Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:

Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3090_Библиотеки_им_академика_М_И_Перельмана

.pdf
Скачиваний:
0
Добавлен:
12.10.2026
Размер:
6 Мб
Скачать
☆
148 Chapter 11
Nonmalignant causes of obstruction or gut paresis must
be considered, which may be amenable to surgical or other
appropriate intervention. These include adhesions, consti-
pation, drugs, unrelated benign conditions, and metabolic
abnormalities.
Investigations can be helpful and may include a biochemical
profile (hypokalaemia may cause ileus; hypercalcaemia may
cause pseudo-obstruction due to constipation). A plain
abdominal X-ray will demonstrate constipation, but can be
misleading when multiple levels of obstruction are present. A
CT/MRI scan can be indicated if surgery is to be considered.
Chemotherapy may offer a palliative option for some
patients with chemosensitive tumours, for example, ovarian
carcinoma. Any surgical or oncological intervention should
run in parallel with more immediate symptomatic treatment.
Expanding stents placed endoscopically or radiologically are
occasionally helpful and are discussed shortly.
Surgical Intervention
Surgery should always be considered in malignant GI
obstruction. However, it will often be inappropriate or
technically impossible. Surgical intervention is unlikely to
be successful in the following situations:
• Radiological or previous surgical evidence indicating
that a surgical procedure will not be technically possible.
•
A stiff, doughy abdomen with little abdominal distension [27].
• Diffuse intra-abdominal carcinomatosis.
• Massive ascites that re-accumulates rapidly after
paracentesis.
•
Poor general physical status [28].
• Previous radiotherapy to the abdomen or pelvis, in
combination with any of the above.
Medical Management
A NG tube and intravenous (IV) fluids are rarely necessary
if the following strategy is used.
Pain
Analgesia for background pain is obtained by using a con-
tinuous SC infusion of an opioid, for example, morphine
(dose: 1/2 total daily oral morphine equivalent
dose ± 30–50% increment as dictated by the pain). If
opioid naive, start on a morphine dose of 10 mg/24 h. Not
all patients require opioid analgesia if no background pain
also have an antiemetic effect in their own right.
Dexamethasone at 2–6 mg OD is useful to add to an anti-
emetic regimen for patients with resistant problems.
Malignant Bowel Obstruction
Malignant GI obstruction occurs most commonly in
patients with advanced abdominal or pelvic cancers: in
25% of patients with a primary bowel cancer; in 6% of
patients with a primary ovarian cancer; and in about 40%
of advanced ovarian cancer patients.
Where surgery is technically not possible, is inappropriate,
or is not acceptable to the patient, medical management of
malignant GI obstruction can offer good symptom control.
Patients may live for surprisingly long periods of time (some-
times months) and be able to take small quantities of food and
fluids as desired, usually without the need for an NG tube or
parenteral fluids. Most patients can be cared for at home.
The clinical scenario may only have some of the classic
features of complete bowel obstruction outlined in Box 3.
Malignant obstruction may present acutely but more com-
monly is gradual in onset, intermittent, and variable in
severity. Gross distension is often absent, even in lower
bowel obstruction since the bowel may be constricted at
several points. Patients with lower bowel obstruction will
often have infrequent, faeculent vomiting, while those
with high bowel obstruction may vomit undigested food. It
is always useful to determine whether colic is present or
absent since this will affect the management strategy (see
following paragraphs).
Box 3: Classical features of complete
intestinal obstruction
• Large-volume vomits.
• Nausea worse before vomiting.
• Nausea relieved by vomiting.
• Nil per rectum or per stoma.
• Abdominal distension.
• Visible peristalsis.
• Increased bowel sounds, classically tinkling, but may be
absent.
•
Background abdominal pain.
• Colicky abdominal pain.
https://t.me/med1917
The Management of Gastrointestinal Symptoms and Advanced Liver Disease 149
series of 51 patients median survival was 17 days with a
range of 1–190 days; 92% of patients gaining symptomatic
improvement of nausea and vomiting with some restora-
tion of diet [26].
Contraindications to the use of a venting gastrostomy
are:
•
The presence of significant ascites as it would precipitate
peritonitis.
•
Tumour infiltration of the stomach.
In an obstructed abdomen with malignant infiltration, the
risk of perforating the bowel with resultant peritonitis is
significant and the patient should be clear about this risk.
It is important that at least a 16–20 F bore gastrostomy
tube should be used to facilitate adequate decompression.
Subcutaneous Drug Delivery
Patients may require the use of more than two drugs to
obtain symptom control and not infrequently two SC infu-
sions are required. Studies of the compatibility of multiple
drug combinations are often not available (see Chapter
22), but clinical observation suggests the following drugs
mixed in water for injection are compatible and maintain
efficacy:
•
Morphine/diamorphine, haloperidol, and cyclizine.
• Morphine/diamorphine, haloperidol, and hyoscine butyl-
bromide (compatibility may depend on order of mixing).
•
Morphine/diamorphine and octreotide.
• Morphine/diamorphine, haloperidol, and octreotide.
Diet and Hydration
Sensitive, pre-emptive discussion of the situation is a vital
part of care for the patient and family. Many patients with
obstruction can eat and drink in modest amounts when
symptoms are controlled. A liquid, low-residue diet may be
the least problematic.
Hydration should be considered on an individual basis.
Oral discomfort and dryness can largely be relieved by fre-
quent, attentive mouth care, ice to suck, and drinks as desired
and tolerated. Profound thirst is not common but some
patients may benefit from parenteral fluids, for example, SC
infusion of 1–2 litres 0.9% saline/24 h or IV fluids. The use of
parenteral fluids can impact on choices regarding place of care.
Hiccup
This is an abnormal respiratory reflex characterised by spasm
of one or both sides of the diaphragm, causing sudden inspira-
tion with associated closure of the vocal cords. The phrenic
nerve, vagus nerve, thoracic sympathetic fibres, brainstem,
and hypothalamus are all involved in the reflex arc. An
is present and colic can be relieved by more appropriate
drugs (see following paragraphs).
Colic and Gut Motility
If colic is present avoid all drugs that could worsen this
(i.e., metoclopramide, bulk-forming, osmotic, and stimu-
lant laxatives). If colic persists, add hyoscine butylbromide
SC, starting at 60 mg/24 h (up to 200 mg/24 h as needed).
If colic is absent, a trial of metoclopramide SC 30–90
mg/24 h should be cautiously instigated with close moni-
toring for development of colic. In the absence of colic,
incomplete obstruction in the large bowel may be helped
by a stool-softening laxative, such as docusate sodium 200
mg BD-QDS. Corticosteroids may reduce bowel obstruc-
tion in those with advanced malignancy, particularly GI
and ovarian cancer. A 5-day trial of dexamethasone 6–16
mg SC/IV should begiven [29].
Nausea
The choice of antiemetic depends on whether the patient is
experiencing colic. If colic is not a feature, metoclopramide
is administered SC 30–90 mg/24 h (see earlier paragraph).
If colic is present, give haloperidol (SC 3–5 mg/24 h) or
cyclizine (SC 50–100 mg/24 h). A combination of haloper-
idol and cyclizine is sometimes necessary.
5HT 3 antagonist antiemetics may have a role in relief of the
nausea induced by bowel distension and stimulation of the
vomiting centre through vagal afferents (see above), but this is
unclear. They can be given rectally or subcutaneously.
Vomiting
Reduction in the volume of GI secretions will reduce colic,
nausea, pain, and the need to vomit. This can usually be ade-
quately achieved with hyoscine butylbromide (SC 60–200
mg/24 h [30]) with or without an H
2
antagonist or PPI.
If large-volume vomiting persists despite hyoscine butyl-
bromide, the somatostatin analogue, octreotide, will further
decrease the volume of intestinal secretions in the gut
lumen [31]. A trial of octreotide, given at a rate of 300 μg/24
h by SC infusion, should be performed. The dose can be
titrated over 2–3 days to 600 μg/24 h; If there is no benefit
at 600 μg/24 h it should be stopped. The dose should be
reduced daily by 100 μg/24 h to the lowest effective dose
(mean dose 300 μg/24 h) [32].
In some cases, particularly in high obstructions such as
gastric outlet obstruction, these strategies are not effective.
It may then be helpful to use a NG tube or consider a vent-
ing gastrostomy to allow the patient to continue to drink
and eat as desired without the fear of provoking immediate
vomiting. Venting gastrostomy can be performed under
local anaesthetic either endoscopically or radiologically
and may facilitate discharge and dying at home. In one
https://t.me/med1917
150 Chapter 11
hospital stays and fewer procedures than non-stenting
options. Covered stents are particularly effective in tra-
cheoesophageal fistula. Stents are most useful in mid to-
low oesophageal tumours. Tumours of the gastroesophageal
junction respond well, but stent migration is more
common and the function of the lower oesophageal
sphincter is lost and can result in problematic gastro-
esophageal reflux (patients will need PPIs). Stenting of
high oesophageal tumours can cause significant and per-
sistent discomfort.
Complications:
•
0.5–2% mortality as a result of stent insertion. [33].
• Pain/mediastinal discomfort (NB: surgical emphysema
may indicate perforation).
•
Bleeding.
• 3% perforation rate.
• Stent migration (more common following chemo-
therapy and tumour regression).
•
Tumour overgrowth.
• Food blockage.
After stenting patients need to modify their diet: more
liquidised/sloppy food, avoid leafy vegetables and chunks
of steak, etc. Possible acute food blockage may be relieved
by carbonated drinks. Total dysphagia with drooling and
aspiration requires emergency review.
Tumour overgrowth can be dealt with by laser, alcohol
injection, or argon (see recanalisation earlier).
Gastroduodenal Stents
Pancreatic, duodenal, and gastric cancers frequently pre-
cipitate gastric outflow obstruction, and EMS are as effec-
tive in relieving this as palliative bypass surgery. Most
patients gain significant clinical improvement. Where
there is functional gastric-outlet obstruction due to
tumour invasion of neural supply or diffuse peritoneal
infiltration with bowel encasement and gut failure,
improvement will not be seen.
The EMS are best placed using the combined modalities
of endoscopic and fluoroscopic guidance; however, this
can be achieved fluroscopically alone. Gastroduodenal
stents can be inserted as an outpatient procedure. Patients
with duodenal involvement frequently develop biliary
obstruction, and it is advisable that the biliary obstruction
is treated first. Complications are similar to those men-
tioned earlier.
Biliary Stents
Patients with biliary obstruction experience nausea,
anorexia, weight loss, fat malabsorption with steatorrhoea,
itch, and occasionally cholangitis, although the severity of
these symptoms varies between individual patients.
inhibitory pathway through the pharyngeal and glossopha-
ryngeal nerves is present. Disturbance of any of these compo-
nents may cause hiccup. Identification of cause may sometimes
enable a logical and successful approach to treatment.
Management
Stimulation of the pharynx may be successful in reducing
hiccup. This can be achieved in various ways, including
holding iced water in the oropharynx, soft palate massage,
oropharyngeal, or nasopharyngeal catheter placement.
Common empirical treatments are:
•
A defoaming antiflatulent before and after meals and at
bedtime (e.g. Simeticone).
•
Domperidone 10–20 mg TDS; or metoclopramide 10
mg TDS half an hour before meals if delayed gastric
emptying.
• Nifedipine 10–20 mg BD-TDS (assess effect on blood
pressure).
•
Midazolam 5–10 mg SC/24 h (this option is for those in
the last days of life; the dose can be titrated to a maximum
of 60 mg/24 h).
• Baclofen 5–10 mg BD-TDS (higher doses can be used
with caution).
•
Chlorpromazine – use with care and only if simpler
measures fail: 10–25 mg PO TDS (it has a diffuse depres-
sant effect on the reticular formation).
•
Sodium valproate – for hiccup of central origin.
In general, the drugs should be started at low dose and
gradually increased to avoid side effects.
Phrenic nerve stimulation or ablation is only occasionally
an appropriate treatment in patients with advanced disease.
Endoluminal Stents
Stenting is a widely used therapeutic intervention for palli-
ation of GI and hepatobiliary malignant obstruction. Stents
are available as expandable metal systems (covered or
uncovered) or in plastic (for biliary obstruction). Stents are
usually placed through a guidewire under endoscopic and
fluoroscopic guidance, although radiologists do place them
under fluoroscopic guidance alone. Uncovered stents
embed well in luminal tissues but may become occluded by
further tumour growth. Covered stents prevent the ingress
of tumour but are more prone to migration and displace-
ment. Stenting is usually a day case procedure but depends
on patient performance status and complications.
Oesophageal Stents
Expandable metal stents (EMS) provide relief or improve-
ment of dysphagia in 90% of cases and result in shorter
https://t.me/med1917
The Management of Gastrointestinal Symptoms and Advanced Liver Disease 151
advanced chronic end-stage liver disease represent a major
public health and potential palliative burden. Worldwide
hepatitis B and C are the most common causes of cirrhosis.
In the developed world, alcohol is the most common cause,
but viral infections and liver disease associated with obesity
(non-alcoholic steatohepatitis) are both increasing.
The UK incidence of cirrhosis is approximately 17 per
100,000 (prevalence 76 per 100,000) in adults over 25
years. More than 80% of liver-related deaths in the
United Kingdom are due to cirrhosis secondary to
alcohol [35].
Prognosis is related to the severity of the underlying
disease (see Figure 4) and the development of disease-
related complications. In stable compensated cirrhosis
(Childs A) the five-year survival is excellent; however, in
decompensated cirrhosis (development of portal hyper-
tension, ascites, portal hypertensive bleeding, encepha-
lopathy), the five-year survival is 50%. The model for
end-stage liver disease (MELD) is a validated scoring
system used to predict the survival of patients with end-
stage liver disease in America and Europe [36]. The UK
equivalent is UKELD, and a UKELD score of greater
than 49 is the minimum criteria for entry onto the trans-
plant waiting list.
Complications of Cirrhosis
The development of complications (see Figure 5) associ-
ated with decompensated cirrhosis have a marked impact
on survival:
•
Refractory Ascites (RA).
• Spontaneous Bacterial Peritonitis (SBP).
• Hepatorenal Syndrome (HRS).
• Variceal Bleeding (VB).
•
Hepatocellular Carcinoma (HCC).
• Portosystemic Encephalopathy (PSE).
Ascites and Refractory Ascites
While response to the use of diuretics in malignant ascites is
variable and unpredictable, they are highly effective in
ascites of decompensated liver disease. Response may be
seen using spironolactone up to 400 mg/day and furosemide
up to 160 mg/day. Diuretics should be titrated to effect while
monitoring electrolyte balance and renal function.
RA is associated with a high frequency of complications
(PSE and infections). The 1-year survival is approximately
50%. Patients should have the patency of the portal vein
checked (ultrasound) and development of a HCC excluded
(serum alpha feto protein and imaging if appropriate).
Jaundice can also be a significant visual reinforcement
affirming the disease process. The obstructed biliary tree is
decompressed by endoscopic retrograde cholangiopancrea-
tography (ERCP) or percutaneous transhepatic cholangiog-
raphy (PTC). Plastic stents are subject to bacterial and
biliary encrustation resulting in occlusion and usually last
between three and four months. The more expensive EMS
have larger diameters and longer patency than plastic stents.
If patient survival is greater than four to six months, then
metal stents appear more cost-effective with fewer endo-
scopic interventions and hospital admissions required.
Patients may benefit from re-stenting and recurrence of
jaundice should not be assumed to be due to tumour
progression.
Complications of biliary stenting (ERCP and PTC):
•
Pancreatitis
• Bleeding
• Perforation
• Biliary leak and peritonitis
• Malposition
• Cholangitis.
Colorectal Stents
Colorectal stents can be used as a bridge to surgery or in
patients with extensive disease who are poor surgical can-
didates. Covered stents are also useful in assisting closure
of colo-vesical and colo-vaginal fistulas. Right-sided
colonic stents require endoscopic placement. Left-sided
stents can be placed radiologically.
Complications:
• Perforation (devastating as it will cause a florid faecal
peritonitis)
•
Stent migration
•
Stool occlusion
• Bleeding
• Tenesmus1
• Faecal incontinence.
1
Patients should be advised to consume a low residue diet
and take faecal softeners.
Liver Disease
Liver disease is the only major cause of death that is
continuing to rise year on year, and it is now the fifth “big
killer” in England and Wales after heart disease, cancer,
stroke, and respiratory disease [34]. Therefore, cirrhosis and
1
In stents placed in the lower rectum.
https://t.me/med1917
152 Chapter 11
CHILDS-PUGH A
(SCORE 5-6
POINTS)
CHILDS-PUGH B
(SCORE 7-9
POINTS)
Bilirubin (µmol/ L) <34
34–51 >51
<28
>6
3–4 (moderate to
severe)
Moderate to severe
(poorly controlled)
28–35
4–6
1–2 (slight)
Mild (easily controlled)
>35
1–4
Absent
None
1 point 2 points 3 points
Albumin (g/L)
Prothrombin time (s)
Ascites
Encephalopathy
CPS
SCORE
(10-15)
POINTS
Figure 4 The Childs-Pugh classification of cirrhosis.
Complications
of
advanced liver
disease
Hepatorenal
syndrome
(HRS)
albumin and
glypressin
HCC
SBP
Ceftriaxone
Quinolone
(primary or
secondary)
Drug resistant
ascites (RA)
High volume
paracentesis.
TIPSS
Bleeding
varices
mortality
35–50%
Resusitate
Glypressin
Antibiotics
Endoscope
Jaundice
Pruritis
Relieve
obstruction
or
Pharmaco-
therapy
Hepatopulmonary
syndrome
O
2 therapy
(Recognise as a
cause of hypoxia)
PSE
Look for
precipitant
Enemas
Lactulose
Sepsis
Figure 5 Summary of the complications that may occur in advanced liver disease. HCC, hepatocellular carcinoma; TIPSS, transjugular
intrahepatic portosystemic shunt; SBP, spontaneous bacterial peritonitis; PSE, portosystemic encephalopathy.
https://t.me/med1917
The Management of Gastrointestinal Symptoms and Advanced Liver Disease 153
Treatment includes the following:
•
Correction of the reversible (sepsis, SBP, dehydration,
hypokalaemia, underlying bleeding, constipation).
•
Enemas to achieve bowel clearance.
• Laxatives: lactulose has traditionally been used as it
reduces colonic pH and nitrogen load in the gut. However,
in practice it is acceptable to use alternatives that may be
better tolerated.
Variceal Bleeding
Varices are related to elevated portal pressure and the
development of a portosystemic shunt through collateral
vessels, allowing portal blood to be diverted to the systemic
circulation. The size of the varix and the severity of the
underlying liver disease are risk factors for bleeding.
Propanolol (40 mg BD) reduces the incidence of first vari-
ceal bleeds by 50%. Alcohol causes marked increase in
portal hypertension, and every effort should be made to
get patients to cease drinking. Banding of varices has a role
in preventing further bleeds, and if practical, should be
carried out on a regular basis until the varices are
obliterated.
The average mortality of a first variceal bleed is approx-
imately 50%; however, this is closely related to the under-
lying severity of liver disease. Bleeding may result in severe
decompensation and fatal liver injury. Variceal bleeding is
always a frightening and dramatic occurrence.
Prescribing in Liver Disease
Patients with advanced liver disease are symptomatic and
therefore need their symptoms to be appropriately assessed
and treated. Concern exists in prescribing for patients with
liver disease as there is little evidence to guide practice. The
liver has a huge reserve and has to be damaged significantly
before it starts to have an effect; however, this is unpredictable
and each patient should therefore be assessed as an individual
and closely monitored after any medication is prescribed.
Treatment of RA includes the following:
• Transplantation: By far the best treatment but not all
patients will be suitable.
•
Transjugular intrahepatic portosytemic shunt (TIPSS):
Reduces the rate of ascites recurrence and the development
of HRS, has no effect on survival and is associated with a
20% incidence of encephalopathy. The ongoing
management of patients with TIPSS is hospital intensive,
and it is not recommended for those with severe liver
failure, concomitant active infection, progressive renal
failure, or severe cardiopulmonary disease.
•
Paracentesis (see Box 4) [37]: The treatment of choice for
most patients. Large volume paracentesis (>5 L) requires hos-
pitalisation and concurrent administration of IV albumin;
however, smaller volume paracentesis (<5 L) can be done as
an outpatient, and the need for volume expansion is less clear
and needs to be considered within the overall goals of care for
a patient*. A palliative procedure out of the hospital setting
may be appropriate, but the risks and benefits for the patient
need to be considered carefully. Palliative long-term abdom-
inal drains (LTADs) are routinely used in refractory malig-
nant ascites but are not standard of care in cirrhosis, pending
results of a national definitive trial. Currently, outside of a
research setting, LTADs should only be considered in cir-
rhosis on a case by case basis after careful patient selection.
Spontaneous Bacterial Peritonitis (SBP)
SBP carries a 10–30% mortality with a 1-year survival of
38% after the first episode. It may lead to circulatory
dysfunction and HRS that has a very poor survival rate.
Administration of albumin with antibiotic therapy pre-
vents HRS and improves prognosis.
There is good evidence for the administration of pro-
phylactic quinolone antibiotics in patients with ascites due
to cirrhosis for the prevention of SBP however concerns
exist over the emergence of quinolone-resistant species of
bacteria and antibiotic-induced complications. The sug-
gested schedule is ciprofloxacin 250 mg OD.
Hepatorenal Syndrome (HRS)
In patients whose renal function deteriorates, HRS should
be considered and urgent specialist advice sought. HRS
occurs in 5–10% of cirrhotic patients with ascites and is a
very sinister development with greater than 90% mortality.
Portosystemic Encephalopathy
This is common and if mild is easily controlled. There are
multiple causes; however, the most common are sepsis,
dehydration, GI bleed, and the co-administration of
sedating drugs. It is a marker of decompensation and
therefore potentially reversible.
Box 4: Large volume paracentesis (>5 L)
• If patient on diuretics, withhold.
•
Under local anaesthetic insert paracentesis catheter into
peritoneal cavity.
• Give albumin 8 g/L of ascitic fluid drained.
•
Drain to dryness.
•
Remove catheter after 24 h to reduce chances of infection
and peritonitis.
• Place stoma bag over site if ascites leakage. Start albumin
infusion before or at same time as starting paracentesis.
*Note that for malignant ascites in patients without cirrhosis,
IV albumin is not required.
https://t.me/med1917
154 Chapter 11
correlation between plasma bilirubin concentration and
intensity of pruritus. Approximately 20–25% of jaundiced
patients complain of itch. There is no standard or generally
accepted regimen for treatment and many different medica-
tions, with a limited evidence base, have been tried. The most
effective treatment is to achieve biliary drainage, although
this is not always possible and not without complications.
Drugs for pruritis include the following:
•
Antihistamine: Sedating antihistamine has no effect on
the itch but may assist in promoting sleep through their
sedating effect, best avoided during the daytime.
•
Exchange resins: Colestyramine is a bile salt binder, give
4 g bd. Best taken on an empty stomach first thing in the
morning and before the evening meal (can add to orange
juice to improve palatability).
•
Choleuretic agents: Ursodeoxcholic acid 250 mg TDS.
• Enzyme inducers: Rifampicin 150 mg daily or phenobar-
bital. Moderate to low efficacy with variable response.
•
5HT3 antagonists: Anecdotal reports of therapeutic
response to ondansetron.
•
Selective serotonin reuptake inhibitor (SSRI) antidepres-
sants: Sertraline 25 mg OD and titrating to effect.
•
Opioid antagonists: specialist guidance is required as
opioid withdrawal may be provoked.
Jaundice
In cholestatic or obstructive jaundice, patients frequently
feel unwell, anorexic, and nauseated. Bile is essential for
digestion and absorption of fat, an essential fuel source.
They may develop symptoms of malabsorption. Active
palliation through decompression of the biliary system
(see endoluminal stents mentioned in the earlier section)
is the only effective treatment, if at all practical. The
approach can be through an ERCP or PTC, either as a day
case or a short stay in hospital. However, on many occa-
sions, decompression is not practically possible and there-
fore active palliation of the resulting symptoms with
medication needs to be aimed for.
Constipation
Constipation is a big problem for patients with advanced
disease. For instance more than 50% of patients admitted to
hospices in the United Kingdom complain of constipation
[38]. Physical illness, immobility, poor oral intake, opioids,
and many other drugs are risk factors for constipation.
Constipation can be prevented in the majority of patients
by prescription of appropriate laxatives and careful review.
Pain Management in Advanced Liver Disease
The dose of paracetamol should be reduced to a maximum
of 3g/24h for those with liver disease. Further dose reduction
is required if the patient’s weight is less than 50 kg.
Nonsteroidal anti-inflammatory drugs (NSAIDs) should be
avoided since their salt retention and other renal effects may
lead to decompensation in patients with cirrhosis.
All opioids require liver metabolism and may accumu-
late in liver impairment. There are also many other factors
that impact on the effects of opioids, for example, under-
lying diagnosis and speed of deterioration, presence of
ascites. There is no evidence base to inform prescribing
advice and we therefore suggest:
• Use reduced doses and consider increasing the dosing
interval.
•
Avoid drugs with long half-lives.
• Titrate slowly against effect.
• Re-evaluate daily.
Liver Transplantation Issues
Liver transplant is the gold standard treatment for
advanced chronic liver disease and fulminant hepatic
failure with a one-year survival of 80–90% and 5-year
survival of 60–80%. However, for various reasons not all
patients will be eligible for transplantation, and there is a
limited pool of donor grafts available. Four people will die
for every one transplanted.
For those who are not suitable for transplantation (e.g.
those with alcoholic cirrhosis who cannot cease drinking
or those whose performance status precludes transplanta-
tion) palliative care is the key focus of care. Even for those
who are suitable for transplantation and on the waiting
list, one in five will die. Appropriate symptom
management and assessment of quality of life needs
therefore to be considered for all those with advanced dis-
ease whether they are listed or not. This will include
support for patients and their families often at a time of
uncertainty and consideration of place of death when
patients are removed from the transplant list because of
deterioration.
Cholestatic Liver Disease
The key symptoms resulting from stasis of bile are pruritus
and jaundice.
Pruritus
The pruritic effect is mediated through a central mechanism,
a response to a rise in endogenous opioid levels. Large varia-
tions in individual response are seen and there is no
https://t.me/med1917
The Management of Gastrointestinal Symptoms and Advanced Liver Disease 155
If the rectum is empty and stool is high in the colon,
enemas should be administered through a rubber Foley
catheter. Oil enemas should be warmed before use.
Bulk-forming laxatives have a very limited place in the
management of constipation in patients with advanced
disease, since they are generally troublesome to take, rely
on a high oral fluid intake, and are not appropriate for the
management of opioid-induced constipation. All laxative
doses should be titrated according to response.
In 2008 methylnaltrexone (an opioid antagonist) was
licensed for use in the United States and Europe. This is
given subcutaneously and may be appropriate to consider
using when standard management of constipation has
failed in those patients with opioid-induced constipation.
Oral opioid antagonists such as naloxegol are now avail-
able for opioid-induced constipation too. Specialist advice
should be sought when considering the use of opioid
antagonists for constipation [39].
Rectal Problems of Advanced Cancer
The presence of tumour in the rectum may lead to bleeding,
faecal incontinence, and offensive discharge, in addition to
pain. The quality of life may be severely impaired. Such
problems occur not only in patients with primary rectal
cancers but also in patients with other pelvic cancers: cervix,
vagina, uterus, and bladder. Treatment options include:
• radiotherapy;
• palliative surgery with stoma formation;
• endoscopic injection of absolute alcohol;
• laser therapy and diathermy;
• metal stent alone or in combination with laser or
alcohol; and
•
pharmacological palliation.
The stool should be kept very soft to pass through the
obstructive lesion. Docusate sodium is given at a dose of
200 mg at least TDS but titrated to stool consistency; it can
be combined with a stimulant laxative. Careful insertion of
softening enemas may be useful.
Pain and Tenesmus
Pain from rectal cancer may be troublesome in a number
of ways; constant nociceptive, visceral and bone, which
may be worsened by movement. In some cases, sitting may
be impossible. The pain may be present only on, or wors-
ened by, either standing or defecation. Neuropathic pains
can result from infiltration of the lumbosacral plexus.
Some patients experience tenesmus: a painful sensation of
rectal fullness and an urge to defecate.
All patients prescribed a weak or strong opioid should
be advised to also take a stimulant laxative unless a contra-
indication exists. The dose of laxative will usually need to
be increased as the dose of opioid is increased. It is not
appropriate to wait until (predictable) constipation occurs
before commencing laxative treatment. The vicious cycle
of inappropriately treated abdominal pain and constipa-
tion should be anticipated in all patients with cancer, or
others taking opioid analgesics.
Management
Management will involve removing any underlying causes
if possible, prescribing an appropriate oral laxative and
considering the use of per rectal/stomal measures (see
Table 3). It should be remembered that one of the com-
monest reasons for failure of therapy is prescription of a
laxative that the patient dislikes.
Table 4 shows the various types of laxative that are avail-
able. Macrogols and sodium picosulfate are probably best
used as second-line laxatives for patients with established
constipation resistant to other laxatives. Lactulose may
cause substantial gaseous distension, especially in resistant
constipation.
Rectal laxatives may be needed and include:
•
Suppositories: glycerine (softening and mild stimulant);
bisacodyl (stimulant).
•
Enemas: arachis (peanut) oil (130 ml) (softening); phos-
phate, sodium citrate (stimulant).
Table 3 Treatment of constipation.
Examination finding Treatment
Rectum full of hard faeces Soften with glycerin
suppositories+/−arachis oil
enema. Commence combined
stimulant and softening oral
laxative
Rectum full of soft faeces Stimulate evacuation with
bisacodyl
suppository+/−stimulant
enema. Commence stimulant
oral laxative
Empty distended rectum Exclude obstruction.
Stimulant suppository or
enema will enhance colonic
contraction. Commence oral
laxative
https://t.me/med1917
156 Chapter 11
Stoma Care
Patients with stomas require both physical and psychological
support. Good preparation before stoma formation and
adequate time spent with the patient after stoma formation
by a specialist (stoma care) nurse help in the transition and
continued successful management. Patients vary in the time
needed to adapt to and manage their stoma.
The most common physical difficulties are:
• when a bowel stoma becomes overactive, often with a
more fluid faecal output;
•
when constipation occurs; and
• when patients are less able to manage their own stoma
care because of the effects of their treatment or their
disease.
Evaluation and management of these problems will involve
examination of the stoma and effluent, including a digital
examination of the stoma. There must also be a review of
skin protectives/adhesives and bag size, together with a
review of laxatives and antidiarrhoeal agents along with all
other drugs.
If a stoma is impacted, suppositories and enemas can be
given as for rectal impaction; however, a stoma has no
sphincter. Suppositories should be gently pushed through
the stoma as far as possible and gauze held over the stoma
for a few minutes. If an enema, either oil or phosphate, is
used it should be administered through a medium-sized
Foley catheter. This should be passed well into the stoma
(identify direction of the bowel by digital examination
beforehand). Inflate the balloon to 5 ml for 10 min while
instilling the enema.
Control of fluid loss from an overactive ileostomy can be
troublesome and specialist advice may need to be sought.
The WHO ladder (see Chapter 9) will be helpful for all
of these pain syndromes. Pain will be additionally helped
by keeping the faeces soft. For some patients, a palliative
colostomy will be the best form of pain relief.
Neuropathic pain, of which tenesmus is one type, may
be helped by opioids but will probably require adjuvant
analgesics such as amitriptyline 10–75 mg nocte. Tenesmus
may also be helped by:
• steroids – dexamethasone 4–16 mg daily;
• calcium channel antagonists – nifedipine 10–20 mg
BD-TDS (smooth muscle relaxant);
•
radiotherapy;
• bupivacaine enema;
• sacral epidural injection of steroid and local anaesthetic,
and
•
intrathecal 5% phenol to posterior sacral nerve roots.
Occasionally epidural infusion of opioids and local
anaesthetic may be appropriate for relief of pain at rest and
on defecation, particularly if the obstructive lesion is very
low in the bowel.
Rectal Bleeding and Discharge
While radiotherapy, alcohol injection, diathermy, or
laser therapy is being planned, or if these are not pos-
sible or helpful, other measures may be needed to
reduce the distress and discomfort from rectal
bleeding. Enemas may be performed using various
active ingredients, including: tranexamic acid (2–4 g/
day made up in KY jelly) [40]; and aluminium coating
through an enema (1% alum or sucralfate in KY jelly)
[41]. Distress or discomfort due to rectal discharge
may be alleviated by steroid enemas and metronida-
zole suppositories.
Table 4 Laxatives and their characteristics.
Laxative type Drugs Starting dose Latency of action
Stimulant Bisacodyl 10 mg nocte 6–12 h
Senna 15 mg nocte
Sodium picosulfate 5 ml nocte
Softening Docusate sodium 200 mg BD-TDS 1–2 days
Lactulose 15 ml BD
Macrogol 1 sachet daily in 125 ml water
https://t.me/med1917
The Management of Gastrointestinal Symptoms and Advanced Liver Disease 157
9. HM Government UK (2005). Mental Capacity Act. London:
The Stationary Office.
10. Bruera, E. and Sweeney, C. (2003). Pharmacological
interventions in cachexia and anorexia. In: Oxford Textbook of
Palliative Medicine, 3e (ed. D. Doyle, G.W.C. Hanks, N. Cherney,
and K. Calman), 552–560. Oxford: Oxford University Press.
11.
Ruiz Garcia, V., Lopez-Briz, E., Carbonell Sanchis, R., Gonzalvez
Perales, J.L., Bort-Marti, S. (2013). Bort-Marti S. Megestrol
acetate for treatment of anorexia-cachexia syndrome. Cochrane
Database of Systematic Reviews, Issue 3. CD004310. https://www.
cochranelibrary.com/cdsr/doi/10.1002/14651858.CD004310.
pub3/full
12.
Stratton, R.J. and Elia, M. (2007). A review of reviews: A new
look at the evidence for oral nutritional supplements in
clinical practice. Clinical Nutrition Supplements 2: 5–23.
13. Elia, M. (Chairman and ed.) (2000). Guidelines for detection
and management of malnutrition. Maidenhead: Malnutrition
Advisory Group (MAG), Standing committee of British
Association of Parenteral and Enteral Nutrition (BAPEN).
14.
National Institute for Clinical Excellence (2006). CG32
guidance for nutrition support in adults.
15. Royal College of Physicians (2010). Oral feeding difficulties
and dilemmas. A guide to practical care, particularly towards
the end of life. Report of a working party. Royal College of
Physicians.
16.
Mathus-Vliegen, E.M.H. (2000). Feeding tubes and
gastrostomy. In: Practice of Therapeutic Endoscopy (ed. G.N.J.
Tygat, M. Classen, J.D. Waye, and S. Nkazawa), Philadelphia,
PA: Saunders.
17.
NCEPOD (2004). Scoping our practice. The 2004 report of
the national confidential enquiry into patient outcome and
death. London: NCEPOD.
18.
Wilcock, A., Howard, P., and Charlesworth, S. (ed.). (2020).
Drug administration to patients with swallowing difficulties
or enteral feeding tubes. In: Palliative Care Formulary, 7e,
837–867. Nottingham: Pharmaceutical Press.
19.
Scannapieco, F.A. (2010). Pneumonia in nonambulatory
patients: The role of oral bacteria and oral hygiene. The
Journal of the American Dental Association 137: 21s–25s.
20. Bassim, C.W., Gibson, G., Ward, T. et al. Modification of the risk
of mortality from pneumonia with oral hygiene care. Journal of
the American Geriatrics Society 2008 56: 1601–1607.
21.
National Patient Safety Agency. (2010). Rapid response alert–
Early detection of complications after gastrostomy No.1214
NPSA/2010/RRR010.
22. Petrina Sweeney, M. and Bagg, J. (2000). The mouth and
palliative care. American Journal of Hospice and Palliative
Medicine 17: 118–124.
23.
Muscaritoli, M., Arends, J., Bachmann, P. et al. (2021). ESPEN
practical guideline: Clinical Nutrition in cancer. Clin Nutr
40(5): 2898–2913.
24. Davies, A. and Finlay, I. (eds.) (2005). Oral Care in Advanced
Disease, 97–114. Oxford: Oxford University Press.
25. Harris, D.G. (2010). Nausea and vomiting in advanced cancer.
British Medical Bulletin 96: 175–185.
Various treatments are available. The administration of
opioids can reduce bowel motility; for example, loper-
amide 4–8 mg BD or codeine phosphate 30–60 mg QDS If
the patient is already taking morphine for pain relief, an
increase in this may reduce bowel motility further but will
also increase sedation and other central effects, and is not
the preferred option unless it is also useful to improve pain
control. A reduction of bowel motility and secretions may
be achieved by use of anticholinergics, for example, hyo-
scine butylbromide SC 60–200 mg/24 h, while H
2
antago-
nists or PPIs can reduce gastric secretions.
Ispaghula (1–2 sachets TDS) aids thickening of the
motions, as does the use of isotonic and avoidance of hypo-
tonic oral fluids. Marshmallows may also help increase
stool consistency. An SC infusion of octreotide can reduce
small bowel secretions (see previous section). However,
doses required can be much greater than in treating
obstruction.
The principles of management of a stoma and stomacare
equipment can also be used to contain the output from fae-
cal fistulae and protect the skin. SC octreotide has been
used to decrease the volume of fistula effluent and in some
cases has aided healing.
References
1. Roth, K., Lynn, J., Zhong, Z. et al. (2000). Dying with end
stage liver disease with cirrhosis: Insights from SUPPORT.
Study to understand prognoses and preferences for outcomes
and risks of treatment. Journal of the American Geriatrics
Society 48 (5 Suppl): S122–S130.
2.
Hansen, L., Saaski, A., and Zucker, B. (2010). End-stage liver
disease: Challenges and practice implications. Nursing Clinics
of North America 45: 411–426.
3.
Dewys, W.D., Begg, D., Lavin, P.T. et al. (1980). Prognostic
effect of weight loss prior to chemotherapy in cancer patients.
American Journal of Medicine 69: 491–496.
4.
Wagner, P.D. (2008). Possible mechanisms underlying the
development of cachexia in COPD. European Respiratory
Journal 31: 492–501.
5. Anker, S.D., Negassa, A., Coats, A.J. et al. (2003). Prognostic
importance of weight loss in chronic heart failure and the
effect of treatment with angiotensin-converting-enzyme
inhibitors: An observational study. Lancet 361: 1077–1083.
6. Plauth, M. and Schutz, E.T. (2002). Cachexia in liver cirrhosis.
International Journal of Cardiology 85: 83–87.
7. Grunfield, C. (1995). What causes wasting in AIDS? NEJM
333: 123–124.
8. General medical Council (2010). Treatment and Care Towards
the End of Life: Good Practice in Decision Making. London:
GMC.
https://t.me/med1917