Gastrointestinal system

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CHAPTER 6 GASTROINTESTINAL SYSTEM

Gastrointestinal tract in critical illness 168
Reduced gastrointestinal motility 170
Diarrhoea 170
Stress ulceration 172
Gastrointestinal ischaemia 172
Gastrointestinal bleeding 172
Intra-abdominal sepsis 174
Abdominal compartment syndrome 174
Hepatic dysfunction during critical illness 176
Hepatic failure 176
Acute pancreatitis 181

GASTROINTESTINAL TRACT IN CRITICAL ILLNESS

The gastrointestinal tract plays a major role in the pathophysiology of critical illness. In addition, to being a common site for surgical intervention and a common source of intra-abdominal sepsis, the gut is pivotal during critical illness in a number of ways:

image As a large ‘third space’ for fluid loss within the lumen of the gut.
image As a bed for altered blood flow (AV shunting) during shock states.
image As a reservoir for bacteria and endotoxins, which may translocate into the portal, lymphatic and systemic circulations, producing systemic inflammatory response syndrome, sepsis and multiorgan failure, particularly during periods of altered blood flow. (See Sepsis, p. 326).
image As a reservoir for bacteria which may colonize/infect the respiratory tract. (See Ventilator associated pneumonia, p. 143)
image As a site of secondary nosocomial infections e.g. Clostridium difficile.
image The maintenance of gastrointestinal integrity and function is therefore of major importance during critical illness.

Maintenance of gastrointestinal tract integrity

The pathophysiology of gastrointestinal integrity is complex. Maintenance of adequate splanchnic blood flow is thought to play a key part. In this respect, early aggressive resuscitation in shock states is crucial. Several studies have shown that both volume resuscitation and the maintenance of adequate perfusion pressure using vasopressor agents are independently important. In the ‘Rivers study’, early effective resuscitation, as guided by optimization of mixed venous oxygen saturation (a good surrogate for adequacy of tissue oxygen supply), was shown to reduce the patient’s stay in the intensive care unit, reduce the number of organ failures and reduce eventual mortality in patients undergoing early resuscitation in sepsis. Importantly, resuscitation goals had to be achieved early (i.e. within the first 6 h). In those patients who are adequately resuscitated, early enteral nutrition may also be of value in helping to preserve mucosal integrity and gastrointestinal function.

Manifestations of gastrointestinal tract failure

Failure of the gastrointestinal tract during critical illness may present in a number of ways. These are listed in Box 6.1.

Box 6.1 Clinical features of gastrointestinal tract failure

Delayed gastric emptying

Failure to absorb feed

Ileus, pseudo-obstruction

Diarrhoea

Stress ulceration

Gastrointestinal tract haemorrhage

Gastrointestinal ischaemia

Acalculous cholecystitis

Liver dysfunction

Systemic infl ammatory response syndrome

The principle aim of investigation of gastrointestinal dysfunction in the critically ill patients is to exclude serious, remediable, intra-abdominal pathology. In some cases, the combination of history, clinical examination and blood results in the context of the overall clinical picture will suffice. In many cases however, intra-abdominal imaging will be required. Occasionally laparotomy or laparoscopy may be necessary to exclude serious pathology.

Plain abdominal X-rays

This is a first-line investigation in most cases. Check the position of the nasogastric tube and any other intra-abdominal drains. Look for gastric air and normally distributed gas pattern throughout the large bowel. Check for distended loops of thickened bowel walls and for any air bubbles visible in the gut walls (implies ischaemic gut). Check outline of major viscera and psoas shadow. Look for free air, suggesting perforation of a viscus, and air in the biliary tree, suggestive of biliary tract sepsis.

Ultrasound

This is a valuable imaging technique, which can be performed at the bedside. It is particularly useful for imaging around the liver, biliary tract, kidneys, spleen and pelvic organs and can be used to identify intra-abdominal collections of fluid for drainage. It may be difficult to obtain good images because of obesity or the presence of excessive gas in the bowel.

CT scan

This is the definitive investigation for most acute intra-abdominal problems. CT generally requires oral and intravenous contrast. Its value may be limited in the very unstable patient by the need to transport the patient to the CT scanner. Images require expert interpretation.

REDUCED GASTROINTESTINAL MOTILITY

Delayed gastric emptying and persistent ileus

Failure of gut motility is common in the critically ill. It is usually manifest as a simple ileus, with large nasogastric losses and failure to absorb feed. It will usually improve spontaneously as the patient’s condition improves. Ensure that the patient’s electrolyte balance is normal. Disturbances of potassium and magnesium in particular can contribute to gastrointestinal tract dysfunction. Prokinetic agents such as metoclopramide and low dose erythromycin may promote motility

Rarely, cholinergic agents such as neostigmine may be required, either as a low dose bolus (up to 1 mg) or by infusion. Neostigmine has potentially alarming cardiovascular and systemic side-effects, including abdominal pain, salivation and bradycardia. Do not embark upon this treatment lightly, and only if you are certain that there is no mechanical gut obstruction. Seek advice from your consultant.

(See Common problem: Feed not absorbed, p. 59.)

Pseudo-obstruction

Occasionally ileus will progress to marked intra-abdominal distension, with obvious signs of gut obstruction in the absence of any apparent mechanical cause. This is called pseudo-obstruction. The diagnosis is supported by plain abdominal X-ray or CT, which shows widely dilated loops of bowel.

If the colon is distended to greater than 10–12 cm in cross-section, there is a risk of colonic rupture. The use of prokinetic agents in this setting may be hazardous, and mechanical decompression is usually necessary to prevent colonic rupture. This may be achieved by flexible sigmoidoscopy, or may require surgical intervention. Seek surgical opinion.

DIARRHOEA

Diarrhoea is a common manifestation of gastrointestinal tract failure in the intensive care unit and may arise in a number of ways

image As a manifestation of multisystem disorder. For example, generalized tissue hypoxia, tissue oedema and vascular endothelial failure affect the function of all tissues. The gut is no exception to this. These pathological abnormalities are associated with a failure in cellular function and metabolic pathways, which may persist for some time. Consequently, gut failure (either diarrhoea or constipation) is often a characteristic feature of the patient in the intensive care unit.
image As a result of the osmotic load placed on the gut. This may reflect overfeeding, or feeding with a diet whose electrolyte composition is unsuitable for a particular patient.
image As a consequence of more sinister conditions, such as ischaemic colitis.
image As a consequence of infection with a gut pathogen. This is a particular problem in intensive care patients, as the widespread use of broad-spectrum antibiotics suppresses the normal gut flora and allows the emergence and predominance of potentially pathogenic organisms such as Clostridium difficile.

Clostridium difficile

Clostridium difficile is a spore forming organism that produces an enterotoxin. Clostridium difficile infection is a serious problem, as in addition to torrential diarrhoea, it gives rise to an inflammatory condition in the gut which results in pseudomembranous colitis, and potentially toxic megacolon and gut perforation. The diagnosis can be made on clinical grounds, by stool culture or by detection of the Clostridium difficile toxin. Additionally, pseudomembranes may be visible on sigmoidoscopy, or gut dilatation on X-ray (toxic megacolon).

Clostridium difficile is readily transmitted from patient to patient. It is transmitted by contact, for example on the hands of health care workers. Unfortunately, because it is a spore forming organism, it is resistant to decontamination by alcohol hand rub. Rigorous hand washing using soap and water is much more effective. Patients suffering from Clostridium difficile diarrhoea, should be barrier nursed while in the critical care unit.

The specific treatment of Clostridium difficile relies on appropriate antibiotics. You should seek guidance from your unit microbiologist, as local infection control policies are an important element in limiting the spread of this pernicious infection. Antibiotics that are most commonly effective (usually enterally) include metronidazole and vancomycin. Occasional patients may require a colectomy.

Management of diarrhoea

Supportive measures include:

image Fluid resuscitation if evidence of hypovolaemia.
image Replacement of on-going losses with an appropriate electrolyte solution usually 0.9% or 0.45% saline.
image Sending of stool samples for culture and Clostridium difficile toxin.

In mild cases enteral feed can be continued. Seek advice from a dietician as to the most appropriate feed. In severe cases consideration should be given to ‘resting the gut’ by stopping enteral feeds and instituting parenteral nutrition.

STRESS ULCERATION

Stress ulceration may occur anywhere in the gastrointestinal tract but, is most common in the duodenum and stomach. Bleeding from ulceration is common and may present as obvious haematemesis or as an unexplained fall in haemoglobin. Perforation needs to be considered in any patient with abdominal signs who deteriorates, and is suggested by the presence of free air on a plain abdominal X-ray or CT.

Stress ulceration is thought to be primarily due to inadequacy of mucosal blood flow, although concurrent use of non-steroidal anti-inflammatory drugs is a risk factor. General resuscitation measures including adequate fluid loading and maintenance of adequate perfusion pressures, together with early feeding, are more important than prophylactic measures.

(See Stress ulcer prophylaxis, p. 62.)

GASTROINTESTINAL ISCHAEMIA

This should be considered as a possible cause of deterioration, particularly in the elderly patient with pre-existing vascular disease or vasculitis. Systemic inflammatory response, oliguria, persistent acidosis, raised amylase and bloody diarrhoea may all occur but none is specific. Thickened loops of bowel with gas present in the wall may be seen on plain abdominal X-ray. CT scan may be helpful, but the diagnosis is usually made at laparotomy. Treatment requires resection of the ischaemic bowel. Difficulty at laparotomy in determining the demarcation between viable and non-viable bowel often necessitates a ‘second look’ laparotomy at 24 – 48 h. Extensive infarction is often fatal.

GASTROINTESTINAL BLEEDING

Slow bleeding from the gastrointestinal tract may occur, and is a common cause of reduced haemoglobin in the critically ill. Less commonly, but of greater immediate concern is acute massive GIT haemorrhage, which may be life threatening. The source is usually the upper GIT. Common causes are listed in Box 6.2. Bleeding of this sort can result in haematemesis, melaena or even frank rectal blood loss. Lower GIT bleeding is less common, but may still be life threatening.

Box 6.2 Causes of upper gastrointestinal tract haemorrhage

Duodenal ulceration

Gastric erosion and ulceration

Oesophageal varices

Portal gastropathy / gastric varices

Aortoenteric fistulae

AV malformations

Other small bowel lesions

Clinical features

The history may be suggestive of the underlying diagnosis; predisposing factors include previous peptic ulceration, non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, anticoagulants, liver disease, portal hypertension and critical illness. Brisk GI bleeding is complicated by hypovolaemic shock and oliguria. Myocardial ischaemia may occur. Patients with liver disease develop worsening encephalopathy. Patients with reduced conscious level are at risk of aspiration pneumonia.

Investigations

Full blood count and cross-match are followed by regular monitoring of haemodynamic status, urine output, haemoglobin, coagulation and electrolytes. The site of the bleeding may be identified by endoscopy or arteriography.

Management

image Large-bore vascular access is obtained and resuscitation of hypovolaemia commenced. In massive bleeds full haemodynamic monitoring, including arterial line, CVP or some other measure of volume status, are valuable.
image Coagulopathy should be corrected.
image Analgesics and anxiolytics are used judiciously in conscious patients. Massive bleeds, however, frequently necessitate intubation and ventilation.
image Endoscopy allows injection of bleeding ulcers and banding or sclerotherapy of varices. The co-administration of a proton pump inhibitor (e.g. omeprazole 40 mg once or twice daily) is frequently all that is required to prevent recurrence.
image Persistent uncontrollable GI bleeding may necessitate surgery. Radiological embolization of actively bleeding vessels may occasionally be useful.

Variceal bleeding

Persistent variceal bleeding carries a high mortality (up to 50% from a first presentation). In addition to the above, management includes:

image Use of a Linton or Sengstaken – Blakemore tube to compress varices in the gastric fundus.
image The administration of vasopressin (up to 20 units by s.c. injection or slow i.v. infusion: beware vasopressor effects) and octreotide to reduce portal hypertension.
image Endoscopy and variceal banding once bleeding is controlled.

If these measures are ineffective, portosystemic shunting will be required. Transhepatic intravenous portosystemic shunt (TIPSS) is a radiological procedure that has a lower mortality than surgical shunt procedures, but is not considered definitive. Surgical options include splenorenal shunting, mesocaval shunting, oesophageal transection and liver transplantation. These interventions carry a high mortality.

(See Practical procedures: Sengstaken–Blakemore tube, p. 422.)

INTRA-ABDOMINAL SEPSIS

Subphrenic, pelvic and other intra-abdominal collections are an ever-present threat in critically ill patients, particularly following any intra-abdominal surgery. The clinical signs and symptoms may be vague. Persistent ileus, with failure to absorb feeds, ‘grumbling sepsis’ and altered liver function tests, should raise suspicion. Wound infections, urinary tract infections and genital tract infection should all be considered.

Assessment is by clinical examination followed by ultrasound or CT imaging. Management depends on the clinical condition of the patient. Options include radiologically guided drainage or open surgical drainage.

ABDOMINAL COMPARTMENT SYNDROME

The presence of blood, free fluid or gas in the abdominal cavity, splanchnic and tissue oedema and organomegally can lead to a progressive increase in the intra-abdominal pressure and to decreased splanchnic perfusion. This may result in gut, renal and liver hypoperfusion with associated clinical features. If suspected, intra-abdominal pressure can be measured via an indwelling urinary catheter (Fig. 6.1).

image

Fig. 6.1 Measurement of intra-abdominal pressure via urinary catheter.

Normal intra-abdominal pressure is less than 15–20 mmHg. Intra-abdominal pressures above 20 mmHg with evidence of end organ dysfunction are suggestive of abdominal compartment syndrome. Decompression of the abdomen may be required. Seek surgical advice. Once opened, it may be impossible to close the abdomen at first laparotomy. The abdomen may be left ‘open’ under sterile plastic coverings for later closure when the swelling has subsided.

HEPATIC DYSFUNCTION DURING CRITICAL ILLNESS

Liver dysfunction (as opposed to liver failure) is common during critical illness, particularly in association with severe shock states in which there is relative splanchnic and liver hypoperfusion. It is characterized by progressive rise in bilirubin, abnormalities of liver enzymes, coagulopathy with raised prothrombin time (PT) and delayed drug metabolism. Ultrasound or CT scan should be performed to exclude localized collections of infected fluid or biliary tract obstruction. The management is essentially supportive. Hepatotoxic drugs should be stopped. Liver function should improve as the patient’s general condition improves.

Cholestasis and cholangitis

Cholestasis is common in the critically ill, particularly in the absence of enteral feed, and may result in jaundice. The alkaline phosphatase may be raised. This usually resolves as the patient’s condition improves and enteral feeds are established. Abdominal ultrasound and endoscopic retrograde cholangiopancreatography (ERCP) may be necessary to exclude mechanical causes of biliary obstruction. Agents such as ursodeoxycholic acid may be used but there is little evidence for their benefit. Occasionally cholestasis leads to ascending cholangitis, which may require antibiotic treatment.

Acalculous cholecystitis

Rarely, critically ill patients may develop an acute, necrotizing inflammation of the gallbladder, known as acalculous cholecystitis. The aetiology of this is multifactorial, but includes bile stasis and splanchnic hypoperfusion. It should be considered in any patient with right upper quadrant pain, jaundice, raised alkaline phosphatase, abdominal signs and evidence of sepsis. There is no definitive test. Abdominal ultrasound or CT may demonstrate an enlarged, oedematous gallbladder with thickened wall and free fluid around the site. Management options include CT-guided drainage and acute cholecystectomy. Seek surgical opinion.

HEPATIC FAILURE

Liver failure is defined as hyperacute where the onset of encephalopathy occurs within 7 days of the onset of jaundice, acute where the interval is 7–28 days, and subacute where it is between 28 days and 6 months. Longer intervals represent chronic liver failure. The term fulminant liver failure refers to an earlier classification where encephalopathy occurs within 8 weeks of the onset of jaundice. It thus encompasses acute and hyperacute liver failure.

Aetiology

The commonest cause worldwide remains hepatitis B. In the UK, this is second to paracetamol poisoning. Other common causes include hepatitis A, drug idiosyncrasy and non-A non-B viral hepatitis. (Note: this does not equate to hepatitis C, which is not thought to be a cause of fulminant liver failure. Up to 20% of cases may, however, be hepatitis E.)

Pathophysiology

The final common pathway is hepatocellular failure, with a reduction or loss of the synthetic, homeostatic and filter functions of the liver. This results in a failure of carbohydrate metabolism, depletion of glycogen stores and consequent hypoglycaemia. Deranged amino acid metabolism results in accumulation of ammonia and other intermediate compounds, which account in part for the development of encephalopathy.

Protein synthesis is arrested, and this includes the synthesis of albumin and clotting factors. Coagulopathy is invariable. PT is the most sensitive index of hepatocellular failure and recovery. The coagulopathy may be exacerbated by activated fibrinolysis.

The filter (reticuloendothelial) functions of the hepatic Kupffer cells are central to the prevention of translocation of gut-derived endotoxin to the systemic circulation. In acute liver failure, there is systemic endotoxaemia. Further, the massive necrosis of hepatocytes releases high levels of tumour necrosis factor (TNF), platelet-activating factor (PAF) and other proinflammatory cytokines. Systemic inflammatory response syndrome (SIRS) and multisystem organ failure (MOF) follow. Moreover, there is a steep rise in circulating ammonia concentration. This is thought to mediate an increase in excitatory neurotransmitters in the central nervous system. The combination of these effects gives rise to failure of the blood–brain barrier, with cerebral oedema and altered consciousness (encephalopathy).

Clinical features

Hypoglycaemia is common and develops any time in the first few days of the condition. It gradually resolves as the liver failure improves. Acid – base homeostasis is altered and either alkalosis or acidosis may complicate this. A metabolic acidosis is the more sinister. Concurrently with the development of the metabolic derangement, conscious level may become impaired. Encephalopathy is graded as in Table 6.1.

TABLE 6.1 Grading of hepatic encephalopathy

Grade 0 Normal
Grade 1 Mild confusion (may not be immediately evident)
Grade 2 Drowsiness
Grade 3 Severe drowsiness, inappropriate words/phrases, grinding teeth
Grade 4 Unrousable

The onset of encephalopathy is followed in some patients by cerebral oedema and raised intracranial pressure (ICP). The risk of raised ICP is greatest in hyperacute liver failure (in excess of 50% of cases), and much lower in acute failure. It is much less common in subacute failure (around 4%). A baseline elevation in ICP up to 20–25 mmHg may be followed by surges, which are transient but severe (up to 80–90 mmHg). This stage may be followed by inexorably rising ICP and brain death.

The haemodynamics of SIRS develop as conscious level reaches grade III–IV. The characteristic hypotension is associated with a high cardiac index and low systemic vascular resistance. Vasodilatation and increased capillary permeability contribute to reduced circulating volume and may predispose to renal failure. Acute tubular necrosis may also occur as a result of SIRS or directly as a result of the precipitating insult, e.g. paracetamol-induced renal damage.

The coagulopathy seldom gives rise to de novo bleeding, even though very high PT values are seen (>100 s). Generalized oozing around cannulation sites is common but is seldom of great significance. Thrombocytopenia may also occur, either due to DIC or hypersplenism. It is occasionally necessary to perform invasive procedures under platelet cover.

True‘infective’ sepsis may occur. A rising WCC, falling platelet count, a PT whose recovery becomes arrested or a worsening acidosis should all be regarded as suspicious.

Management

image Acute hepatic failure carries a high mortality and treatment options include transplantation. Early discussion with a specialist centre is therefore mandatory.

image The development of grade III–IV encephalopathy or the onset of SIRS is an indication for tracheal intubation and mechanical ventilation. This protects the airway, reduces the work of breathing and protects against the risk of secondary hypoxic damage.
image Fluid and haemodynamic management is guided by invasive monitoring. Maintain adequate filling to ensure optimal CO while avoiding the risk of interstitial oedema of the lung, brain and gut.
image Noradrenaline (norepinephrine) is used to keep the mean arterial pressure above 70–80 mmHg and the CPP >50 mmHg (see below).
image Renal failure can make fluid balance difficult. Continuous renal replacement therapy is frequently necessary, but is often associated with transient haemodynamic instability and ICP surges.
image All patients should receive continuous N-acetylcysteine infusion (100 mg/kg per 24 h). This has been shown to improve outcome in fulminant liver failure irrespective of aetiology, even when instituted relatively late in the disease process.
image Stress ulcer prophylaxis with an H2 antagonist or proton pump inhibitor should be prescribed.
image Prevention of sepsis is a major problem. Prophylactic antibiotics should be discussed with a microbiologist. Selective decontamination of the digestive tract is practised in some centres, but is probably of marginal value.

image The prothrombin time (PT) is one of the key prognostic factors determining whether the optimal treatment of acute liver failure is likely to be medical or surgical. Therefore, do not treat coagulopathy (by, for example, giving fresh frozen plasma) except in cases of life threatening aemorrhage.

Metabolic issues

image Hypoglycaemia is common. All infusions should be made up in dextrose solutions (5–20%), and dextrose (5–50%) infused to maintain a normal blood sugar.
image Nitrogenous feeds are avoided (no TPN or nasogastric feed should be administered until metabolic resolution of acute liver failure).
image Sodium and potassium are maintained within the normal range; this may involve judicious use of potassium infusions at 10–40 mmol/h.
image The liver is unable to metabolize citrate used as an anticoagulant in blood products. Consequently, persisting citrate chelates calcium, and may drastically reduce ionized calcium levels. Calcium chloride 10 mmol may be given by slow bolus to maintain the ionized calcium to above 0.8 mmol/L.
image Metabolic acidosis is a useful prognostic indicator and is in any case best left untreated on theoretical grounds. The exception to this is where a severe acidosis is associated with haemodynamic instability. It is acceptable to correct the pH slowly to 7.2 if this improves the haemodynamic status. Rapid correction of acidosis with boluses of sodium bicarbonate should be avoided. The use of sodium bicarbonate can result in a transient dramatic elevation in the carbon dioxide tension, with consequent cerebral vasodilatation and a surge in ICP.

Control of ICP

image Nurse patient at a 20º head-up tilt.
image Keep physiotherapy, tracheal suctioning and turning to a minimum until the risk of ICP surges resolves (usually 5 days after the onset of grade IV encephalopathy).
image Ensure adequate sedation and paralysis.
image Primary surges in ICP (often followed by a reflex rise in arterial pressure) are treated acutely by hyperventilation. The response to hyperventilation is not maintained, so it should be discontinued as soon as a fall in ICP is seen. Mannitol 20% 100 ml is used to sustain the reduction in ICP and also where the baseline ICP remains above 25 mmHg. Other hyperosmolar therapies, for example hyperosmolar saline are also of value. The use of these agents should be discussed with your regional centre.
image Cooling the patient and liver support systems have been shown to help control ICP.

Even where the ICP remains very high, a good neurological outcome is possible provided CPP is maintained at or above 40–50 mm Hg.

Prognosis

Without transplantation, the prognosis is poorest in the subacute group and best in the hyperacute group. Within this group, the prognosis is poorer in those at the extremes of age, those with non-A, non-B hepatitis and drug dyscrasia. The overall mortality in patients with grade IV encephalopathy is 70%. With liver transplantation (i.e. in those patients at the highest risk of death with optimal medical management), the 1-year mortality is between 30 and 50%.

ACUTE PANCREATITIS

Inflammation of the pancreas and autodigestion may be precipitated by a number of triggers, some of which are listed in Box 6.3. The commonest causes are alcohol and biliary obstruction. Frequently no cause can be identified.

Box 6.3 Common causes of pancreatitis

Alcohol

Biliary obstruction (gallstones) / ERCP

Viral infection (CMV, EBV, etc.)

Surgical injury or trauma

Hypothermia

Cardiopulmonary bypass

Corticosteroids

Oral contraceptives

Clinical features

A spectrum of severity exists from mild pain to severe shock. Epigastric pain radiating to the back and a history of risk factors (including previous episodes) suggest the diagnosis. Examination may reveal flank discoloration (Grey – Turner sign) and peritonism. SIRS, ARDS, coagulopathy and renal failure may develop. The action of digestive enzymes on fat leads to ‘soap formation’ hypocalcaemia and hypomagnesaemia. Diabetes mellitus arising de novo may be permanent.

Investigations

A raised serum amylase (>1000 IU/1) is diagnostic but is often absent. Values in the range 100–1000 suggest alternative intra-abdominal pathologies, including perforated viscus. CT imaging investigation of first choice. MRI is also useful in more difficult cases. Culture of aspirated fluid can be used to guide surgical drainage, i.e. if heavily infected indication for surgery or drainage.

Localized posterior perforations of duodenum or stomach may be difficult to distinguish. Chest and abdominal plain films should confirm the absence of free gas or pneumonia, and may show calcium deposition. In severe cases the typical radiographic features of ARDS may be present. Plain film and ultrasound may confirm the presence of gallstones or other underlying biliary lesion. Blood glucose and arterial gases should be closely monitored. As the condition progresses, serial CT scanning is valuable to monitor pancreatic viability and to diagnose pancreatic cysts and pseudocysts.

Management

Severe cases should be referred to specialist centres. In milder cases supportive treatment and analgesia are the main requirements. Pethidine theoretically causes less spasm of the sphincter of Oddi than morphine. Hyperglycaemia is managed by sliding scale insulin infusion. Traditionally, the GI tract is rested by insertion of a nasogastric tube and regular drainage/aspiration. Total parenteral nutrition is frequently introduced early in the condition. These views are currently undergoing reappraisal; some studies suggest that very early enteral feeding reduces mortality.

In some centres, octreotide (25 μg hourly by infusion) or lanreotide are used to reduce exocrine activity. Patients who develop SIRS/ARDS require intubation, ventilation and haemodynamic optimization. These patients may benefit from antioxidant regimens. Acute renal failure may require renal replacement therapy. Particular attention should be paid to acid – base balance and electrolyte disorders. Repeated calcium, phosphate and magnesium supplementation are often required.

Pancreatic cyst/pseudocyst formation requires expert surgical intervention. Treatment may be conservative, by radiologically guided drainage, or by surgical excision. The latter may require repeated laparotomy for intra-abdominal sepsis.

The role of prophylactic antibiotics in severe pancreatitis has been widely debated and controversial in recent years. The best evidence currently available suggests that prophylactic use of antibiotics is associated with an increased mortality, and that antibiotic use should be guided according to culture results. Because pancreatitis is associated with a brisk SIRS response, it is tempting to introduce antibiotics in the absence of infection. This temptation should be resisted!

Prognosis

This depends on the severity and duration of the disease and the occurrence of complications including SIRS, ARDS and ARF. In general, the prognosis is poorer in the elderly, in those with pre-existing diabetes mellitus and those with alcohol-related disease.

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