Monitoring Gastrointestinal Function

Hiatus hernia
Gastritis
Peptic ulcers
Tumours
Oesophagogastric dismotility
Pyloric stenosis result of chronic peptic ulcerationBiliary tractGallstones
Hepatoma
Metastic liver diseaseSmall and large intestineCrohn’s disease
Irritable bowel syndrome
ObstructionMetabolicUraemia
Diabetic ketoacidosis
Hepatic failure
HypercalcaemiaNeurologicalRaised intracranial pressure
Labyrinthine pathology
Brain-stem pathologyOtherDrugs, e.g. opiates, chemotherapy, sulphonamides
Hyperemesis gravidarum
Viral, e.g. norovirus
Viral hepatitis
Food or drink infected with organisms, e.g. staphylococci
Sepsis
Severe constipation especially in elderly people

The timing of vomiting together with the volume and consistency of the vomit are also helpful.

Timing of Vomiting

Vomiting that occurs more than an hour after eating is characteristic of obstruction of the gastric outlet, whereas early morning vomiting is typical of pregnancy, alcoholism and raised intracranial pressure.

Volume of Vomit

The volume of the vomit is important: a large volume may be indicative of gastric outflow obstruction. If there are small amounts of vomit it is important to ensure that the patient is actually vomiting and not just expectorating – testing for acidity is recommended.

Consistency of Vomit

The consistency is important:

‘Coffee-grounds’: old blood clots in vomit; can also be caused by iron tablets, red wine and, of course, coffee ingestion
Fresh blood: the presence of fresh blood is indicative of bleeding from the upper gastrointestinal tract
Yellow/green: presence of bile and upper small bowel contents is suggestive of obstruction
Faeculent: brown offensive material from the small bowel, a late sign of small intestinal obstruction (Bickley and Szilagyi 2009)
Projectile: causes include pyloric stenosis and raised intracranial pressure.

MONITORING STOMAS AND FISTULAS

Stomas

Several factors can influence the characteristics of output from stomas including medication, diet and amount of bowel removed. The position of the stoma is also significant: basically the more proximal the stoma, the more fluid the effluent and the more caustic its effect on the skin, due to the presence of chemical irritants effluent from the stoma (Rolstad and Erwin-Toth 2004). In addition to chemical irritants, other causes of loss of skin integrity include stripping off the ostomy bag adhesive, infection, allergy to the stoma bag adhesive and underlying skin disease, e.g. eczema (Rolstad and Erwin-Toth 2004).

The skin surrounding the stoma should be closely observed for early signs of maceration (Herlufsen et al. 2006). Documentation of the size, length and colour of the stoma should be regularly undertaken as should volume and consistency of the output recorded.

Fistulas

An enterocutaneous fistula is an abnormal communication between a section of the GI tract and the skin (Renton et al. 2006). It usually arises from the small or large intestine, from an underlying area of diseased bowel or as a complication of abdominal surgery (Hollington et al. 2004). These are rare complications but pose serious problems because of the serious underlying gastrointestinal comorbidity, e.g. inflammatory bowel disease, intestinal malignancy, pancreatitis as well as concurrent severe sepsis (Streat 2009). The location of the fistula along the bowel will determine the type of effluent produced, e.g. a small bowel fistula can lead to the leaking of copious volumes of corrosive fluid (Renton et al. 2006). Monitoring priorities include recording the consistency and volume of the effluent and observing the surrounding skin for maceration. Monitoring skin integrity is a key priority (Renton et al. 2006).

ACUTE UPPER GASTROINTESTINAL TRACT BLEEDING

Acute GI bleeding is a common cause for admission to the intensive care unit (ICU) and a major cause of morbidity and mortality (Sung 2009). The mortality rate from upper GI bleeding has remained at 10% for decades (Sung 2009). Peptic ulcer and oesophageal varices are the two most frequent causes of upper GI bleeding (Fiore et al. 2005).

Gastrointestinal bleeding usually manifests itself through haematemesis and melaena or more dangerously through an enlarged abdomen with associated abdominal pain. The vomit may be either bright red or coffee-ground in appearance, depending on the length of time the blood that has been in contact with gastric secretions (gastric acid converts bright red haemoglobin to brown haematin). A history of vomiting and retching preceding the GI bleeding suggests a Mallory–Weiss syndrome – a tear at the junction of the stomach and the oesophagus secondary to forceful vomiting/coughing (Sung 2009).

Although most GI bleeds stop spontaneously, approximately 20% will re-bleed in hospital and many of these will need surgical intervention. Upper GI bleeds are commonly seen in the ICU or high dependency unit (HDU) because of the vast blood supply to the stomach and oesophagus. Bleeding is therefore more likely to be severe causing haemodynamic instability requiring massive fluid resuscitation.

Monitoring priorities include:

Assessing for signs of hypovolaemia and shock
Estimating blood loss and accurate maintenance of fluid balance
Determining the cause of the bleed if possible (Table 8.2)

Monitoring fluid balance
Monitoring the function of other major systems
Laboratory investigations, e.g. full blood count (FBC), prothrombin time, liver function tests (LFTs), platelet count, urea and electrolytes (U&Es)
Monitoring intra-abdominal pressures for signs of increasing pressure.

Table 8.2 Causes of acute upper gastrointestinal (GI) bleeding

Adapted from Steele and Sabol (2009), Sung (2009) and Jenkins and Johnson (2010).

Oesophageal	Oesophageal varices Coagulopathy Oesophagitis Tumours Mallory–Weiss tear
Gastric	Peptic ulcers Gastritis Tumours Angiodysplasia (arteriovenous malformation of the GI tract) Dieulafoy’s lesions
Duodenal	Duodenal ulcers Angiodysplasia Duodenitis Crohn’s disease Meckel’s diverticulum

If the upper GI bleed is due to persistent bleeding ulcers, haemostasis is recommended by endoscopic and pharmacological means, i.e. endoscopic injection of adrenaline or by clipping with adjunct therapy proton pump inhibitors, e.g. esomeprozole (Sung 2009). Mainstay treatment of bleeding oesophageal varices is endoscopic sclerotherapy. Balloon tamponade, i.e. with a Sengstaken–Blakemore tube, may be helpful to apply pressure on the bleeding points in exceptional cases when other therapies fail to effect control of bleeding (Sung 2009). Balloon tamponade tubes can only remain in situ for 24 hours because of the risk of necrosis and close monitoring of tube position, together with the patient’s airway and respiratory status is important.

ASSESSMENT OF INTESTINAL OBSTRUCTION

Intestinal obstruction can occur in either the small or the large bowel. It can lead to bowel strangulation, infarction and perforation, resulting in potentially life-threatening peritoneal and systemic infection (Steele and Sabol 2009). It can be classified as mechanical or non-mechanical. Mechanical obstruction results from a physical blockage of the intestinal lumen which may be complete or incomplete. Causes include adhesions, malignancy, hernias, bolus obstruction and bowel strangulation, e.g. volvulus. Non-mechanical obstruction is caused by ineffective intestinal peristalsis (paralytic ileus) which is an ileus without the presence of mechanical obstruction, causes of which include trauma, handling of the bowel during surgery, peritonitis and electrolyte imbalance (Steele and Sabol 2009).

Detailed below are the key monitoring considerations:

Blood pressure and pulse measurements to detect early signs of shock
Temperature – pyrexia is usually present
Vomiting: the higher the obstruction, the more profuse the vomit
Fluid and electrolyte balance
Abdominal pain and distension: characteristics and severity
Bowel function: consistency of faeces, regularity, volume.

PRINCIPLES OF MONITORING PANCREATIC FUNCTION

The pancreas secretes water to dilute chyme, bicarbonate to neutralise postgastric chyme and enzymes to help with digestion. Its endocrine function is discussed in Chapter 10.

Severe acute pancreatitis (SAP) is an acute inflammation of the pancreas that can also involve surrounding tissues and/or remote organs (Steele and Sabol 2009). The more severe form of pancreatitis, acute necrotizing pancreatitis (ANP), is mainly responsible for the associated high mortality rates (15%) (Wyncoll 2009). Biliary disease and alcohol remain the causative factors in 70% of cases (Wyncoll 2009). Pancreatitis can compromise most of the major systems in the body. Therefore close monitoring is required. The key priorities are:

Fluid and electrolyte monitoring: fluid and electrolyte imbalances may be present (large volumes of fluid can leak into extravascular spaces).
Pulse oximetry and arterial blood gas analysis: respiratory failure can be a complication.
ECG monitoring: electrolyte imbalances can cause arrhythmias.
Blood sugar estimations: hyperglycaemia may occur as a result of impaired insulin production and increased release of glucagon.
Temperature: the main cause of pyrexia is hypermetabolism, although infection may also be the cause
Nutritional status: may have paralytic ileus patient will be nil by mouth, parenteral nutrition will probably be commenced or enteral feeding to bypass the stomach, i.e. into distal duodenum or jejunum, is considered safe (Steele and Sabol 2009). If there is long-term alcohol abuse, nutrition is an even greater priority.
Serum amylase: peaks at 4–8 hours after onset and returns to baseline within 3–5 days with SAP (Steele and Sabol 2009)
Serum lipase: elevated only in pancreatitis, remains elevated after serum amylase returns to normal (Steele and Sabol 2009)
Pain: the patient may have severe abdominal pain.

Scenario

David a 130-kg 56-year-old welder who presented to the emergency department acutely unwell, with a 5-day history of severe epigastric pain, distension and vomiting. Initial physical assessment was undertaken and bloods taken for a full biochemical and haematological screen. David was given a subcutaneous morphine injection for his pain, which he rated at 7 out of 10, and commenced on intravenous (IV) fluids for hydration.

The initial assessment was:

A – airway was patent and David was speaking in short sentences due to abdominal discomfort

B – respiratory rate (RR) was 30/min, SpO₂ was 91% on room air, and poor bilateral basal air entry was heard on auscultation. Oxygen via a non-re-breather mask was applied at 15 L/min

C – BP was 88/55 mmHg, heart rate (HR) 125/min regular, core temperature 40°C, peripheries were warm and capillary refill was >3 s. A urinary catheter was inserted and 70 ml of dark urine obtained. The 12-lead ECG was normal

D – pupils were equal and briskly reacting to light. AVPU was A and David was oriented to time and place

E – David’s abdomen was moderately distended and tense with Grey–Turners sign (haemorrhagic discoloration).

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