portal

Urgent ascitic tap

check for spontaneous bacterial peritonitis (Ep. 330). for varices and check for upper GI bleed as cause of decompensation.

8

European guidelines available free at Mhttps://doi.org/0.06/j.jhep.209.02.04

Acute liver failure Paracetamol overdose

Chronic liver failure Alcohol,

- antitrypsin deciency.



8

Paracetamol,

sats, GCS, blood glucose, urine output.

Chronic liver diseaseCachexia, palmar ery-

Urine

MSU;

blds

FBC, clotting,

(E pp. 578–9) and white cell count to

OGD

may help assess

327LIVER FAILURE

328 CHAPTER0 Gastroenterology

3Acute liver failure (E OHAM4p. 276.)

$ Acute encephalopathy, coagulopathy, and jaundice without previous

cirrhosis (Table0.0).

Table0.0 Types ofacute liver failure

Liver failure <7d of disease onset Hyperacute fulminant hepatic failure

Liver failure – 4wk of disease onset Acute fulminant hepatic failure

Liver failure 4– 2wk of disease onset Subacute fulminant hepatic failure

Liver failure 2– 26wk of disease onset Late- onset hepatic failure

SymptomsBruising/ bleeding, drowsy ±confusion, abdopain. Signs Drowsiness, confusion, slurred speech, jaundice, apping tremor

(asterixis), poor coordination, bruising, hepatomegaly, ascites.

Investigations Initiate liver screen as detailed (E p. 327); blds iPT/

APTT, ii ALT, iALP, ibilirubin, iammonia, iWCC, dglucose, dMg

3–

dPO

; ABG Respiratory alkalosis, metabolic acidosis (poor prognosis);

USSMasses, echogenicity, portal veinow.

TreatmentDiscuss with a senior early, often needs ICU/ HDU with inva-

sive monitoring, and may need transfer to a specialist liver centre, where may be considered for transplantation. Monitor blood glucose every 2h; insert a catheter and monitor uid balance.

• i

PT Give one- o dose of vitamin K 0mg IV. PT prolongation is used

to monitor disease progress; FFP and/ or platelets may be indicated if the patient is bleeding or needs an invasive procedure

•

Stop Aspirin, NSAIDs, and hepatotoxic drugs (E p. 327); check all drugsinBNF

•

Antibiotic Prophylaxis in all patients (eg cefotaxime) ±antifungals

•

Daily bloods FBC, U+E, LFT,PT

9

• Steroids May improve survival in more severe alcoholic hepatitis

•

Lactulose 0– 20mL/ 8h PO in all patients (helps remove ammonia)

•

Close monitoring of cardiovascular status and blood glucose; if need IV

uids, avoid Na

Complications Renal failure (hepatorenal syndrome), respiratory failure

(ARDS), cerebral oedema, bleeding, sepsis, dglucose, iNa

if chronic liver disease/ ascites.

Alcoholic hepatitis

$ Acute liver inammation on a background of chronic alcohol excess.

Symptoms and signsJaundice, anorexia, fever, and RUQpain. Investigations blds iWCC, ibilirubin, iALT ±iPT, −ve hepatitis/ auto-

immune serology;

Ascitic tapto exclude spontaneous bacterial peritonitis.

Treatment As for acute liver failure. Transplantation may have a role in

highly selected patients.

Vascular liver disease

$ Diagnosed by Doppler USS; these diseases can cause hepatic jaundice or

acute liver failure, often treated by anticoagulation or endovascular methods.

• Budd– Chiari hepatic vein obstruction

•

Portal vein obstruction (pain and deranged LFTs; jaundice only if other

causes of liver disease coexist)

•

Liver ischaemia due to hypotension and/ or hepatic artery stenosis.

Typically causes massive ALTrise.

9

Strictl y, the INR is specic for warfarin therapy; the abnormal clotting pattern in liver disease is

dierent and more reliably reported as PT and APTT prolongation.

,dK+.

Glandular fever(Infectious mononucleosis, Epstein– Barr virus(EBV).)

Symptoms Usually young (0– 30yr), sore throat >wk, fever, lethargy,

malaise, rash, lumps in the neck, anorexia.

Signs Red tonsils ±white exudate, tender lymphadenopathy, splenomegaly,

rash (especially with amoxicillin/ ampicillin), palatal petechiae, jaundice.

Investigations blds ilymphocytes (atypical on lm), iALT, +ve Monospot/

Paul Bunnell, +ve IgM forEBV.

Management Rest, rehydration, analgesia, gargle with warm saline/

aspirin, avoid amoxicillin/ ampicillin, avoid alcohol, consider short course of oral steroids if very severe (eg hepatic encephalopathy).

Complications Hepatitis, liver failure, thrombocytopenia, splenic rupture,

haemolysis, encephalitis.

Acute viral hepatitis(E OHCM1p. 274.)

Causes Hepatitis A, B, C, and E, CMV andEBV. Symptoms Jaundice, rash, diarrhoea, abdo pain, u- like symptoms (eg

fever, malaise, anorexia, fatigue, nausea, vomiting, arthralgia, sore throat).

Signs Patient may have no signs, itemp, urticarial rash, jaundice, hepato-

megaly, splenomegaly, lymphadenopathy.

Investigations blds iWCC, ibilirubin, iALT ±iPT, +ve hepatitis serology (eg

check anti- hepatitis A, B, C, ±E, see Table0. for hepatitis B interpretation).

ManagementAvoid alcohol, supportive treatment, monitor for progres-

sion to acute liver failure (E p. 328) which may need antiviral treatment.

Complications Natural history varies widely depending upon virus and

host; risks include acute liver failure or chronic disease.

Chronic viral hepatitis(E OHCM1p. 274)

$ Hepatitis >6mth, caused by hepatitis B (±D) and C.

Symptoms and signsUsually asymptomatic, signs of chronic liver disease. Investigations bldsDeranged LFT ±iPT; abnormal viral serology (check anti-

hepatitis C antibody then PCR for viral load if positive; see Table0. for hepatitis B serology);

USSLiver may be suggestive of cirrhosis.

TreatmentAvoid alcohol; refer to a hepatologist for antiviral treatment. ComplicationsCirrhosis (20%), hepatocellular carcinoma (espHBV).

329LIVER FAILURE

Table0. Serology inhepatitisB

Surface antigen (HBsAg) Active virus replication— acute or chronic disease

Anti- core (anti- HBc) IgM Acute infection

Anti- core (anti- HBc) IgG Chronic infection (or previous infection if HBsAg– ve)

‘e’ antigen (HBeAg) High infectivity

Anti- e (Anti- HBe) Low infectivity

$ In chronic hepatitis B infection, HBeAg negativity is associated with immune

control of the virus and low/ undetectable viral DNA. Beware, however, the subset of patients in whom the virus develops a precore mutation leading to absent production of HBeAg, despite loss of immune control and rising viral DNA titres. These patients are at high risk for disease complications.

A wide range of currative treatment options exist for hepatitis C.For a range of current

European guidelines, see Mwww.easl.eu

330 CHAPTER0 Gastroenterology

Decompensated chronic liver failure(E OHCM1p. 272.)

$ Cirrhosis is the nal common histological pathway for a variety of

liver diseases; problems relate to synthetic function (coagulopathy, ascites 2° to hypoalbuminaemia), decreased detoxication (encephalopathy), or portal hypertension (variceal bleeding).

Symptoms and signsAs for acute liver failure (E p. 328) but look for stigmata

of chronic liver disease:spider angioma, palmar erythema, gynaecomastia.

Investigations Measure severit y LFTs, U+E, and clotting prole; Establish

underlying cause

ferritin, α

tant of decompensation FBC, bld cultures, ascitic tap,OGD; Treatment This

Hepatitis serology, immunoglobulins, liver autoantibodies,

- antitrypsin, caeruloplasmin, USS, liver biopsy; Identify precipi-



requires hepatology input and transplant assessment; deal with upper GI bleeding (E pp. 313–14), treat sepsis, support alcohol cessation, lactulose (to reduce ammonia levels);

Ascites Low- salt diet, daily weights, spir-

onolactone 00mg/ 24h PO increasing dose every 48h to 400mg/ 24h ±furosemide; ascitic tap for diagnosis (E pp. 578–9) and to exclude spontaneous bacterial peritonitis; may need long- term antibiotics, therapeutic paracentesis, or TIPS if recurrent;

Complications High mortality, portal

hypertension, bleeding varices, encephalopathy, hepatocellular carcinoma.

Spontaneous bacterial peritonitis

Symptoms Abdominal pain in the presence of ascites, associated

with fever;

Signs Fever, iHR ±dBP, abdo tenderness ±peritonitis;

Investigations blds iWCC, iCRP; Ascitic tap >250 white cells/ mm

identication of organisms (E pp. 578–9); biotics: (eg Tazocin

4.5g/ 8hIV).

Treatment Prompt IV anti-

Autoimmune liver disease(E OHCM1p. 278.)

Causes Primary biliary cholangitis (E p. 333), primary sclerosing cholan-

gitis (E p. 333), autoimmune hepatitis (types Iand II— see Table0.2); primary biliary cirrhosis and type I autoimmune hepatitis may overlap;

Symptoms Often asymptomatic, may have fever, malaise, rash, joint pain,

or symptoms of chronic liver disease;

Signs Signs of chronic liver disease;

Investigations blds Deranged LFT ±iPT, +ve autoantibodies (Table0.2);

USSAnd liver biopsy; Treatment Autoimmune hepatitis Prednisolone 30mg/

24h PO initially then azathioprine;

Other diseases E p. 333; Complications

Acute liver failure, cirrhosis, hepatocellular carcinoma.

Table0.2 Autoantibodies inautoimmune liver disease

Primary biliary cholangitis (780% •)

Primary sclerosing cholangitis (770% ♀, 780% IBD)

Autoimmune hepatitis typeI(80% ♀)

Autoimmune hepatitis type II (mainly children; 90% ♀)

Anti- mitochondrial (AMA) present in 95% and 98% specic

Anti- smooth muscle (SMA), antinuclear (ANA), p- ANCA

Anti- smooth muscle (SMA), antinuclear (ANA)

Anti- liver/ kidney microsomal type  (LKM)

Haemochromatosis(E OHCM1p. 284.)

$ Autosomal recessive disease causing excess iron accumulation.

Symptoms

megaly, signs of chronic liver disease, cardiac failure, or conduction defects, hypogonadism ±impotence, tanned skin; (>60% in ♂ and >50% in ♀ highly specic, but false- negatives esp. in younger ♀),iALT, iglucose, genetic testing (2 common mutations account for 70% of Cau- casian patients); severity);

Fatigue, lethargy, arthralgia, hyperpigmentation, DM;

ECG

Cardiomyopathy or conduction delays;

Treatment

Venesection ( unit/ wk) until ferritin normalizes then every

Investigations blds

itransferrin saturation

Liver biopsy

Signs

Hepato-

(Diagnosis,

3– 6mth; transferrin saturation or genetic screening of relatives.

Non- alcoholic fatty liver disease(E OHCM1p. 281.)

$ Spectrum of damage from fat deposition in absence of other causes.

Symptoms and signsObesity, hypertension, diabetes, liver failure; Investigations

bldsFull liver screen to rule out other causes;HbA

show fat deposition and evidence of cirrhosis;

; USS ± elastographyMay

C

Liver biopsy; TreatmentWeight

loss; manage cardiovascular risk; monitor for transplantation.

- antitrypsin deciency(E OHCM1p. 286.)



$ Genetic disease with complex inheritance causing liver and lung damage.

Symptoms and signs Breathlessness, liver failure, family history; Investigations blds dα

smoking, may need liver transplant, COPD treatment.

- antitrypsin levels, genetic testing; Liver biopsy; Treatment Stop



Wilson’s disease(E OHCM1p. 281.)

$ Autosomal recessive disease; copper accumulates in the liver andCNS.

Symptoms Tremor, slurred speech, abnormal movements, clumsiness, depres-

sion, personality change, psychosis, liver failure, family history; Fleischer rings in eyes, signs of liver failure;

Investigations blds dcaeruloplasmin,

dtotal serum copper, iserum free copper, genetic testing; excretion (especially if a dose of penicillamine is given); copperon

Treatment

Lifelong penicillamine, may need liver transplant, screen relatives.

Signs Kaiser–

Urine i24h copper

liver biopsy;

Weil’s disease (leptospirosis)

$ Bacterial infection transmitted via exposure to water contaminated with rat urine.

Symptoms Recent contact with dirty water, high fever, malaise, anorexia, fatigue,

nausea, vomiting, arthralgia, pharyngitis, conjunctival oedema, neck stiness, photophobia, jaundice, bleeding, and kidney failure; bruising, tender RUQ, myocarditis;

blds dHb (haemolytic), iurea, icreatinine, ibilirubin, iALT, serology; Treatment

Investigations Urine Dipstick haematuria, culture;

Doxycycline 00mg/ 2h PO or benzylpenicillin 600mg/ 6h IV and supportive care of renal/ liver failure.

Predicting outcomes inchronic liver disease This is of considerable

importance, not least in prioritizing use of organs for transplantation. The ‘Child’ scoring system originated in 964 from attempts by Child and Turcotte to assess operative risks for cirrhotic patients undergoing porto- systemic shunt surgery. Later modications to include albumin and INR led to the ‘Child– Turcotte– Pugh’ score which is still widely used. With the advent of liver transplantation, more precise stratication of patients with advanced disease was needed:for the NHS transplantation programme, the UKELD (UK end- stage liver disease) score is calculated from serum Na The original description of the UKELD score (Neuberger J, Gut 2008;57:252) is available online at Mhttps://gut.bmj.com/content/57/2/252.long (subscription required, but many NHS trusts provide access through ATHENS). Online calculators for the Child score and UKELD are widely available (eg

Mwww.mdcalc.com). Information on the NHS transplantation programme, including liver transplants, is available at: Mwww.organdonation.nhs.uk

Signs Acute liver failure, meningism,

, creatinine, bilirubin, andINR.

331LIVER FAILURE

332 CHAPTER0 Gastroenterology

Jaundice

2Worrying features iHR, dBP, drowsiness, dGCS, bleeding, slurred

speech, poor coordination, tremor/ ap, renal failure, weightloss.

Thinkabout

Pre- hepatic Haemolysis, malaria. Hepatic Paracetamol overdose, viral hepatitis, alcohol, chronic liver disease,

Gilbert’s syndrome, pregnancy, medications (E p. 327), toxins (eg poi- sonous fungi), vascular disease (eg ischaemia, Budd– Chiari), sepsis.

Cholestatic Choledocholithiasis, ascending cholangitis, pancreatic cancer,

cholangiocarcinoma, primary biliary cirrhosis, primary sclerosing cholangitis.

Ask about Tiredness, jaundice (+onset), abdo pain, itching, dark urine,

pale stools, drowsiness, confusion, bruising, bleeding (skin, nose, bowel, urine), bloating, vomiting, rashes, recent infections (sore throat), weight loss, generalized aching, hair loss, darkening skin, jointpain; dice, gallstones, breathing problems, blood transfusions; and medications (Ep. 327);

FHLiver disease, recent jaundice; SHAlcohol,

IVDU, tattoos, piercings, foreign travel, sexual activity (?abroad).

Obs Temp, RR, HR, BP, urine output, O

sats, glucose,GCS.

Look for Volume status (E p. 402), bruising, evidence of bleeding,

drowsiness, confusion:

Pre- hepaticSplenomegaly, pale conjunctiva, breathlessness. HepaticSigns of acute or chronic liver failure (Epp. 327–31). Cholestatic Abdominal tenderness ±peritonism, Charcot’s triad (fever,

jaundice, and RUQ pain=cholangitis), palpable gallbladder, cachexia.

Initial investigations Urine MSU, bilirubin, urobilinogen; blds FBC,

reticulocytes and LDH (both elevated in haemolysis), blood lm, clotting, U+E, LFT (total and conjugated bilirubin), amylase, lipase, paracetamol levels, hepatitis, EBV and CMV serology, bld cultures;

USS Abdo (?dilated bile ducts, cirrhosis, pancreatic mass, metastases).

See Table0.3 and Box0.4.

Table0.3 Laboratory investigation ofjaundice

Urine Liver tests Other tests

Pre- hepatic jaundice

Hepatic jaundice

Cholestasis Bilirubin, dark

Cholangitis Bilirubin, dark

Urobilinogen

urine

iunconjugated bilirubin

imixed bilirubin, iALT/ AST

iconjugated bilirubin, iALP, iγGT

PMH Previous jaun-

DH Paracetamol

dHb, nMCV, dhaptoglobin, ireticulocytes

May have positive hepatitis serology or iparacetamol levels

Dilated ducts on USS

iWCC, iCRP, dilated biliary ducts

Urgent

I Box 0.4 Causes ofjaundice covered elsewhere

HaemolysisEp. 416 Liver failureEpp. 327–31

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