The patient with gastrointestinal disease
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Transcript of The patient with gastrointestinal disease
PERIOPERATIVE MANAGEMENT OF CO-MORBID CONDITIONS
The patient withgastrointestinal diseaseJohn McKenna
Chris Sadler
AbstractThe gastrointestinal system is responsible for digestion of food, absorp-
tion of nutrients and excretion of waste. It consists of the mouth, oesoph-
agus, stomach, small intestine, large intestine, liver, gall bladder and
pancreas. Many patients managed by surgical teams will suffer from
some form of gastrointestinal disease.
To aid with the management of these patients we will look at a logical,
systemic approach to the assessment of gastrointestinal disease and
common signs and symptoms found. We will discuss the investigation
of gastrointestinal disease and the common abnormalities found.
This article will then discuss in further detail the perioperative
management of some common gastrointestinal problems, namely fluid
therapy, nutrition, gastrointestinal bleeding, hepatic dysfunction, bowel
obstruction, inflammatory bowel disease and pancreatitis.
Keywords Assessment; bleeding; fluid therapy; gastrointestinal;
inflammatory bowel disease; investigation; management; nutrition;
obstruction; pancreatitis; perioperative
Introduction
Many patients present to the surgical team with a primary
gastrointestinal complaint, or have coexisting gastrointestinal
problems that complicate their perioperative management. This
article will cover the clinical assessment and investigation of
these patients, and the management of some common gastroin-
testinal presentations.
Broadly, the function of the gastrointestinal system is to digest
and absorb nutrients to support the functions of the body. It is
also involved in excretion of waste from the body. Therefore
dysfunction of the gastrointestinal system can affect many of the
body’s organ systems.
Assessment of the patient with gastrointestinal disease
It is important to have a logical and systemic approach to
assessment.
Airway and breathing
� Check airway patency and look for soiling or obstruction,
especially from vomit and blood.
John McKenna MBBS FRCA is a Specialist Registrar in Anaesthetics at
Barts & The London School of Anaesthesia, London, UK. Conflicts of
interest: none declared.
Chris Sadler MBBS FRCA PhD is a Consultant Anaesthetist at Barts & The
London NHS Trust, London, UK. Conflicts of interest: none declared.
SURGERY 28:9 437
� Check that the patient is able to swallow as this could lead to
airway compromise.
� Examine the mouth. Poor dentition may reflect nutritional
status and oral infection is a potential source of sepsis.
� Examine the chest, and measure the respiratory rate and
peripheral oxygen saturation.
Any condition causing the airway to fill with fluid such as
vomiting or an upper gastrointestinal bleed can cause potential
airway compromise. Pulmonary aspiration may occur as
a consequence of reflux or vomiting. It may present early as
respiratory distress, or late as pneumonia if aspiration is silent.
Increased intra-abdominal pressure can cause splinting of the
diaphragm. This can lead to basal atelectasis and hypoxia
secondary to ventilation and perfusion mismatch. Deficiencies in
nutrition lead to muscular weakness that, if severe, can weaken
the muscles of respiration. Fluid shifts, as a consequence of
sepsis, liver dysfunction or nutritional status may lead to capil-
lary leak, ascites and pulmonary oedema.
Circulation
� Assess the cardiovascular system, with particular regard to
fluid status.
� Record blood pressure, heart rate, and capillary refill time.
Hypovolaemia can be due to either inadequate intake, distribu-
tion of fluid outside the vascular compartment, or excessive
losses. Cardiac conduction and contractility can be adversely
affected by nutritional deficiencies and electrolyte disturbances,
in particular hypokalaemia or hyperkalaemia. Anaemia may be
secondary to haemorrhage or dietary haematinic deficiency.
Abdominal compartment syndrome can lead to cardiovascular
collapse due to compression of the major abdominal blood
vessels. This may be seen postoperatively in an intensive therapy
unit (ITU) setting.
Neurological
� Basic assessment of conscious level e Alert, Verbal, Pain,
Unresponsive (AVPU) score or Glasgow Coma Scale (GCS) e
is necessary.
� A Mini Mental State Examination (MMSE) and a full neuro-
logical examination may aid diagnosis.
Both acute and chronic alcohol use lead to neurological symp-
toms, ranging from acute intoxication to delirium tremens in the
withdrawing patient. Dietary thiamine deficiency may produce
the WernickeeKorsakoff syndrome. Chronic liver disease causes
accumulation of toxic metabolites, leading to encephalopathy.
Gastrointestinal
� Full assessment from mouth to anus.
� Bodymass index (BMI)may indicatenutritional status (Table 1).
Excessive vomiting can be indicative of gastrointestinal
obstruction and should also raise suspicion of dehydration.
Constipation, diarrhoea and altered bowel habit are significant
symptoms and may be associated with massive fluid losses.
Obesity may be associated with obstructive sleep apnoea, dia-
betes, and ischaemic heart disease. Jaundice may be pre-hepatic
(e.g. haemolytic diseases), hepatic (e.g. hepatitis) or post-hepatic
(e.g. biliary obstruction) in origin. Jaundice can lead to brain
damage in neonates, and intense itching if secondary to biliary
obstruction.
� 2010 Published by Elsevier Ltd.
World Health Organization classification of BMI1
Classification Body mass index (kg/m2)
Underweight <18.50
Normal range 18.50e24.99
Overweight >25.00
Obese >30.00
Table 1
PERIOPERATIVE MANAGEMENT OF CO-MORBID CONDITIONS
Renal
� Assessment of fluid status is vital. Look for skin appearance,
turgor and cardiovascular parameters.
� Consider fluid balance monitoring. Oliguria is a good indi-
cator of a dehydrated patient. Dipstick the urine.
Dehydration cannot be overemphasized in these patients. Hypo-
volaemia leads to hypoperfusion of the kidneys, which can lead to
acute renal failure. Renal calculi can be formed or exacerbated by
dehydration. Patients with advanced hepatic disease can develop
hepatorenal syndrome. This is caused by renal vascular vaso-
constriction in response to hepatic mediated hypotension.
Infection and immunity
� Examine the patient for any signs of infection e fever,
rigours.
� Record temperature.
Investigations in patients with gastrointestinal disease (adap
Full blood count Guides transfusion requirements.
Characterize anaemia.
Aid diagnosis of sepsis.
Urea and electrolytes Vomiting can lead to loss of potassium, sod
Serum urea rises in an upper gastrointestin
Hypocalcaemia due to reduced dietary intak
Iatrogenic disturbances caused by inapprop
Coagulation Liver dysfunction causes a prolongation in p
due to reduced production of clotting facto
Liver function tests Aspartate transaminase (AST) and alanine t
Alkaline phosphatase (ALP) raised in choles
Gamma glutamyl transferase (gGT) is induce
Microbiology If infection is suspected, blood and stool cu
Viral markers are important in establishing
Electrocardiogram Conduction problems caused by electrolyte
Peaked T waves suggest hyperkalaemia.
Radiology Air under the diaphragm on a plain erect ch
Patterns of intestinal gas on abdominal film
Ultrasound provides excellent images of sol
and may be used to identify ascites.
Computed tomography is useful in intra-abd
Endoscopy May be diagnostic or therapeutic.
Table 2
SURGERY 28:9 438
Perforation of the gut can cause faecal peritonitis. Patients with
jaundiceor liverdysfunctionshouldbe investigated forviralhepatitis.
Food-borne infection leading to gastroenteritis is a common presen-
tation. Immune function can be compromised in malnutrition and
hepatic dysfunction.Bacterial translocationoccurswhen the integrity
of the gut is compromised. Gut flora can reach the bloodstream
causing a bacteraemia. Obesity is a risk factor for wound infection.
Investigations
Investigations are summarized in Table 2.
Arterial blood gas analysis provides information about
pulmonary gas exchange and acidebase status (Table 3).
Perioperative management of gastrointestinal problems
Fluid therapy
When a patient is kept ‘nil by mouth’ in preparation for surgery
or because of gastrointestinal disease, the clinician is responsible
for maintaining fluid balance. The approach to fluid therapy
should include clinical assessment of hydration, calculation of
fluid deficit, maintenance requirements, replacing ongoing los-
ses, and monitoring response to fluid therapy (Figure 1).
Maintenance fluid requirements should be based on body
weight (Table 4). Maintenance requirements in a 70 kg patient
are (1000 þ 500 þ 1250) 2750 ml/day.
Ongoing losses (e.g. haemorrhage, diarrhoea, vomiting and
third space loss) must be quantified and replaced. Evaporative
fluid losses during laparotomy may exceed 15 ml/kg/hour.
ted from Allman and Wilson2)
ium, chloride and hydrogen ions.
al bleed due to digestion of blood in the stomach.
e of calcium or vitamin D.
riate fluid therapy.
rothrombin time (PT) or activated partial thromboplastin time (APTT)
rs.
ransaminase (ALT) released when hepatocytes are damaged.
tasis.
d by certain drugs and, notably, ethyl alcohol.
ltures should be sent to identify a causative organism.
a cause for liver disease.
disturbances.
est X-ray is suggestive of intestinal perforation.
s can be used to diagnose bowel obstruction.
id intra-abdominal organs such as the liver and gall bladder,
ominal trauma and suspected intra-abdominal sepsis.
� 2010 Published by Elsevier Ltd.
Acidebase disturbances in gastrointestinal disease
Condition Acidebase disturbance Cause
Diarrhoea Metabolic acidosis Bicarbonate loss
Pancreatic fistulae Metabolic acidosis Bicarbonate loss
Acute alcohol
intoxication
Metabolic acidosis Toxins metabolized
to acids
Ileostomy Metabolic acidosis Bicarbonate loss
Pyloric stenosis Metabolic alkalosis Hydrogen ion loss
Excessive vomiting Metabolic alkalosis Hydrogen ion loss
Table 3
Fluid requirements according to patient weight
Weight Fluid requirement (ml/kg/day)
First 10 kg (i.e. 1e10 kg) 100
Second 10 kg (i.e. 11e20 kg) 50
Each kg >20 kg 25
Table 4
PERIOPERATIVE MANAGEMENT OF CO-MORBID CONDITIONS
Fluid therapy is a dynamic process and it is important to
monitor response to fluids administered. With an appropriate
response to fluid, tachycardia should settle, blood pressure will
normalize, urine output should be >0.5 ml/kg/hour and, if
available, a sustained rise in central venous pressure (0e8
mmHg). Serum urea and electrolytes should be monitored, as
disturbances are common. For example, overuse of 5% dextrose
can lead to hyponatraemia, and overuse of normal (0.9%) saline
can lead to a hyperchloraemic metabolic acidosis.
The choice of fluid remains the subject of debate. Fluid
therapy should target the fluid compartment (intravascular,
extracellular, intracellular) that is depleted (Table 5).
Nutritional support
Catabolism is the normal response to sepsis, trauma and surgery.
Catabolic patients have higher energy requirements than normal
patients, and need their nutritional intake supplemented
accordingly. While it is preferable to achieve these nutritional
requirements by oral intake of normal diet, alternatives to oral
nutrition may be required.
Enteral feeding is preferred to parenteral feeding as it is more
physiological, maintains enterocyte integrity and reduces bacte-
rial translocation from the gut to the bloodstream. If the oral
route is unavailable, for example due to high aspiration risk, feed
can be administered via a nasogastric tube (NGT). For longer
term enteral feeding a gastrostomy or jejunostomy can be sited.
Parenteral nutrition, via a central vein, is considered when
gastrointestinal motility or absorption is impaired. Parenteral
Percentage fluid loss Signs and symptoms
5% Thirst
Peripheral shutdownTachycardiaReduced skin turgorOliguria
10%Tachypnoea HypotensionConfusionAnuria
15%Life threatening
Clinical signs of fluid loss2
Figure 1
SURGERY 28:9 439
nutrition carries more risks than enteral nutrition, namely
metabolic disturbances, hyperlipidaemia, and deficiencies in
trace elements. The fluids used for parenteral nutrition are an
excellent culture medium and great care is required to prevent
septicaemia.
Gastrointestinal bleeding
Upper gastrointestinal haemorrhage can occur anywhere from
the pharynx to the ligament of Treitz. It is characterized by
haematemesis, coffee ground vomitus and malaena. Upper
gastrointestinal haemorrhage may be amenable to endoscopic
therapy. Certain lesions can be treated with sclerotherapy or
injection of adrenaline. Variceal lesions can be banded. Full
anaesthetic precautions and monitoring are required for endos-
copy under sedation. Pharmacological management includes
proton pump inhibitors, and octreotide and terlipressin to reduce
splanchnic perfusion.
Lower gastrointestinal haemorrhage can occur anywhere from
the ligament of Treitz to the anus and is characterized by malaena
or fresh blood per rectum. Lower gastrointestinal haemorrhage
can be caused by diverticular disease, colitis and malignancy.
Hepatic dysfunction
Hepatic failure can be acute or chronic, and unless absolutely
necessary, those with acute hepatic failure should have their
operation postponed due to an increase risk of mortality.
Common causes include infection (hepatitis A-E) and toxins
(alcohol, paracetamol). In addition to having altered drug
metabolism, patients with hepatic dysfunction are at increased
risk of coagulopathic haemorrhage, hypoglycaemia, infection
and encephalopathy (Table 6).
Gastrointestinal obstruction
Gastrointestinal obstruction may be mechanical (e.g. foreign
body, malignancy, adhesions, strictures) or functional (e.g.
ileus). These patients frequently present for emergency surgery if
obstruction is prolonged or the gut is ischaemic. The clinical
picture will give clues to the site of the obstruction. Oesophageal
obstruction presents with dysphagia, odynophagia, regurgitation,
malnutrition and dehydration. Small bowel obstruction presents
Choice of fluid
Compartment Fluid
Intravascular Colloid (gelatin, starch, albumin), blood
Extracellular Electrolyte crystalloid (saline, Hartmann’s)
Intracellular Dextrose 5%
Table 5
� 2010 Published by Elsevier Ltd.
ChildePugh Score3
Measurement 1 point 2 points 3 points
Bilirubin (mmol/litre) <34 34e50 >50
Albumin (g/litre) >35 28e35 >28
International
normalized ratio
<1.7 1.71e2.20 >2.20
Ascites None Mild Severe
Hepatic
encephalopathy
None Grades IeII (drowsy
0 disorientated)
Grades IIIeIV
(stupor 0 coma)
Class Points 2-year survival (%)
A 5e6 85
B 7e9 57
C 10e15 35
Table 6
Ranson criteria.4 Each category carries 1 point
On admission After 48 hours
Age >55 years Serum calcium <2 mmol/litre
Leukocyte count >16 � 109/litre Fall in
haematocrit
>10%
Serum glucose >11.1 mmol/litre Rise in urea >1.8 mmol/litre
AST >250 IU/litre Base deficit >4 mmol/litre
LDH >350 IU/litre Artrial pO2 <60 mmHg
Fluid
sequestration
>6000 ml
Score <2 3e4 4e6 7e8
Mortality (%) 2 15 40 100
AST, aspartate transaminase; LDH, lactate dehydrogenase.
Table 7
PERIOPERATIVE MANAGEMENT OF CO-MORBID CONDITIONS
with early vomiting and colicky central abdominal pain. In large
bowel obstruction, constipation and lower abdominal pain are
more prominent features.
The principal complications of gastrointestinal obstruction are
eventual perforation and peritonitis, malnutrition and impaired
fluid balance. Fluid can be lost in vomit, or sequestered into the
bowel lumen. Up to 6 litres of fluid can be lost into the bowel in
severe small bowel obstruction; therefore adequate fluid resus-
citation is essential. Patients with severe vomiting are at risk of
aspiration and significant hypokalaemia.
Inflammatory bowel disease
Ulcerative colitis is restricted to the gut mucosa and affects the
colon and anus. Crohn’s disease can occur anywhere from the
mouth to the anus and affects the whole gut wall. Patients
typically present with fever, vomiting, abdominal pain, diar-
rhoea, and rectal bleeding during an acute exacerbation.
Inflammatory bowel disease may be associated with arthropathy,
anaemia, primary sclerosing cholangitis, uveitis and a pro-
thrombotic tendency.
Non-surgical management includes general supportive
measures (fluids, analgesia, etc.) and immunosuppression with
corticosteroids, methotrexate and azathioprine. Immunosup-
pression places patients at increased risk of infection risk and
may mask the symptoms and signs of gastrointestinal perforation
and peritonitis. Long-term steroid therapy may cause Cushing’s
syndrome and Addisonian crisis following abrupt withdrawal.
Methotrexate can cause neutropenia and is teratogenic. Surgery
is restricted to patients who have failed to respond to medical
treatment and those who have developed complications, such as
stricture, perforation, haemorrhage, abscess or fistula.
SURGERY 28:9 440
Pancreatitis
The severity of acute pancreatitis can be assessed in a variety of
ways based on biochemical, haematological, clinical (Glasgow &
Ranson) and radiological (Balthazar) criteria. The purpose of
scoring is to predict mortality and morbidity (Table 7).
Conclusion
Patients with gastrointestinal disease can be challenging to
manage in the perioperative period. Thorough assessment and
attention to simple problems, such as fluid balance, nutrition and
analgesia can greatly improve patient outcome. A
REFERENCES
1 World Health Organization Body Mass Index Classification. http://apps.
who.int/bmi/index.jsp?introPage¼intro_3.html.
2 Allman K, Wilson I. Oxford handbook of anaesthesia. 2nd edn. Oxford:
Oxford University Press, 2006.
3 Pugh RN, Murray-Lyon IM, Dawson JL, Pietroni MC, Williams R. Tran-
section of the oesophagus for bleeding oesophageal varices. Br J Surg
1973; 60: 646e9.
4 Ranson JH, Rifkind KM, Roses DF, Fink SD, Eng K, Spencer FC.
Prognostic signs and the role of operative management in acute
pancreatitis. Surg Gynecol Obstet 1974; 139: 69e81.
CROSS-REFERENCE
Peterson M, Thomas WEG. Gastrointestinal haemorrhage. Surgery 2008;
26: 113e9.
FURTHER READING
Rassam SS, Counsell DJ. Perioperative fluid therapy. BJA CEPD Rev 2005;
5: 161e5.
� 2010 Published by Elsevier Ltd.