Gastrointestinal emergencies

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Chapter 25 Gastrointestinal emergencies

Greg McDonald

The aim of emergency department assessment of patients with gastrointestinal (GIT) emergencies is to rapidly detect and stabilise those patients requiring urgent surgical or procedural intervention. In pursuing this aim the processes of assessment, investigations appropriate to the disease and management should be followed in an orderly and purposeful manner and must be performed simultaneously in the seriously ill.

ACUTE ABDOMEN

An ‘acute abdomen’ may be defined as an acute intra-abdominal condition causing severe pain and often requiring urgent surgery. The causes may be:

• inflammatory, e.g. appendicitis, diverticulitis, cholecystitis, perforated viscus
• mechanical, e.g. incarcerated hernia, band adhesions, volvulus, intussusception
• vascular, e.g. aortic aneurysm, mesenteric infarction
• neoplastic, e.g. carcinoma colon
• congenital, e.g. malrotation, congenital atresia/stenosis, Meckel’s diverticulum
• trauma.

The priority is to resuscitate the patient as needed and exclude a life-threatening cause of abdominal pain. In-hospital investigation and management is usually required.

Assessment

History

• Who is your patient? Age and sex are two important aetiological factors.

• Patients over the age of 65 years are twice as likely as younger patients to require surgical intervention.
• Gynaecological disorders obviously need to be excluded in women, particularly in their childbearing years. Young women are also more likely to have a final ‘uncertain’ diagnosis (up to one-third of cases).
• Previous medical and surgical histories and a drug history will give important clues to diagnosis and need to be considered for operative fitness.

• When did the pain start? Acute onset of severe pain implies vascular events, perforated viscus or renal colic. Inflammatory causes tend to arise more slowly.
• Where is the pain? Has it moved? Initial visceral pain is usually diffuse and in the midline. Later somatic pain localises better to the site of pathology.
• What is the pain like? The colicky pain of bowel obstruction is typically episodic and gripping with pain-free intervals. In the case of biliary and renal colic, there is more constant pain rising to a crescendo. Constant severe pain indicates advanced or serious illness.
• Which other symptoms accompany this illness? The onset of nausea and vomiting after the onset of pain suggests surgical illness. Constipation is non-specific but absolute constipation (neither faeces nor flatus) indicates bowel obstruction. Diarrhoea, jaundice, haematuria, haematemesis or melaena leads to specific diagnoses.

Remember: Only two-thirds of patients with acute surgical conditions have a ‘typical’ history of illness. Children and the elderly are more likely to have atypical presentations.

Examination

General

Appearance is apprehensive and motionless with peritonitis, unsettled and agitated with colicky pain, and pale and ‘Hippocratic’ with advanced disease. Check temperature, hydration, pulse and blood pressure (with postural drop).

Abdomen

• Inspection—rigid, distended or scaphoid, visible peristalsis, operative scars
• Palpation—guarding, diffuse or local tenderness, rebound tenderness

Note: ‘Rebound’ is not pathognomonic of peritonitis. It is false positive in up to one-quarter of patients and is an observer-dependent sign. Cough and percussion tenderness are often more reliable.

• Percussion—local peritonism, air, fluid, masses, organs

Note: Loss of liver dullness with pneumoperitoneum.

• Auscultation—peristaltic noises coinciding with colic in small bowel obstruction, diffuse increased bowel sounds in gastroenteritis, silent abdomen or occasional tinkling sounds in late bowel obstruction or diffuse peritonitis

Special signs

• Murphy’s sign in cholecystitis; Rovsing’s, psoas and obturator signs in appendicitis; Cullen’s and Grey-Turner’s signs in pancreatitis; costovertebral tenderness with pyelonephritis or perinephric abscess.
• Hernial orifices/scrotum and testes should never be forgotten.
• Rectal examination looking for blood (bright, melaena or occult), faecal loading, local tenderness, masses, prostatomegaly.
• Pelvic examination: incorrect and uncertain diagnoses occur much more frequently in women. A careful vaginal examination will help differentiate pelvic pathology.

Note: Cervical excitation is a ‘classic’ sign of ectopic pregnancy and pelvic inflammatory disease but is an observer-dependent sign.

OTHER SYSTEMS

Exclude non-abdominal pathology causing abdominal pain, e.g. pneumonia, pulmonary embolus and myocardial infarction. Assess operative fitness (cardiovascular and respiratory).

Investigations

Immediate

• Urine—urine analysis, microscopy and culture, pregnancy test (if appropriate)
• Blood—haemoglobin; haematocrit (PCV); white cell count and differential; electrolytes, urea and creatinine (EUC); amylase/lipase (if appropriate); blood gases (if appropriate); group-and-hold serum/cross-match (if blood loss or operation likely)
• Stool—occult blood
• Organ imaging—abdominal X-ray, supine and erect, chest X-ray, erect

Semi-urgent (with appropriate indications)

• Blood—liver function tests, coagulation studies
• Stool—smear and culture for colitis, enteritis
• Organ imaging—abdominal, ultrasound CT scan, angiography
• Endoscopy—proctosigmoidoscopy, panendoscopy

Value of investigations

Pregnancy should be considered and excluded in all women of child-bearing years with acute abdominal pain.

White cell count is non-specific unless a marked neutrophilia (over 20 × 109/L) is present. It is often a late manifestation of significant pathology.

Serum amylase is frequently elevated in a variety of surgical conditions. Levels greater than three times normal strongly suggest pancreatitis. Lipase is more sensitive and specific for pancreatitis and is the test of choice for this disease.

Abdominal X-rays are a poor tool for diagnosing non-specific abdominal pain, but are valuable in confirming specific and serious pathology. Bowel obstruction, paralytic ileus, caecal and sigmoid volvulus have typical findings. A paucity of bowel gas may be the only clue to mesenteric infarction. Don’t forget to check the psoas shadows, the size and shape of solid organs, for calculi and for air in the biliary tree. Avoid abdominal X-rays in pregnancy if possible.

Erect chest X-ray will detect subdiaphragmatic free air, exclude pulmonary pathology and help preoperative assessment. Free air will be absent in about 20% of perforated peptic ulcers. Massive pneumoperitoneum suggests colonic perforation. The chest X-ray is the definitive investigation for Boerhaave’s syndrome (oesophageal rupture).

Abdominal ultrasound is usually indicated for right upper quadrant pain and cholelithiasis, obstructive uropathy, pelvic pathology, suspected abdominal aortic aneurysm (in stable patients) and abdominal masses. It is the investigation of choice in many paediatric patients, e.g. intussusception, pyloric stenosis, appendicitis. Pelvic ultrasound is essential for the diagnosis of gynaecological and pregnancy-related diseases.

CT scanning: spiral non-contrast CT is the initial test of choice for renal colic. Contrast CT is useful in diagnosing many acute surgical conditions, e.g. acute pancreatitis, intra-abdominal sepsis, intra-abdominal trauma. It is increasingly used to confirm the preoperative diagnosis before laparotomy.

Angiography may be both diagnostic and therapeutic in intestinal haemorrhage, mesenteric ischaemia and abdominal trauma.

Proctosigmoidoscopy is a diagnostic tool in bright rectal bleeding, rectal mass and colitis, and is therapeutic in sigmoid volvulus.

Panendoscopy is indicated urgently in life-threatening upper GIT bleeding and semi-electively in stable patients with suspected peptic ulcer or other inflammatory conditions of the upper GIT.

Management

Surgical emergency

Examples of a surgical emergency include perforated viscus, advanced peritonitis, mesenteric infarction and strangulated bowel.

Common indications for laparotomy

Most patients with an acute abdomen will undergo specific imaging prior to surgery. Adequate resuscitation and prophylactic antibiotics will allow imaging before operation.

• Physical findings—diffuse or spreading rigidity; tense or progressive distension; increasing or severe localised tenderness and peritonism; tender abdominal mass with high fever or sepsis; equivocal clinical signs with septicaemia, uncontrolled bleeding, suspected mesenteric ischaemia, deterioration with conservative treatment
• Radiological findings—pneumoperitoneum; gross or progressive bowel obstruction; free contrast extravasation; perforation abscess on ultrasound/CT scan
• Endoscopic findings—perforation or uncontrolled bleeding

Preoperative treatment

1. Airway.
2. Breathing—oxygen by mask.
3. Circulation—intravenous access and appropriate blood tests; volume resuscitation; urinary catheter.
4. Analgesia should be given after initial medical assessment and establishment of a working diagnosis. Small increments of intravenous narcotics greatly benefit the patient.

Note: Narcotics do not mask clinical signs in abdominal pain; they may help in assessment by reducing patient distress and anxiety. Do not deny analgesia to patients in pain.

5. Antibiotic prophylaxis is required with diffuse peritonitis or if infective pathology is suspected. Ampicillin, gentamicin and metronidazole is the usual combination therapy.
6. Preoperative preparation—nasogastric tube; operative fitness; consent (by surgeon).

Surgical admission

Some conditions for which admission to hospital for conservative treatment, observation and semi-elective operation is appropriate are discussed later.

Emergency department observation and discharge

Patients with mild or equivocal tenderness, minor or no laboratory abnormalities and whose condition settles can be discharged for follow-up in the community, after observation in the department. Certain diagnoses, e.g. uncomplicated renal or biliary colic and peptic ulceration, are discharged in most cases for further investigations and referral.

SPECIFIC SURGICAL CONDITIONS

Acute appendicitis

This is the most common general surgical emergency. Most problems occur with extremes of age, < 5 and > 60 years, mostly due to atypical presentation and late diagnosis.

Assessment

• Typical history is vague periumbilical pain, anorexia, nausea, vomiting, pain migration to right iliac fossa, fever. This only occurs in about half of cases.
• Clinical features include: mild/moderate pyrexia; anorexia; McBurney’s point tenderness and peritonism with or without mass; ruptured appendix will often have a quiet peritonitic abdomen with few localising signs.
• Perform vaginal examination to exclude pelvic pathology in women.
• Differential diagnoses: mesenteric adenitis in children; diverticular disease/caecal carcinoma in adults; ovarian cyst, pelvic inflammatory disease, ectopic pregnancy.

Investigations

• Convincing clinical appendicitis—no investigations are required, other than for preoperative assessment if needed.
• Uncertain diagnosis—urine analysis/MSU to exclude urinary tract infection; white cell count is moderately raised (10 to 15 × 109/L with left shift) and is often a late indicator; AXR/CXR rarely necessary, perform only if you suspect another diagnosis or complications.
• Ultrasound is preferred for evaluating right iliac fossa pain in children and fertile female patients if the diagnosis is uncertain.
• CT is more sensitive than ultrasound and may reveal alternative diagnoses; contrast is not needed with newer CT scanners.

Management

1. Surgery as soon as practical. Overnight delay in the stable patient does not significantly worsen outcome.
2. Suspected perforation/generalised peritonitis—urgent surgery.
3. Prophylactic antibiotics reduce infective complications. They should be given in the emergency department if peritonitis or abscess is suspected or if surgery will be delayed. Otherwise antibiotics can be given at induction of anaesthesia.
4. Mass/phlegmon—intravenous antibiotics and fluids; nil by mouth; ultrasound/CT scan; operation at surgeon’s discretion.
5. Uncertain diagnosis—non-specific clinical findings and investigation results; admit; nil by mouth; intravenous fluids; analgesia; close review; ultrasound/CT scan.

Acute cholecystitis

Assessment

• 25% of women and 12% of men have gallstones.
• Past history of fat intolerance, belching and flatulence.
• Right upper quadrant pain becoming constant and severe.
• Mild fever and tachycardia; mild icterus in 10% of cases.
• Tender right upper quadrant with positive Murphy’s sign.
• Palpable gallbladder in about one-third of cases.
• Empyema—toxic/shocked, high spiking temperatures.
• Local perforation—progressing fever, symptoms and signs. Local mass and peritonism.
• Free perforation—general peritonism.
• Cholangitis—common duct stone; right upper quadrant pain; jaundice; fever/rigors.

Investigations

• Urine analysis—bilirubin; exclude renal pathology.
• White cell count—moderate neutrophilia is usual. Marked neutrophilia suggests complications.
• Liver function tests—bilirubin > 60 mmol/L suggests common duct obstruction.
• Abdominal X-ray is often not helpful but may be ordered to exclude other pathology and complications.
• Ultrasound demonstrates stones, debris within the gall bladder, wall thickening, masses or abscesses.
• Hepatobiliary iminodiacetic acid scan (HIDA) may be used if the ultrasound is non-diagnostic, e.g. acalculous cholecystitis.
• Operative fitness assessment (e.g. ECG, CXR, Hb, renal function).

Management

Uncomplicated biliary colic

Discharge home for outpatient investigation and referral if:

• pain resolves
• no significant local signs
• normal laboratory investigations.

Cholecystitis/cholangitis

1. Admit to hospital
2. Nil by mouth and intravenous fluids
3. Analgesia
4. Antibiotics intravenously (ampicillin/gentamicin)
5. Ultrasound, usually within 24 hours
6. Endoscopic retrograde cholangiopancreatography (ERCP) if obstructing bile duct stone
7. Early cholecystectomy when condition settles

Advanced/complicated disease

Examples of this are empyema, abscess, free perforation, septicaemia.

1. Rapid stabilisation and assessment as for ‘surgical emergency’
2. Antibiotics (ampicillin, gentamicin and metronidazole or equivalents)
3. Urgent cholecystectomy or cholecystostomy

Diverticular disease

Fifty percent of people over 40 years of age have diverticular disease.

Assessment

• Previous history—irregular bowel habit; diffuse, non-specific lower abdominal pain
• Diverticulitis—fever; altered bowel habit; left iliac fossa (LIF) pain and tenderness with or without local peritonism; LIF or pelvic mass
• Diverticular abscess—toxic; palpable mass
• Free perforation—generalised peritonitis
• Bleeding (See ‘Lower GIT bleeding’ below.)

Investigations

• Urine analysis and midstream urine (MSU)
• White cell count
• Occult blood
• Abdominal X-ray usually non-specific, but will reveal perforation, local or generalised ileus or large mass
• Contrast CT scan to distinguish abscess/local perforation

Management

• Diverticulitis—admit; nil by mouth; intravenous fluids; intravenous antibiotics (ampicillin/gentamicin/metronidazole)
• Complicated/severe disease (e.g. advancing peritonitis; CT findings)—as above; urgent surgery

GASTROINTESTINAL BLEEDING

Upper GIT bleeding

Aetiology

• 50% peptic ulceration
• 5% erosive gastritis/oesophagitis/duodenitis
• 15% oesophageal varices
• 5% Mallory-Weiss syndrome
• 5% others (tumour, blood dyscrasias etc)

Note: 30% of patients with known varices will bleed from other non-variceal causes.

Assessment

History

• Amount and nature of bleeding (haematemesis/melaena)
• Symptoms of occult bleeding
• Drug history—alcohol; non-steroidal anti-inflammatories; steroids
• Past GIT disease/other conditions

Examination/immediate intervention

• Airway
• Breathing—oxygen by mask
• Circulation—pallor/shock; pulse/blood pressure with postural drop; intravenous access—1 or 2 large-bore cannulae with pump set
• Blood for—haemoglobin; haematocrit; crossmatch; electrolytes; urea/creatinine; coagulation studies; liver function
• General—evidence of chronic liver disease and hepatic encephalopathy; abdominal examination including rectal exam with or without proctoscopy; cardiorespiratory status

Investigations

• Nasogastric tube may be inserted for:

• stable patients as a diagnostic tool if upper GIT bleeding is occult
• profuse haematemesis to empty stomach prior to endoscopy.

• Panendoscopy is the definitive investigation and in many cases an effective immediate treatment of upper GIT bleeding. Panendoscopy within 24 hours in stable patients reduces rebleeding rates and shortens length of stay. Information regarding the aetiology, site and prognosis of the bleeding is gained. Urgent panendoscopy should be performed in cardiovascularly unstable patients and in those with profuse or persistent bleeding.

Management

1. Volume resuscitation with colloid and/or blood and/or clotting factors.
2. Close monitoring of vital signs, hourly urine output and haemoglobin/haematocrit. Central venous pressure (CVP) monitoring should be used in the cardiovascularly unstable patient and patients who are elderly or have cardiorespiratory disease.
3. Urgent panendoscopy on high-risk patients with: shock; blood requirements > 5 units; serious underlying disease; recurrent bleeding, especially if over 60 years of age.

Non-variceal bleeding

• Eighty per cent of cases will settle spontaneously; 20% will require intervention for recurrent bleeding within 48 hours.
• Poor prognostic endoscopic findings in non-variceal bleeding are: gastric ulcer, especially lesser wall; posterior site in duodenum; visible vessel; sentinel clot or black spot in ulcer base.

Further management

• Notify a surgeon of high-risk patients, either on clinical criteria or endoscopic finding.
• Commence proton pump inhibitors (PPIs): orally if bleeding ceased and patient stable; intravenously with active bleeding or if nil by mouth, e.g. IV pantoprazole 80 mg stat and 8 mg/hour for 10 hours. PPIs reduce bleeding recurrence and shorten length of stay.

Definitive treatment:

• endoscopic haemostasis
• surgery
• angiographic haemostasis (depending on availability).

Variceal bleeding

Poor prognostic factors include large blood requirements (over 4 units), active bleeding at endoscopy and Child’s category C patients (advanced hepatic failure).

Further management

1. Endoscopic banding or sclerosis is 90% effective in controlling variceal bleeding. Balloon compression prior and/or simultaneously aids sclerotherapy.
2. Sangstaken-Blakemore/Minnesota tube—careful placement by an experienced person is necessary. Endotracheal intubation beforehand is preferred. Careful observation of position and balloon pressures with deflation at 24 hours minimise traumatic complications. About 50% of patients will rebleed within 24 hours.
3. Octreotide—lowers azygous vein blood flow in patients with portal hypertension. Dosage is 50–250 μg bolus and infusion of 50–250 μg/hour.
4. Vasopressin infusion at an initial dose of 0.2–0.4 units/minute controls variceal bleeding in about two-thirds of cases. Side effects include hypertension, nausea/vomiting and ischaemia of myocardium, bowel or skin. Intercurrent vasodilator infusion (glyceryl trinitrate or nitroprusside) may be necessary to reduce complications.

Note: Both octreotide and vasopressin are temporary measures with similar efficacy and a high incidence of rebleeding after cessation.

5. Angiographic embolisation.
6. Transjugular intrahepatic portosystemic shunt (TIPPS).

Lower GIT bleeding

Causes of profuse bright per rectal bleeding are: diverticular disease; polyps; angiodysplasia; carcinoma/colitis/solitary ulcer; Meckel’s ulcer in children.

Note: Bright or maroon rectal bleeding can occur with profuse upper GIT bleed.

Assessment

History, examination and immediate intervention are as for upper GIT bleeding. Note that a high urea/creatinine ratio (> 100:1) suggests an upper GIT site of bleeding.

Investigations

• Sigmoidoscopy should be performed as the initial investigation.
• Nasogastric tube for exclusion of upper GIT bleeding if suspected and/or for preoperative preparation.
• Radioisotope red cell scan or mesenteric angiography should be performed urgently if bleeding persists. A negative scan indicates bleeding rate less than 0.1 mL/minute (see below, ‘Further management’).

Management

1. Volume resuscitation.
2. Monitor vital signs, urine output, haemoglobin/haemocrit with or without CVP.
3. Notify surgeon.
4. Bleeding stops spontaneously in 75% of cases with conservative treatment. If bleeding is profuse or recurrent, undertake further management.

Further management

1. Negative isotope scan—semi-elective colonoscopy and/or other investigations.
2. Positive isotope scan (i.e. active bleeding)—further urgent investigation and/or treatment required.
3. Angiography—selective arterial catheterisation is 60% successful in identifying the bleeding site and allows treatment with intra-arterial vasopressin infusion or embolisation.
4. Colonoscopy has variable efficacy in brisk acute bleeding and requires experienced hands.
5. Surgery should be undertaken when the bleeding site is known and/or the above two modalities have not controlled the haemorrhage.

ACUTE PANCREATITIS

The causes of acute pancreatitis are: gallstones (40–50%); alcohol (25–35%); idiopathic (20%); and others (5%).

Assessment

History

• Aetiological factors
• Acute epigastric pain through to back associated with nausea and vomiting

Examination/initial intervention

• Airway
• Breathing—oxygen by mask
• Circulation—shock; pulse, blood pressure with postural drop; intravenous line
• Blood for—lipase/amylase; haemoglobin/haematocrit; electrolytes; urea/creatinine; calcium; glucose; liver function tests; arterial gases; coagulation studies; group-and-hold
• Abdominal examination—temperature, jaundice; epigastric tenderness with or without mass; local/diffuse peritonism; Cullen’s (periumbilical) and Grey-Turner’s (flank) signs in haemorrhagic pancreatitis; paralytic ileus; subcutaneous fat necrosis
• Cardiorespiratory examination, especially to exclude complications

Poor prognostic indicators

• Severe necrotising pancreatitis, which may also become secondarily infected, occurs in 10–20% of patients. Clinical and radiological scoring can select those patients with more severe disease requiring ICU admission and consideration for CT-guided drainage or surgery.
• Ranson’s criteria:

• Immediate—age > 55; hyperglycaemia; leukocytosis; LDH; AST
• Two days—drop in haemoglobin/haematocrit; shock; hypocalcaemia; hypoxia; azotaemia (elevated urea)
• Score ≥ 5 (at 48 hours) suggests serious illness

• APACHE score
• Balthazar staging on CT scanning (most sensitive predictor)

Investigations

• Amylase—level more than three times normal confirms the diagnosis in the great majority of cases. Lipase is more sensitive and specific and is better than amylase in diagnosing chronic pancreatitis.
• Abdominal X-ray—exclude perforated peptic ulcer. Look for: pancreatic calcification/gall stones; ascites. ‘Sentinel loop’ is non-specific.
• Chest X-ray—raised left hemidiaphragm; pleural effusion; atelectasis; ARDS.
• ECG to exclude myocardial infarct.
• Ultrasound should be performed within 24 hours to exclude gallstone pancreatitis. CT scanning with contrast is indicated within 48 hours to assess severity.

Management

1. Volume resuscitation.
2. Supplemental oxygen.
3. Monitor observations, urine output with or without CVP.
4. Nasogastric tube for severe cases or if gastric dilation or ileus, otherwise nil by mouth.
5. Analgesia—parenteral narcotics after diagnosis is established.
6. Insulin infusion if blood sugar level > 15 mmol/L.
7. Observe for other complications—shock/acidosis; acute tubular necrosis; ARDS/disseminated intravascular coagulation (DIC); haemorrhagic pancreatitis; pancreatic abscess.
8. Early nutritional support—nasojejunal or parenteral.
9. Prophylactic antibiotics—the evidence is conflicting, but imipenem or imipenem/cilastin has shown benefit in some trials in severe necrotising pancreatitis.
10. CT-guided aspiration if abscess suspected. Laparotomy has up to 40% mortality.

GASTRO-OESOPHAGEAL REFLUX DISEASE (GORD)—OESOPHAGITIS

Remember: Indigestion is not a diagnosis; it is an excuse to stop thinking.

In discussing GORD, it is crucial to consider an acute coronary syndrome. Improvement of ‘indigestion’ with antacids is not proof of upper GIT pathology. ‘Indigestion’ is a common diagnosis in missed acute myocardial infarction (AMI). The mortality rate of missed AMI is around 30%.

About 7% of the population report daily heartburn. Risk factors for GORD include: obesity; alcohol; smoking; diabetes; pregnancy. Exacerbating factors are: chocolate/fatty and spicy foods; drugs, e.g. NSAIDs; cough medicines; bisphosphonates. The commonest symptoms of GORD are: heartburn; regurgitation; dysphagia (oesophageal stricture or spasm). Atypical symptoms relate to gastric reflux, which may be ‘silent’, e.g. cough/wheeze or hoarseness.

Heartburn is the commonest non-cardiac cause of chest pain (∼50% of cases).

Assessment

History

• Aetiological factors.
• Epigastric and/or chest pain, typically burning. Oesophageal spasm may occur without burning pain.
• Reflux, with or without cough/wheeze/hoarseness.
• Haematemesis/melaena.
• Cardiac risk factors and cardiac symptoms—could it be angina?
• Fatty food intolerance; belching; RUQ pain—could it be cholelithiasis?
• Weight loss; anorexia; jaundice—could it be upper GIT malignancy?
• Malignancy/steroid use/HIV/immunosuppression—could it be infective oesophagitis?

Examination

• Airway; breathing; circulation
• Abdominal examination—tenderness (epigastrium/RUQ); liver; masses; aorta + bruit; rectal exam for blood

Investigations

• For simple GORD none may be required, other than an ECG. A trial of antacids or H2-receptor antagonist may give relief and suggest GORD, but does not rule out other diagnoses.
• To exclude other diseases, e.g. ECG/cardiac markers; CXR; LFTs; amylase/lipase; abdominal ultrasound.
• To assess complications of erosive oesophagitis, e.g. FBC; iron studies.

Management

1. Lifestyle modification—weight loss; avoid precipitating foods/smoking; elevate head of bed about 20 cm; eat evening meal 3 hours prior to bed; smaller meals.
2. If simple GORD, commence treatment and refer to local doctor:

a. antacids after meals and at night may control symptoms
b. H2-receptor antagonist.

3. Consult gastroenterologist if: dysphagia; uncertain diagnosis; refractory symptoms requiring PPIs; complicated disease, e.g. aspiration/asthma or bleeding; possible malignancy.

VOMITING

Vomiting is a symptom, not a diagnosis. Most vomiting patients have benign, readily treated illnesses. Occasionally it is a symptom of a life-threatening problem. Management is directed at finding and treating the cause, assessing fluid deficits and controlling the symptoms.

Assessment

History

• Age—nausea and vomiting in infants and children raise certain diagnoses: pyloric stenosis; intussusception; viral gastroenteritis; reflux; sepsis, e.g. meningitis; children also become dehydrated more quickly
• Fever; viral prodrome; contacts with gastroenteritis or suspect foods; diarrhoea—gastroenteritis or food poisoning
• ‘Heartburn’; epigastric discomfort; haematemesis/melaena—peptic ulcer disease; erosive oesophagitis; oesophageal varices; Mallory-Weiss tear
• Chest pain—myocardial infarction; Boerhaave’s syndrome
• Abdominal pain—colicky suggesting bowel obstruction; RUQ suggesting biliary disease; RIF suggesting appendicitis; generalised and severe suggesting peritonitis
• Previous abdominal surgery and colicky pain—adhesions and bowel obstruction
• Jaundice; dark urine—biliary disease; hepatitis
• Headache—migraine; meningitis or meningism; cerebrovascular event; sub-arachnoid haemorrhage
• Vertigo/‘dizziness’—labyrinthitis; vertebrobasilar cerebrovascular accident (CVA) or posterior fossa lesion
• Medications—opiates; antibiotics; chemotherapy; almost any medication
• Pregnant—exclude with beta subunit of human chorionic gonadotrophin (BhCG) in fertile women
• Diabetic or symptoms of diabetes—ketoacidosis
• Marijuana abuse—cyclical vomiting syndrome (repetitive hot showers are pathognomonic)

Examination

• Airway
• Breathing—ketotic; aspiration
• Circulation—vital signs; peripheral perfusion; dehydration
• Disability—pupils; GCS; mental state
• System specific examination—looking for underlying causes as above

Investigations

• Investigations depend upon the clinical context and likely aetiology. They serve two purposes: establishing the underlying cause and assessing complications of vomiting.
• Basic tests should include FBC; EUC; LFTs; BSL; urine analysis; BhCG in fertile women.
• Disease-specific tests depend on the potential diagnoses.

Management

1. IV access is usually required. Children may be managed with oral rehydration ± ondansetron wafer. Some adults will respond to rectal or intramuscular anti-emetics.
2. Resuscitate with normal saline if severe dehydration/shock.
3. Restore fluid deficits depending on degree of dehydration and EUC results. Insert indwelling urinary catheter if severe dehydration or persistent vomiting.
4. Anti-emetics include:

a. dopamine antagonists—metoclopramide IM/IV; prochloperazine PR/IM/IV; promethazine IM/IV slowly (may be useful with vestibular causes and in children); haloperidol/droperidol IM/IV cautiously
b. serotonin antagonists—ondansetron PO (wafer)/IM/IV; dolasetron IM/IV (not in children)
c. adjuncts—ginger, pyridoxine in pregnancy; oral methylprednisolone or dexamethasone.

5. Disease-specific interventions as indicated.

CONSTIPATION

As in vomiting, it is important to rule out serious underlying causes of constipation. It is the commonest GIT complaint, affecting up to 25% of people at some time. Two per cent of the population have chronic or recurrent constipation.

Causes in children:

• functional (over 90% of cases, especially if over 1 year old)
• change in formula or to bottle feeding in infants
• Hirschsprung’s disease
• congenital anorectal or neurological diseases
• cystic fibrosis
• metabolic disorders

Causes in adults:

• primary—functional (normal transit); slow transit; anorectal muscle incoordination
• secondary—medications (up to 40% of cases), e.g. opioids, anti-depressants, calcium channel blockers, diuretics, iron, antihistamines, psychotropic agents; irritable bowel syndrome (IBS); psychological conditions—anxiety, depression; anorectal structural abnormalities, e.g. anal fissure, haemorrhoids, prolapsed; endocrine and metabolic diseases, e.g. diabetes mellitus, hypercalcaemia, hypothyroidism; neurological, e.g. Parkinsonism, multiple sclerosis, spinal cord disease; autonomic neuropathy

Note: Constipation is not a ‘normal’ part of ageing.

Assessment

History

• Frequency and quality of stool; effort of defecation; pain; incomplete evacuation; soiling; bleeding; nausea/vomiting; medications; urinary retention
• ‘Red flags’ in children—delayed meconium; abdominal distension/vomiting; failure to thrive, recurrent pneumonia (cystic fibrosis); abnormal gait or lower limb tone; wheat intolerance (gluten enteropathy)
• ‘Red flags’ in adults—age over 50 years; weight loss; rectal bleeding; family history of colon cancer

Examination

• Directed at finding underlying cause and confirming faecal loading
• Airway; breathing; circulation
• Dehydration if vomiting; abdominal distension
• Abdominal examination—looking for obstruction, masses or hernia
• Anal inspection—congenital abnormality in children; anal fissure; haemorrhoids; rectal prolapse
• Rectal examination—mandatory in an adult; may be replaced by plain abdominal X-ray in children if parents object or child distressed (level C evidence)
• Specific system examination to exclude secondary causes, e.g. neurological (altered anal tone, abnormal lower limb power/tone/reflexes)

Investigations

• None usually required if history of functional constipation in child (see AXR above).
• FBC; BSL; EUC; calcium; thyroid function; urine analysis in adults. AXR may be indicated to exclude obstruction and/or reveal extent of colonic loading.
• Sigmoidoscopy and/or colonoscopy (semi-elective) if ‘red flags’ in adult.
• Specific investigations or consultations if secondary cause suspected.

Management in adults

This is a possible protocol. Local preferences may apply.

1. Distal rectal vault only:

a. 1–2 Microlax enemas → wait 30–60 minutes
b. 1–2 Bisacodyl enemas → wait 30–60 minutes
c. Fleet (phosphate) enema OR 20 mL lactulose in 100 mL water → retain at least 10 minutes; may be repeated once
d. Manual disimpaction (with analgesia; sedation)
e. May need admission for repeat enemas

2. Faecal matter above rectum:

a. Oral sorbitol (70%) 30 mL q2–3 hours PLUS
b. Fleet (phosphate) enema or lactulose enema as above → wait 4–6 hours
c. If no success (or oral sorbitol not available) → glycoprep-C solution 1 sachet/litre orally per hour up to 3 litres OR Movicol 8 sachets in 1 litre over 6 hours OR oral Picosulphate 1–2 sachets in glass of water (causes greater fluid and electrolyte shifts; use cautiously in the elderly; dehydration; renal impairment; cardiac failure)

Admission is often required for observation, repeat enemas and/or oral agents.

Patients may be discharged if they have at least one significant documented bowel action for follow-up by their doctor in 24 hours.

Discharge plan should include dietary advice, fluid intake, exercise, toileting pattern, aperients and review of causative medications.

HEPATIC FAILURE—PORTOSYSTEMIC ENCEPHALOPATHY

Fulminant

• Encephalopathy, jaundice, hepatic fetor, multiple system complications

Aetiology

• Viral hepatitis
• Paracetamol overdose/CCL4
• Drug reactions (e.g. INAH, halothane, methyldopa)

Acute-on-chronic

• Stigmata of chronic liver disease, jaundice, ascites, encephalopathy

Aetiology

• Alcoholic cirrhosis
• Chronic active hepatitis
• Post-necrotic
• Infiltrative
• Other

Precipitating causes of encephalopathy

Fulminant

Encephalopathy from cerebral oedema is the hallmark of the disease. Coma has 80% mortality. Can be exacerbated by the conditions listed below.

Acute-on-chronic

• GIT bleeding (especially upper)—elevated urea/creatinine ratio is suggestive; accounts for about 25% of cases
• Constipation
• Increased protein load
• Azotaemia/volume depletion—hepatorenal syndrome
• Hypokalaemia/alkalosis
• Hypoxaemia/hypoglycaemia
• Infection, including spontaneous bacterial peritonitis in ascites (usually coliforms or pneumococcus)
• Ethanol, sedatives, opiates

Assessment

History

• Alcohol and drug history
• Rapidity of onset of symptoms
• GIT bleeding

Examination/immediate intervention

• Airway
• Breathing—oxygen by mask as necessary
• Intravenous access
• Blood for—haemoglobin/haematocrit; coagulation studies; electrolytes/urea/creatinine; calcium/phosphate/magnesium; blood sugar level; liver function tests; arterial blood gases; viral serology, drug screen, group-and-hold as necessary
• Dextrose—hypoglycaemia needs to be rapidly excluded and treated
• Encephalopathy—GCS; mini-mental state; Star chart; asterixis (flap)
• Further examination—fetor; evidence of chronic liver disease/ascites; liver/spleen/rectal examination; cause of likely decompensation, including rectal exam; complications (e.g. bleeding, cardiorespiratory, infectious disease, alcohol withdrawal)

Investigations

• Septic workup, including ascitic tap
• Arterial blood gases
• Serum ammonia (does not correlate well with severity of illness)
• Occult blood
• Chest X-ray
• ECG
• CT scan and EEG to assess encephalopathy/oedema and exclude other pathology
• Liver biopsy in some cases

Management

1. Treat precipitating causes, e.g. GIT bleeding, constipation, volume depletion, electrolyte abnormality, infection.
2. Reduce protein absorption—low protein diet (20–40 g/day); oral lactulose (30–45 mL q8h); oral neomycin (4–6 g/day) and metronidazole (250 mg q12h).
3. Other nutritional support, e.g. carbohydrates, zinc, magnesium.
4. Flumazenil to reverse intercurrent benzodiazepine ingestion. Bromocryptine may have a role in chronic encephalopathy.
5. Patients in coma will need endotracheal intubation and ICU transfer.
6. Consider radiographic occlusion of spontaneous portosystemic shunts if the patient is not responding to medical management. Surgical shunts, e.g. transjugular intrahepatic portosystemic shunt (TIPS), may also be reversed.
7. Liver transplant in selected patients.

RECOMMENDED READING

Doherty G.M., Way L.W., et al. Current surgical diagnosis and treatment, 12th edn. New York: The McGraw-Hill Companies (Lange); 2006.

eMedicine website. http://www.emedicine.com.

Marx J.A., et al. Rosen’s emergency medicine, concepts and clinical practice, 6th edn. St Louis: Mosby; 2006.

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