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Gastrointestinal care 

Gastrointestinal care
Gastrointestinal care

Heather Baid

, Fiona Creed

, and Jessica Hargreaves

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date: 18 May 2021

Gastrointestinal assessment

If an actual or potential gastrointestinal abnormality has been identified during a general ABCDE assessment (see Gastrointestinal care p. [link]) or while monitoring the patient, a more detailed and focused gastrointestinal assessment can provide further information to guide clinical management.

Focused health history

Subjective information about the gastrointestinal history can be taken from the patient if they are awake, or from other sources (e.g. family, caregivers, or the patient’s notes). See Gastrointestinal care p. [link] for an overview of history taking.

Gastrointestinal symptom enquiry

  • Diet, indigestion, swallowing ability.

  • Appetite, weight loss, weight gain.

  • Nausea and vomiting.

  • Diarrhoea, constipation, melaena.

  • Abdominal pain.

Focused physical assessment

  • Obvious signs of discomfort or distress.

  • Inability to lie flat or cough due to abdominal pain.

  • Nutritional assessment (see Gastrointestinal care p. [link]).

  • Fluid assessment (see Gastrointestinal care p. [link]).

  • Bowel assessment (see Gastrointestinal care p. [link]).

  • Gastrointestinal-focused assessment of the face and abdomen (see Table 10.1).

Figure 10.3 Bristol Stool Chart.

Figure 10.3 Bristol Stool Chart.

(Reproduced by kind permission of Dr. K. W. Heaton, Reader in Medicine at the University of Bristol © 2000 Norgine Pharmaceuticals Ltd.)

Table 10.1 Gastrointestinal-focused assessment




  • Pink, moist mucous membranes

  • White sclera

  • Symmetrical, non-distended abdomen

  • Pallor

  • Jaundice

  • Dry mucous membranes

  • Abdominal distension

  • Abdominal asymmetry

  • Abdominal wounds, drains, scarring, bruising


  • Soft abdomen

  • Non-tender abdomen

  • Firm abdomen

  • Painful abdomen

  • Mass


Tympanic abdominal percussion note

Dullness on abdominal percussion


Bowel sounds present

  • Absent bowel sounds

  • Hypoactive bowel sounds

  • High-pitched, tinkling bowel sounds

Some authors suggest that auscultation should be performed prior to palpation, while others recognize that bowel sounds may not be a reliable assessment finding, due to normal sounds occurring with an abnormal abdomen, and vice versa.1

Abdominal landmarking

Any abnormal findings found during the health history and physical assessment should be documented and reported according to the specific quadrant of the abdomen in which the abnormality was identified (see Figure 10.1).

Figure 10.1 Abdominal quadrants. RUQ, right upper quadrant; LUQ, left upper quadrant; RLQ, right lower quadrant; LLQ, left lower quadrant.

Figure 10.1 Abdominal quadrants. RUQ, right upper quadrant; LUQ, left upper quadrant; RLQ, right lower quadrant; LLQ, left lower quadrant.

(Reproduced from Randle, Coffey, Bradbury, Oxford Handbook of Clinical Skills in Adult Nursing, 2009, with permission from Oxford University Press.)

Causes of key abnormalities

  • Jaundice—liver failure, gallstones.

  • Abdominal distension—ascites, bowel obstruction, bleeding, sepsis, air (e.g. due to non-invasive ventilation without a nasogastric tube).

  • Abdominal pain—abnormality of underlying structure (see Figure 10.1).

  • Dullness on percussion—fluid, mass, faeces.

  • Absent bowel sounds—bowel obstruction.

  • Hypoactive bowel sounds—bowel obstruction, opioids.

  • High-pitched, tinkling bowel sounds—partial bowel obstruction.

Laboratory investigations

Blood tests which are relevant to check in a gastrointestinal review include:

  • FBC and CRP

  • U&E

  • LFTs

  • amylase and lipase.


1 Baid H. A critical review of auscultating bowel sounds. British Journal of Nursing 2009; 18: 1125–9.Find this resource:

Further reading

Cox C and Stegall M. A step-by-step guide to performing a complete abdominal examination. Gastrointestinal Nursing 2009; 1: 10–17.Find this resource:

Stayt L, Randle J and Coffey F. Gastrointestinal system. In: J Randle, F Coffey and M Bradbury (eds) Oxford Handbook of Clinical Skills in Adult Nursing. Oxford University Press: Oxford, 2009. pp. 397–454.Find this resource:

Gastrointestinal monitoring

Gastric residual assessment

Gastric residual contents should be monitored regularly according to local protocol until enteral feeding has been established, or if significant abnormality of the gastrointestinal system is noted (see Gastrointestinal care p. [link]).

Gastric contents are observed for colour, consistency, and amount by aspirating fluid back from a large-bore oral or nasogastric tube. If the patient vomits, the same type of assessment can take place while observing the emesis. Table 10.2 provides an overview of normal and abnormal gastric content findings.

Table 10.2 Normal and abnormal gastric fluid content

Normal gastric content

Abnormal gastric content

Acceptable gastric residual volumes

High gastric residual volumes

(see Gastrointestinal care p. [link])

Fresh blood

Normal gastric fluid colour

Coffee-grounds appearance

pH < 5.5

Faecal smell

Intra-abdominal pressure

The pressure within the abdominal cavity can be estimated by obtaining a pressure measurement in the bladder. This is achieved by using either a Foley manometer or a Foley catheter which can be connected to a transducer (see Figure 10.2).

Figure 10.2 Intra-abdominal pressure monitoring: foley catheter transducer. (Drawing by Mark Gregory.)

Figure 10.2 Intra-abdominal pressure monitoring: foley catheter transducer. (Drawing by Mark Gregory.)

Intra-abdominal pressure (IAP) monitoring is indicated if the abdomen becomes distended, firm, or there is a risk of abdominal compartment syndrome (see Gastrointestinal care p. [link]). Normal and abnormal IAP values are listed in Box 10.1. High-pressure readings are most likely to be clinically significant if they show an upward trend within the context of other abnormal signs and symptoms indicating gastrointestinal dysfunction.

Further reading

Delgado LA. Abdominal compartment syndrome: a guide for the gastrointestinal nurse. Gastrointestinal Nursing 2013; 11: 42–8.Find this resource:

Desie et al. Intra-abdominal pressure measurement using the FoleyManometer does not increase the risk for urinary tract infection in critically ill patients. Annals of Intensive Care 2012; 2 (Suppl. 1 ): S10.Find this resource:

Lee RK. Intra-abdominal hypertension and abdominal compartment syndrome: a comprehensive overview. Critical Care Nurse 2012; 32: 19–31.Find this resource:



Gastrointestinal dysfunction resulting in large amounts of frequent loose stools is commonly found in critically ill patients. Strategies for preventing diarrhoea include strict infection control precautions (see Gastrointestinal care p. [link]), appropriate use of antibiotics, and early enteral nutrition to maintain integrity of the gut mucosa.


Table 10.3 summarizes the infective and non-infective causes of diarrhoea. Medications with the potential to cause diarrhoea include antibiotics, laxatives (if overused), and sorbitol-containing drugs.

Table 10.3 Causes of diarrhoea

Infective causes

Non-infective causes

  • Clostridium difficile

  • E. coli

  • Salmonella

  • Tropical diseases

  • Medications

  • Enteral feeding

  • Malabsorption

  • Inflammatory bowel disease

  • Diverticulitis

  • Overflow with faecal impaction

Assessment findings

  • More than 3 stools a day.

  • Watery, loose stools.

  • Bristol Stool Chart—type 5, 6, or 7 (see Figure 10.3).

  • Stool weight > 200 g/day.


  • Protect the skin from excoriation by means of:

    • careful washing

    • barrier cream or spray

    • a bowel management system (flexible rectal catheter with balloon seal and collection bag).

  • Monitor electrolytes and treat imbalances.

  • Monitor fluid status and treat fluid deficit (see Gastrointestinal care p. [link]).

  • Review current medications and discontinue laxatives or other diarrhoea-inducing drugs that are not essential.

  • Perform a rectal examination to rule out faecal impaction with overflow.

  • Obtain stool specimens for:

    • MC&S (send three samples)

    • Clostridium difficile toxin.

  • Consider fibre-containing enteral feeds and probiotic additives.

  • Provide appropriate antibiotic treatment if culture and isolation identify a bacterial cause (e.g. metronidazole or vancomycin for C. difficile).

  • Take an abdominal X-ray if ischaemic or inflammatory bowel disease is suspected (or if there is bloody diarrhoea).

  • Consider semi-elemental feeds if malabsorption is suspected.

  • Use anti-motility agents (e.g. loperamide or co-phenotrope).



The definition of constipation is subjective, but is usually considered to be more than 3 days without a bowel movement. However, in patients who are fed parenterally there may be minimal gastrointestinal content and waste for excretion, and expected bowel movements may be less frequent. Constipation occurs in up to 70% of critically ill patients, and early initiation of enteral nutrition is associated with improved bowel function of mechanically ventilated patients.2


  • Opiates.

  • Immobility.

  • Dehydration.

  • Vasoconstrictors.

  • Hypoperfusion of the gastrointestinal tract.

Assessment findings

  • More than 3 days without a bowel movement.

  • Bristol Stool Chart—type 1 or 23 (see Figure 10.3).

  • Abdominal palpation—distension, firm or palpable faecal matter.


  • Identify the patient’s normal frequency of bowel movements.

  • Daily assessment and documentation of bowel function, including:

    • number of days since a bowel movement has occurred

    • stool assessment for all bowel movements (see Gastrointestinal care p. [link]).

  • Monitor fluid status and treat fluid deficit (see Gastrointestinal care p. [link]).

  • If the patient is enterally fed, switch to fibre-containing feed.

  • Perform a rectal examination to assess for stool in the rectum.

  • Follow local bowel management protocol, including:

    • laxatives (see Table 10.4)

    • glycerine suppository

    • enema.

  • Perform manual evacuation for faecal impaction if other interventions fail to result in a bowel movement.

Table 10.4 Laxatives




Bulk-forming laxatives

Soluble fibres draw water into the gut and add bulk to the stool

Psyllium, bran, methylcellulose

Stimulant laxatives

Act by irritating and increasing the motility of the gut

Senna, docusate sodium, bisacodyl

Faecal softeners

Ease the passage of the stool by altering consistency

Liquid paraffin, seed oils

Osmotic laxatives

Draw water into the colon and increase volume and water content of stool

Lactulose, phosphate enema


2 Nassar AP Jr, da Silva FM and de Cleva R. Constipation in intensive care unit: incidence and risk factors. Journal of Critical Care 2009; 24: 630.e9–12.Find this resource:

3 Lewis SJ and Heaton KW. Stool form scale as a useful guide to intestinal transit time. Scandinavian Journal of Gastroenterology 1997; 32: 920–24.Find this resource:

Further reading

Bayón García C et al. Expert recommendations for managing acute faecal incontinence with diarrhoea in the intensive care unit. Journal of the Intensive Care Society 2013; 14 (Supp l.): 1–9.Find this resource:

McPeake J, Gilmour H and MacIntosh G. The implementation of a bowel management protocol in an adult intensive care unit. Nursing in Critical Care 2011; 16: 235–42.Find this resource:

Masri Y, Abubaker J and Ahmed R. Prophylactic use of laxative for constipation in critically ill patients. Annals of Thoracic Medicine 2010; 5: 228–31.Find this resource:



When gastrointestinal motility becomes delayed, stomach contents accumulate, leading to abdominal distension, a high gastric residual volume (GRV), and the potential for vomiting and aspiration pneumonia to develop. Even patients with cuffed tracheal tubes are not completely protected from the risk of aspiration, as it is still possible for gastric contents to be aspirated past the cuff.

Normal gastrointestinal motility is indicated if a patient is tolerating enteral feeding which is confirmed by checking the GRV aspirated from a large-bore oro- or nasogastric tube. It is common practice to consider a GRV of up to 200–250 mL to be an indicator that enteral nutrition is being absorbed, although the REGANE study4 concluded that a GRV of up to 500 mL may be a more appropriate threshold value. Another trial by Reignier and colleagues5 indicated that mechanically ventilated patients in whom GRV was not checked were no more likely to develop ventilator-associated pneumonia than patients who received routine care. However, the findings of these studies may not be generalizable, particularly for surgical and severely ill patients. Until the debate about best practice for assessing and acting upon hypomotility of critical care patients has been clarified by further research, local interpretation of what constitutes a high GRV and local enteral feeding protocols should be followed.6 Figure 10.4 shows a general template for the management of high GRVs.

Figure 10.4 Management of high gastric residual volumes.

Figure 10.4 Management of high gastric residual volumes.


  • Medications—opiates, catecholamines, β‎-2 agonists.

  • Post-operative ileus.

  • Sepsis.

  • Trauma.

  • Increased ICP.

  • Gastrointestinal ischaemia.

  • Cellular cytokines and kinases released during reperfusion injury.

  • Release of endotoxin or corticotropin (a stress response agent).

Assessment findings

  • High GRV—as defined by local protocol, which typically considers a GRV of > a number between 200 and 500 mL to be high.

  • Vomiting.

  • Abdominal distension.

  • Hypoactive or absent bowel sounds.


  • Monitor GRV according to local protocol.

  • Continue low-volume enteral feeding.

  • Semi-recumbent positioning (head-up angle of 35–45°).

  • Prokinetics—metoclopramide, erythromycin.

  • Post-pyloric feeding.


4 Montejo J et al. Gastric residual volume during enteral nutrition in ICU patients: the REGANE study. Intensive Care Medicine 2010; 36: 1386–93.Find this resource:

5 Reignier J et al. Effect of not monitoring residual gastric volume on risk of ventilator-associated pneumonia in adults receiving mechanical ventilation and early enteral feeding: a randomized control trial. Journal of the American Medical Association 2013; 309: 249–56.Find this resource:

6 Heyland D and Dhaliwal R. Measuring Gastric Residual Volumes in Enterally Tube Fed Critically Ill Patients: the end of an era? Gastrointestinal

Further reading

Ukleja A. Altered GI motility in critically ill patients: current understanding of pathophysiology, clinical impact, and diagnostic approach. Nutrition in Clinical Practice 2010; 25: 16–25.Find this resource:



Vomiting is a high-risk event for a critically ill patient and should be responded to immediately in order to prevent aspiration of gastric contents into the lungs. Box 10.2 lists the aspiration risk factors for a patient who has vomited.


  • Ileus.

  • Bowel obstruction.

  • Side effect of medication.

  • Chemical irritants.

  • Neurological event (e.g. raised ICP).

  • Gastroenteritis.

  • Pancreatitis.


  • Mouth and pharyngeal suctioning if there is a reduced level of consciousness or poor cough or gag reflex.

  • Endotracheal suction if the patient is intubated.

  • Turn off enteral feed.

  • Aspiration with large-bore oro- or nasogastric tube, and leave on free drainage.

  • Anti-emetics (e.g. metoclopramide, cyclizine, prochlorperazine, or ondansetron).

  • Semi-recumbent positioning (head-up angle of 35–45°).

  • Monitor electrolytes and treat imbalances.

  • Monitor fluid status and treat fluid deficit (see Gastrointestinal care p. [link]).

  • Review enteral feeding regime with doctor and dietitian.

  • Provide mouth care.

Further reading

Collins AS. Postoperative nausea and vomiting in adults: implications for critical care. Critical Care Nurse 2011; 31: 36–45.Find this resource:

Acute abdomen


The phrase ‘acute abdomen’ is used to describe the rapid onset of clinically significant abdominal abnormalities when the underpinning problem is still unknown. There are numerous potential causes of an acute abdomen because the abdominal cavity contains a number of different organs and structures. Due to the potentially life-threatening nature of many of these causes, immediate medical referral is needed.


  • Intestinal ischaemia.

  • Peptic ulcer—perforation, gastrointestinal bleeding (see Gastrointestinal care p. [link]).

  • Bowel obstruction.

  • Cholecystitis.

  • Pancreatitis (see Gastrointestinal care p. [link]).

  • Appendicitis.

  • Peritonitis.

  • Abdominal aortic aneurysm.

  • Ectopic pregnancy.

Assessment findings

  • Severe sudden pain < 24 h in duration.

  • Pain before vomiting.

  • Raised temperature and heart rate.

  • Distended, firm, tender abdomen.

  • Raised WBC count.

  • Bowel sounds—hypoactive, absent, or high-pitched/tinkling.

  • Peritoneal signs—rebound tenderness, guarding, or rigidity.


  • Inform the doctor urgently and refer the patient to the surgical team as required.

  • Give analgesia and anti-emetic for pain and nausea.

  • Monitor gastric aspirates for amount and colour (see Gastrointestinal care p. [link]).

  • Perform a rectal examination to assess for melaena.

  • Give fluid resuscitation and haemodynamic support as required.

  • Blood investigations:

    • FBC

    • U&Es

    • LFTs

    • clotting

    • glucose

    • amylase

    • arterial blood gas.

  • Other investigations as appropriate to the assessment findings:

    • radiology—facilitate CT scan, ultrasound, or X-ray if ordered

    • urine—urinalysis, MC&S, pregnancy test

    • 12-lead ECG to rule out cardiac abnormality

    • intra-abdominal pressure monitoring.

Acute liver failure


Significant liver dysfunction with any degree of altered mentation (hepatic encephalopathy) in the absence of chronic liver disease indicates acute liver failure. Classification of acute liver failure is based on how fast encephalopathy develops after the initial signs of liver abnormality (see Table 10.5). Severe cases of acute liver failure may require transfer to a specialist liver intensive care unit for extracorporeal liver assist device (ELAD) therapy or transplantation.

Table 10.5 Classification of acute liver disease based on development of hepatic encephalopathy

Type of acute liver failure

Time between onset of liver dysfunction signs (e.g. jaundice) and encephalopathy


0–7 days


7–28 days


> 28 days


  • Paracetamol overdose.

  • Acute viral hepatitis or other viruses.

  • Hepatotoxic substances—drugs, excessive alcohol, mushrooms, chemicals, herbal remedies.

  • Vascular causes—ischaemic hepatitis, Budd–Chiari syndrome.

  • Pregnancy—acute fatty liver, HELLP syndrome.

  • Autoimmune hepatitis.

  • Metabolic causes—Wilson’s disease, Reye’s syndrome.

Assessment findings

  • Hepatic encephalopathy (see Table 10.6).

  • Cerebral oedema leading to raised ICP.

  • Hypotension and tachycardia.

  • Coagulopathy and bleeding.

  • Jaundice and raised LFTs.

  • Acute kidney injury.

  • Metabolic disturbances.

  • Infection.

Table 10.6 Classification of hepatic encephalopathy


Clinical presentation


Mood change, slow mentation, disturbed sleep, usually alert and lucid


Drowsiness, inappropriate behaviour, easily arousable, conversant


Marked confusion and disorientation, agitation, stuporous but rousable


Coma—unrousable to verbal or noxious stimuli, abnormal motor response to stimuli


  • Haemodynamic monitoring to assess for distributive shock.

  • Fluid resuscitation, avoiding excessive volume overload.

  • Vasoconstrictor if hypotension does not respond to IV fluids.

  • Inotropic support as required.

  • Antibiotics for prophylaxis or an identified infection.

  • Blood components as required—FFP is only given if the patient is actively bleeding or prior to invasive procedures (INR is a highly sensitive marker of liver function and helps to monitor the progression and severity of liver injury).

  • Give 50% glucose for hypoglycaemia.

  • Renal replacement therapy for oliguria and/or significant acidosis.

    • Use bicarbonate-buffered replacement solution (see Gastrointestinal care p. [link]).

    • Avoid using heparin as anticoagulant if the patient has a low platelet count or is actively bleeding—use epoprostenol as an alternative.

  • Blood investigations:

    • FBC

    • U&Es, phosphate, calcium, magnesium

    • LFTs

    • clotting

    • glucose

    • amylase

    • arterial blood gas and arterial ammonia

    • paracetamol level and toxicology screen

    • hepatitis screen

    • autoantibodies and immunoglobulins (autoimmune hepatitis).


  • Avoid the use of sedatives, or give short-acting agents (e.g. propofol and fentanyl) if required for intubation or patient safety.

  • Maintain cerebral perfusion pressure if cerebral oedema develops:

    • ICP monitoring is required in severe cases

    • see Gastrointestinal care p. [link] for care of the patient with a raised ICP.

N-acetylcysteine infusion

  • Paracetamol overdose (see Gastrointestinal care p. [link]).

  • Consider for non-paracetamol-induced liver failure.7


7 Lee WM et al. Intravenous N-acetylcysteine improves transplant-free survival in early stage non-acetaminophen acute liver failure. Gastroenterology 2009; 137: 856–64.Find this resource:

Further reading

Sargent S (ed.) Liver Diseases: an essential guide for nurses and health care professionals. Wiley-Blackwell: Chichester, 2009.Find this resource:

Chronic liver failure


Patients with chronic liver failure who are admitted to an intensive care unit have an overall hospital mortality rate of 55%, but those with cirrhosis, sepsis, and organ failure have an even higher mortality rate, ranging from 65% to 90%.8 The intensive care management is not curative of the chronic liver disease itself, but is more supportive in nature, addressing secondary problems resulting from an acute on chronic episode. Common causes of acute on chronic liver failure are listed in Box 10.3.


  • Alcoholic liver disease—progresses in severity through three stages:

    • fatty liver—fibrosis with recovery is still possible

    • alcoholic hepatitis—inflammation, necrosis, and fibrosis

    • cirrhosis—irreversible nodule formation due to hepatocyte destruction being more rapid than regeneration.

  • Non-alcoholic fatty liver disease:

    • associated with metabolic syndrome (obesity, hyperlipidaemia, type 2 diabetes, and hypertension)

    • non-alcoholic steatohepatitis (NASH)—severe form with inflammation leading to fibrosis and cirrhosis.

  • Viral causes—hepatitis, cytomegalovirus, Epstein–Barr virus.

  • Metabolic cause—Wilson’s disease.

  • Autoimmune causes—primary biliary cirrhosis, autoimmune chronic hepatitis.

  • Right-sided heart failure.

Assessment findings

  • Jaundice.

  • Ascites.

  • Hepatic encephalopathy (see Table 10.5).

  • Coagulopathy.

  • Gastrointestinal haemorrhage (see Gastrointestinal care p. [link]).

  • Chronic signs—spider naevi, caput medusae, palmar erythema, asterixis, leukonychia, Dupuytren’s contracture, and finger clubbing.


  • Haemodynamic monitoring, fluid resuscitation, and vasoconstrictor and inotropic support as required.

  • Monitor for and treat acute respiratory failure secondary to abdominal distension or pleural effusions.

  • Give 50% glucose for hypoglycaemia.

  • Renal replacement therapy for oliguria and/or significant acidosis:

    • use bicarbonate-buffered replacement solution (see Gastrointestinal care p. [link]).

  • Monitor for coagulopathy and gastrointestinal bleeding (see Gastrointestinal care p. [link]).

  • Blood investigations:

    • FBC

    • U&Es, phosphate, calcium, magnesium

    • LFTs

    • clotting

    • glucose

    • amylase

    • arterial blood gas.


  • Paracentesis and IV fluid replacement as prescribed.

  • Antibiotics for spontaneous bacterial peritonitis.

  • Sodium restriction.

  • Diuretics.


  • Rule out other causes, such as sepsis, acidosis, uraemia, alcohol or drug withdrawal, and hypoxia.

  • Avoid the use of sedatives, or give short-acting agents (e.g. propofol and fentanyl) if required for intubation or patient safety.

  • Give lactulose—this osmotic laxative increases gastrointestinal motility, so there is less time for intestinal bacteria to metabolize protein to ammonia.

  • A protein-restricted diet is no longer recommended.10


8 O’Brien AJ et al. Prevalence and outcome of cirrhosis patients admitted to UK intensive care: a comparison against dialysis-dependent chronic renal failure patients. Intensive Care Medicine 2012; 38: 991–1000.Find this resource:

9 Wadei HM and Gonwa TA. Hepatorenal syndrome in the intensive care unit. Journal of Intensive Care Medicine 2013; 28: 79–92.Find this resource:

10 Caruana P and Shah N. Hepatic encephalopathy: are NH4 levels and protein restriction obsolete? Practical Gastroenterology 2011; 35: 6–18.Find this resource:



Inflammation of the pancreas can result from an acute, chronic, or acute on chronic process. Pancreatic enzymes are prematurely activated in the pancreas instead of within the duodenum, leading to autodigestion. The localized injury resulting from this autodigestion triggers the release of cytokines, hormones, and other vasoactive substances as part of the inflammatory response. This leads to the development of oedema, bleeding, necrosis, pseudocysts, and abscesses (see Figure 10.5). Initially, systemic inflammatory response syndrome (SIRS) occurs, with the potential for sepsis and multi-organ dysfunction syndrome (MODS) to develop if the initial precipitating factor is not resolved and the pancreatitis becomes progressively more severe (see Gastrointestinal care p. [link]).

Figure 10.5 Progression of acute pancreatitis. SIRS, systemic inflammatory response syndrome; MODS, multi-organ dysfunction syndrome.

Figure 10.5 Progression of acute pancreatitis. SIRS, systemic inflammatory response syndrome; MODS, multi-organ dysfunction syndrome.


  • Biliary disease—gallstones or common bile duct obstruction.

  • Alcohol.

  • Endoscopic retrograde cholangiopancreatography (ERCP).

  • Medications—diuretics, sulfonamides, ACE inhibitors, valproic acid.

  • Abdominal trauma.

  • Infection.

  • Idiopathic causes.

Assessment findings

  • Nausea and vomiting without relief.

  • Abdominal pain.

  • Abdominal distension and tenderness.

  • Fever.

  • Jaundice.

  • Elevated serum pancreatic enzymes—amylase and lipase.

  • Raised WBC count, CRP, and lactate dehydrogenase (LDH).

  • Raised bilirubin, AST, and PT (liver disease).

  • Elevated alkaline phosphatase (biliary disease).

  • Hyperglycaemia.

  • Electrolyte imbalances.

  • Metabolic acidosis.

  • Retroperitoneal bleeding—Cullen’s sign (bruising near the umbilicus) and Grey Turner’s sign (flank bruising).

  • Steatorrhoea —oily, foul-smelling, grey faeces secondary to excess fat in faeces.


  • Haemodynamic monitoring to assess for distributive shock from systemic inflammatory response syndrome (SIRS) (see Gastrointestinal care p. [link]).

  • Fluid resuscitation, avoiding excessive volume overload.

  • Vasoconstrictor if hypotension does not respond to IV fluids.

  • Inotropic support as required.

  • Monitor for and treat acute respiratory failure secondary to abdominal distension.

  • Insulin therapy for hyperglycaemia.

  • Renal replacement therapy for oliguria and/or significant acidosis.

  • Analgesia and anti-emetics as required.

  • Monitor electrolytes and treat imbalances.

  • Antibiotics for an identified infection—the evidence for the effectiveness of their prophylactic use is inconclusive.11

  • Confirm nutritional regime with doctor:

    • nasogastric or nasojejunal enteral feeding

    • total parenteral nutrition only if necessary—routine bowel rest is no longer recommended.12

  • Blood investigations:

    • FBC

    • U&E, phosphate, calcium, magnesium

    • LFTs

    • clotting

    • glucose

    • amylase and lipase

    • arterial blood gas.

  • ERCP or surgery as required.


11 Villatoro E et al. Antibiotic therapy for prophylaxis against infection of pancreatic necrosis in acute pancreatitis. Cochrane Database of Systematic Reviews 2010; Issue 5: CD002941.Find this resource:

12 Al-Omran M et al. Enteral versus parenteral nutrition for acute pancreatitis. Cochrane Database of Systematic Reviews 2010; Issue 1: CD002837.Find this resource:

Gastrointestinal haemorrhage


Bleeding can occur in either the upper or lower regions of the gastrointestinal tract. If there are significant amounts of continual haemorrhage, referral to endoscopy and/or general surgery will be required for definitive treatment.


  • Peptic ulcers.

  • Varices secondary to portal hypertension.

  • Mallory–Weiss tear.

  • Tumours.

  • Ischaemic colitis.

  • Crohn’s disease.

  • Ulcerative colitis.

  • Diverticulitis.

Assessment findings

  • Upper gastrointestinal bleeding:

    • bloody or coffee-ground gastric aspirates or emesis

    • melaena.

  • Lower gastrointestinal bleeding—rectal passing of fresh blood or clots.

  • Signs of hypovolaemic shock (see Gastrointestinal care p. [link])—hypotension, tachycardia, prolonged capillary refill time, cool skin, and weak pulse.

  • Abdominal distension and tenderness.

  • Hyperactive bowel sounds.


  • Monitor gastric contents aspirated from oro- or nasogastric tube.

  • Monitor bowel movements for melaena.

  • Use semi-recumbent positioning (head-up angle of 35–45°).

  • Haemodynamic monitoring to assess for hypovolaemic shock.

  • Monitor fluid status and treat fluid deficit (see Gastrointestinal care p. [link]).

  • Blood components as required (see Gastrointestinal care p. [link]).

  • Gastric acid suppressive therapy—proton-pump inhibitor.

  • Confirm with doctor the enteral feeding regime, depending on the amount of bleeding, cause of bleeding, and need for endoscopic investigation.13

    • Clarify whether enteral feeding should be initiated, continued at the same rate, or stopped.

    • Active bleeding may result in high gastric residual volumes, thus increasing the risk of pulmonary aspiration.

    • Low-rate enteral feeding may protect the gut mucosa and prevent further bleeding.

  • Blood investigations:

    • FBC

    • U&E

    • LFTs

    • clotting

    • arterial blood gas

    • cross-matching.

  • Use medication with a gastrointestinal vasoconstrictor effect—vasopressin, terlipressin, or octreotide.

  • Endoscopy treatment—sclerotherapy or banding.

  • Use balloon tamponade if bleeding is not controlled by medication or endoscopy treatment (see Table 10.7).

    • The Sengstaken–Blakemore tube contains three lumens (oesophageal balloon, gastric balloon, and a gastric aspiration port) (see Figure 10.6).

    • The Minnesota tube contains the same three lumens as a Sengstaken–Blakemore tube, but in addition has a fourth lumen for oesophageal aspiration.

Table 10.7 Nursing management of the patient with balloon tamponade*



Continuous monitoring

Balloon could burst or migrate to oropharynx

Sedation and analgesia

Nasogastric tube is uncomfortable and patient must remain still

Elevated head of bed

To prevent pulmonary aspiration of gastric contents

Aspiration or frequent suction of nasogastric tube

To monitor gastric content and prevent pulmonary aspiration

Irrigation of nasogastric tube

To maintain patency, as the tube may become blocked with clots

Deflate balloon every 6–8 h

To prevent oesophageal necrosis

*Traction is no longer recommended.14

Figure 10.6 Balloon tamponade using a Sengstaken–Blakemore tube.

Figure 10.6 Balloon tamponade using a Sengstaken–Blakemore tube.

(Reproduced from Waldmann, Soni and Rhodes, Oxford Desk Reference: critical care, 2008, with permission from Oxford University Press.)


13 Hébuterne X and Vanbiervliet G. Feeding the patients with upper gastrointestinal bleeding. Current Opinion in Clinical Nutrition and Metabolic Care 2011; 14: 197–201.Find this resource:

14 Sargent S. Liver Diseases: an essential guide for nurses and health care professionals. Wiley-Blackwell: Chichester, 2009.Find this resource:

Further reading

Waldmann C, Soni N and Rhodes A. Gastrointestinal therapy techniques. In: Oxford Desk Reference Critical Care. Oxford University Press: Oxford, 2008. pp. 73–80.Find this resource:

Abdominal compartment syndrome


Abdominal compartment syndrome is defined as a continuous intra-abdominal pressure reading of > 20 mmHg with new organ failure15 (for an overview of intra-abdominal pressure monitoring, see Gastrointestinal care p. [link]). The underlying problem can be either a primary cause inside the abdomen itself, or a secondary issue outside the abdomen which results in the accumulation of intra-abdominal fluid.

Increased pressure within the peritoneal or retroperitoneal spaces causes ischaemia of the intra-abdominal organs along with secondary complications of dysfunction of the respiratory and cardiovascular systems. For example, as the pressure continues to rise, lung expansion becomes restricted and the vena cava becomes compressed, consequently reducing the return of blood to the heart and ultimately leading to a reduction in cardiac output.


Capillary leakage during fluid resuscitation

  • Systemic inflammatory response syndrome (SIRS).

  • Sepsis.

  • Burns.

  • Trauma.

Increased abdominal contents

  • Haemorrhage within the abdominal cavity.

  • Ascites.

  • Liver disease.

  • Pancreatitis.

  • Peritonitis.

  • Intra-abdominal mass.

Increased intra-luminal contents

  • Gastroparesis.

  • Paralytic ileus.

  • Bowel obstruction.

Decreased abdominal wall compliance

  • Patient–ventilator dyssynchrony.

  • High levels of intrinsic or extrinsic PEEP.

  • Prone positioning.

  • Abdominal surgery with tight closure.

Assessment findings

  • Intra-abdominal pressure > 20 mmHg.

  • Abdomen distended, firm, and tender.

  • Nausea and vomiting.

  • High gastric residual volumes.

  • Acute kidney injury.

  • Acute respiratory failure.

  • Hypotension, tachycardia, and reduced cardiac output.


  • Avoid excessive fluid resuscitation.

  • Improve abdominal compliance:

    • Optimize mechanical ventilation settings.

    • Give sedation, analgesia, and neuromuscular block as required.

    • Optimize patient positioning—avoid prone positioning and hip flexion.

  • Evacuate intraluminal and abdominal contents:

    • Aspirate oro- or nasogastric tube and leave on free drainage.

    • Give enema.

    • Give prokinetics

    • Drain ascites.

  • Haemodynamic monitoring to assess preload and cardiac output (see Gastrointestinal care p. [link]).

  • Vasoconstrictor to maintain a mean arterial pressure (MAP) sufficiently higher than the intra-abdominal pressure (IAP) to give an abdominal perfusion pressure (APP) of ≥ 60 mmHg:

    • APP = MAP – IAP.

  • Renal replacement therapy for oliguria and/or significant acidosis.

  • Surgical decompression.


15 Kirkpatrick AW et al. Intra-abdominal hypertension and the abdominal compartment syndrome: updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive Care Medicine 2013; 39: 1190–206.Find this resource:

Further reading

Lee RK. Intra-abdominal hypertension and abdominal compartment syndrome: a comprehensive overview. Critical Care Nurse 2012; 32: 19–31.Find this resource:

Malbrain M and De Waele J. Intra-Abdominal Hypertension: core critical care. Cambridge University Press: Cambridge, 2013.Find this resource:

The Abdominal Compartment Society. Gastrointestinal

Refeeding syndrome


Malnourished patients are at risk of developing significant metabolic, electrolyte, and fluid shifts if standard feeding regimes are started too quickly or prior to correcting glucose and electrolyte abnormalities. Refeeding syndrome can be a consequence of either enteral or parenteral feeding, and the risk factors for this syndrome are summarized in Table 10.8.

Table 10.8 Criteria for identifying high risk of refeeding syndrome

Patient has one or more of the following:

Patient has two or more of the following:

  • BMI < 16 kg/m2

  • Unintentional weight loss > 15% within the last 3–6 months

  • Little or no nutritional intake for > 10 days

  • Low levels of potassium, phosphate, or magnesium prior to feeding

  • BMI < 18.5 kg/m2

  • Unintentional weight loss > 10% within the last 3–6 months

  • Little or no nutritional intake for > 5 days

  • History of alcohol abuse or medication including insulin, chemotherapy, antacids, or diuretics

Source: NICE guidelines.16


  • Rapid refeeding in patients who are malnourished due to:

    • prolonged starvation

    • anorexia nervosa

    • chronic alcoholism.

  • Excessive dextrose infusion.

  • Antacids.

Assessment findings

  • Pulmonary oedema.

  • Arrhythmias.

  • Hypophosphataemia.

  • Hypokalaemia.

  • Hypomagnesaemia.

  • Hypocalcaemia.

  • Altered glucose metabolism.

  • Vitamin deficiencies.


  • The NICE guidelines16 make the following recommendations :

    • Commence feeding at 10 kcal/kg/day, increasing the rate slowly to meet or exceed full needs by 4–7 days.

    • Give 5 kcal/kg/day in extreme cases (BMI < 14 kg/m2 or negligible intake for > 15 days).

    • During the first 10 days of feeding give thiamine, vitamin B, and a balanced multivitamin and trace element supplement.

  • Continuous ECG monitoring is required.

  • Monitor fluid status and treat imbalances (see Gastrointestinal care p. [link]).

  • Monitor electrolytes and treat imbalances prior to starting feeding.

  • Coordinate the feeding regime as discussed with dietitian and doctor.


16 National Institute for Health and Care Excellence (NICE). Nutrition Support in Adults: oral nutrition support, enteral tube feeding and parenteral nutrition. CG32. NICE: London, 2006. Gastrointestinal this resource:

Further reading

Adkins SM. Recognizing and preventing refeeding syndrome. Dimensions of Critical Care Nursing 2009; 28: 53–60.Find this resource:

Byrnes MC and Stangenes J. Refeeding in the ICU: an adult and pediatric problem. Current Opinion in Clinical Nutrition and Metabolic Care 2011; 14: 186–92.Find this resource: