Answering bleep/taking referral

• Diarrhoea: is there known IBD? Is or was the patient on antibiotics? Pyrexial, tachycardia, unwell, dehydrated? How many times have bowels opened today and is stool bloody?
  
• Use the Bristol stool chart to characterise diarrhoea (Type 6/7). Suspected infective causes need isolation and stool culture. Wash hands with soap and water. Alcohol hand washes are insufficient.
  
• Why are they in hospital? When did it start? Frequency? Bristol stool chart scale.
  
• Abdominal pain or vomiting, recent antibiotics, excessive laxatives. Known bowel disease. Pain, guarding, tenderness – is this an acute abdomen?

On arrival

• Review early warning score. Review notes and drug chart particularly antibiotics and laxatives and stop them if possible. Discuss with microbiology if need for antimicrobials.
  
• Abdominal examination including PR – may be hard stools with overflow.
  
• Check basic bloods if concerned about dehydration. If severe diarrhoea or poor oral intake then IV fluids.
  
• Caution with loperamide if any suggestion of infective cause. Hand washing. Isolate patient and send stool cultures if infected cause suspected.

Investigations

• Bloods: FBC, U&E, TFT, CRP.
  
• Request stool culture: cysts, ova and parasites and C. difficile toxins A and B.
  
• AXR: features of IBD, toxic megacolon if pseudomembranous colitis.
  
• Sigmoidoscopy: look for inflamed mucosa, rectal biopsy if diarrhoea persists.
  
• Colonoscopy: if colitis or polyps/tumour suspected. Colonoscopy is best investigation to diagnose colonic cancer in those without significant co-morbidities. If there are such issues then CT colonography may be considered or flexible sigmoidoscopy and barium enema.
  
• CT/MRI: rarely needed. Get if suspected intra-abdominal pathology. MRI best for pelvic Crohn’s disease or other inflammatory bowel disease.
  
• Rare: look for carcinoid syndrome, VIPoma, etc.

General management

• Isolation if an infective cause suspected. Gown up and wear gloves, which should be placed in bin in patient’s room. Ensure hands washed with soap and water to remove any C. difficile spores.
  
• See individual cases above, but all patients need to maintain adequate hydration either orally or IV depending on losses. Monitor fluid balance and U&E and general observations.
  
• Use codeine/loperamide sparingly in lowest dose for short period if severe symptomatic diarrhoea if infective causes suspected. Use with caution, concern is that they may delay resolution. Avoid if suspected C. difficile and pseudomembranous colitis. Surgical review if acute abdomen.

Answering bleep (is the patient a bowel obstruction/ileus or simple constipation?)

• Has there been dietary intake? When did bowels last open? Is patient in pain or discomfort?
  
• Patient taking opiates or dehydrated or bed bound or Parkinson’s disease or hypothyroid?
  
• Rarely an acute issue unless nil PR is a sign of obstruction with pain and abdominal distension and abnormal bowel sounds.

On arrival

• Review notes, observations and drug chart. Assess patient and usual bowel frequency. Once a week may be normal for some. Is it physical/psychological, e.g. having to use bed pan or commode?
  
• Pain, e.g. anal fissure or haemorrhoids will make patient avoid defecation. Needs stool softeners.
  
• If there are signs of bowel obstruction then nil by mouth, bloods and AXR and surgical consult.
  
• If not obstructed and mild may simply require improved hydration, high fibre diet and oral laxatives.
  
• If constipated (AXR may show stool ++) with watery diarrhoea and an enema, e.g. Microlax enema or a Picolax (sodium picosulphate) enema, can be very effective in emptying the rectum.
  
• Examination: tenderness, bowel sounds, peritonism, masses. PR examination: anal pain or discomfort, rectal tumour or impacted faeces. Spinal cord disease or multiple sclerosis usually already known. Hirschsprung’s disease usually from childhood. Myxoedema: look for clinical signs, ↑TSH.

Management

• Hydrate orally if possible and high fibre diet and early mobility and provide time and access to optimal toileting conditions with as much privacy as can be provided. Make use of gastrocolic reflex – toileting patient after eating.
  
• On-going or new constipation for several weeks warrants consideration to exclude a colorectal malignancy. Try stool softeners (e.g. SODIUM DOCUSATE 200 mg tds), bulking agents (e.g. FYBOGEL one sachet BD), stimulants (e.g. SENNA 1 tab BD is useful especially if stools are large, soft and bulky).
  
• Osmotic laxatives (e.g. LACTULOSE 10–20 ml BD) really are to be avoided if possible, except to improve stool output with hepatic encephalopathy. Movicol (e.g. contains polyethylene glycol or codanthramer). Enemas (e.g. glycerin suppository or Picolax enema) are useful for distal stool.
  
• Occasionally all fails and you may be asked to perform a manual evacuation, which is digital removal of rectal faeces. Be sure to wear two pairs of gloves and have lots of pads. Constipation is common but significant complications are very rare, but include faecal impaction where the rectum fills with ‘rocks’ of hard stool with soft stool leaking around sides and overflow diarrhoea.
  
• Can even cause intestinal obstruction and perforation and megacolon leading to sigmoid volvulus. Rectal prolapse can be seen. It may provoke urinary retention and UTI.

Laxatives and bowel preparation

• Stimulant laxative: SENNA 15 mg (2 tabs) BD SE: cramps, diarrhoea and low K. Avoid if bowel obstruction. BISACODYL 5–10 mg nocte.
  
• Osmotic laxative: LACTULOSE 10–30 ml 12 h, higher doses in hepatic encephalopathy (30–50 ml TDS) to have 2+ soft stools/day.
  
• Bulk forming laxative: ISPAGHULA HUSK 3.5 g BD or one sachet BD.
  
• Bowel cleansing for severe cases: SODIUM PICOSULPHATE 10 mg single dose and review.
  
• Enema: MICROLAX one PR and the more potent PHOSPHATE enema.

• Investigations: diagnostics can help where cause not evident. Send FBC. U&E, LFT, Ca, amylase/lipase, CRP, troponin (if needed), ECG, USS biliary tracts and pancreas, endoscopy, urea breath test for HP. HP serology identifies only prior exposure.
  
• Management: treatment can be with SUCRALFATE 2 g BD PO, RANITIDINE or PPI. H. pylori eradication – see BNF for latest regimen. Transfuse if anaemia Hb <80 g/L or bleeding. Iron replacement. See below for acute upper GI bleed and for gallstones. Always ask if this could be an ACS.

About: bleeding from above the ligament of Treitz. Nasopharynx, oesophagus, stomach, duodenum. Multiple causes may co-exist – varices and gastritis and a duodenal ulcer. Epistaxis and swallowed blood can mimic GI bleed. If physicians can’t stop life-threatening bleeding it’s a surgical problem. 90% of non-variceal bleeds (VBs) and 50% of VBs stop spontaneously. Mortality is 10%, rising to 26% in patients who bleed when in hospital for other reasons. Use the Blatchford and Rockall score to assess patients.

NB. With a suspect GI bleed first make sure there are at least two good wide bore IV lines before all peripheral venous access disappears.

• Clinical history/risk factors: most of the time the story is difficult with dark material passed orally or rectally and the usual ‘coffee grounds’, which may be bile. Ask about liver disease, peptic ulcer disease, alcohol intake, aspirin usage, NSAIDs, warfarin, steroids. Ask about a history of bleeding problems – dental extractions, etc. Bright red haematemesis implies active bleeding from the oesophagus, stomach or duodenum. This can lead to circulatory collapse and constitutes a medical emergency. Coffee ground vomitus refers to the vomiting of black material assumed to be blood. Its presence implies that bleeding has stopped or has been relatively modest. It may simply be bile. Often over-reported. Melena is the passage of tarry black stool usually due to acute upper GI bleeding but occasionally from bleeding within the small bowel or right colon. Iron preparations will cause some black faeces. Haemochezia is the passage of fresh blood per rectum usually due to colonic bleeding but occasionally due to profuse upper GI bleeding.
  
• Examination: look for signs of liver disease and portal hypertension suggests varices but bleeding may be other pathology. Liver disease – ascites, jaundice, gynaecomastia, Dupuytren’s contracture, clubbing, spider naevi, caput medusae, palmar erythema, etc. Liver decompensation, e.g. jaundice, encephalopathy, asterixis. Liver flap. Evidence of significant blood loss: postural fall in SBP >20 mmHg, postural HR increase >30 bpm (lying/sitting when too ill to stand). Signs of shock and haemodynamic compromise. Thready pulse, thirst, poor skin turgor, cold nose. Increased capillary refill time. Oliguria – measure urine output. Rectal exam for melena. Facial telangiectasias (HHT).
  
• Look for evidence for bleeding: upper GI bleeding manifests as either vomited bright red or altered blood ‘coffee grounds’ called haematemesis, or altered blood products passed PR as melena. Normal dark bile often mistaken for coffee grounds. ‘Coffee grounds’ and melena show bleeding that occurred minutes to hours before. Huge amounts of GI bleed will pass quickly and cause bright red blood passing within minutes. The GI protein load of blood and the anaemia and ↓BP can cause agitation and delirium. Bleeding may, however, be occult with just progressive signs of anaemia.

Investigations

• FBC: initially often normal and misleading because haemodilution yet to take place. Check platelets. Target Hb 80 g/dL. Recent evidence suggests that higher Hb targets associated with increased mortality.
  
• U&E: ↑urea may suggest GI blood loss and protein load in gut. May see AKI.
  
• LFT and coagulation screen: at baseline and repeat as needed.
  
• Blood group and cross-match 2–4 units depending on estimated losses.

Management (see also Haemorrhagic shock Section 2.22)

• Risk assess: use Glasgow Blatchford score to assess on admission and full Rockall post-endoscopy to guide management. Escalate high score or unstable patients. Resuscitate those who are actively bleeding and discuss need for urgent endoscopy. In suspected GI bleeding, consider the patient for non-admission or early discharge if before endoscopy the Blatchford score is 0, i.e. no melena and no haemodynamic disturbance, no significant co-morbidity and normal FBC and normal urea. Low score patients may be managed as outpatients on a next day list.
  
• Get good IV access and protect it: if ↓BP and ↑HR or melena or witnessed haematemesis then need good venous access with 2 GREY VENFLONS in each antecubital fossa. If difficult IV access get immediate help from registrar or anaesthetist. A central line is too long and fine bore for good flow and not good for giving volume quickly. Once access gained send bloods FBC, U&E, LFT, clotting, and group and cross-match 4 units or more if needed. Upper GI endoscopy: usually within 24 h or sooner.
  
• Give crystalloids: start 1 L NS, use Dextrose and transfuse if Liver failure (avoid or caution against saline if liver disease) over 20–60 min and high flow O2 if shocked. Transfuse: if actively bleeding and Hb <9, or the patient is shocked. In stable non-actively bleeding patients, transfuse if Hb <7, or if <8 and there is significant co-morbidity. See massive transfusion protocol. Early effective resuscitation reduces mortality. If patient dying in front of you from obvious active witnessed bleeding consider universal donor O negative blood and send someone to fetch it.
  
• Nil by mouth: keep patients who are actively bleeding, or are shocked at presentation, NBM. Unless actively bleeding, patients should be NBM for 4 h before endoscopy. Otherwise stable non-bleeding patients should be allowed to eat.
  
• PPI: start oral PPI and give IV only if cannot take PO.
  
• Coagulopathy: offer FFP if actively bleeding and INR >1.5. If a patient’s fibrinogen level remains less than 1.5 g/L despite FFP use, offer cryoprecipitate as well. Consider platelet transfusion in those actively bleeding with count <50 × 109/L. Those on warfarin and bleeding need prothrombin complex concentrate and vitamin K. Those on dabigatran need Praxbind. Give FFP at 15 ml/kg (each unit is about 150–200 ml). Give cryoprecipitate (2 units) as per transfusion policy. Patients with critical CAD or new or drug-eluting stents should be discussed with cardiology prior to next dose. Uncontrolled bleeding and anaemia exacerbates IHD.
  
• Endoscopy: most arteries go into spasm and stop bleeding after the initial rupture. In patients who continue to bleed or re-bleed following admission, endoscopic therapy or surgery may be necessary. The decision on the timing of endoscopy is individualised for patients depending on the severity of the bleed and their co-morbidities. If endoscopy is required out of hours contact the on-call consultant endoscopist. All other patients with upper GI bleeding should have endoscopy within 24 h of admission.
  
• Interpretation of endoscopic findings: risks of rebleeding – active bleeding 90%, non-bleeding visible vessel 25%, adherent clot 25–30%, oozing without visible vessel 10–20%, flat spot 7–10%, clean ulcer base 3–5%
  
• Drugs: stop all antiplatelets if possible. Patients with critical CAD or stents <1 year should probably continue these drugs except in the most severe bleeding episodes. Consider seeking advice from a cardiologist.
  
• Observations: repeat frequent assessments of BP, HR and JVP and titrate volume and blood replacement with these. Take care not to volume overload the frail and elderly and those with poor cardiac function. A urinary catheter can be the poor man’s central line because it can give some measure as a surrogate marker of renal and general perfusion. If you can get the patient to an HDU/ITU bed then that is ideal for the shocked bleeder.
  
• Starting PPI: IV PANTOPRAZOLE 40 mg BD is used only in patients with severe active bleeding from ulcers after endoscopy. Otherwise give OMEPRAZOLE 20 mg PO after endoscopy, unless endoscopy is likely to be delayed. NICE recommends that PPI treatment is not started before endoscopy. Although it is logical to begin treating bleeding peptic ulcers with PPIs as soon as possible, there is no evidence that treatment before endoscopy alters outcome. Treatment with PPIs makes testing for H. pylori less reliable.
  
• Recurrent bleeding: patients with one episode of recurrent bleeding following initially successful endoscopic therapy are typically treated with a second attempt at endoscopic therapy. Surgery or angiography-guided intervention is indicated for patients who fail endoscopic therapy (persistent bleeding or recurrent bleeding after two therapeutic endoscopies).
  
• Surgical liaison: if bleeding continues despite endoscopy then surgeons and anaesthetists will be involved, as laparotomy may be the only way to stop the bleeding. The patient becomes a surgical rather than a medical emergency.
  
• ITU/HDU: patients may be best on HDU/ITU, especially if need for intubation or ventilation or inotropic support or multi-organ failure. Speak to ITU team and involve them early in a deteriorating patient.

• Warnings: elderly patients decompensate early; healthy younger patients (under 50) decompensate late and quickly so take care and don’t be lulled into a false sense of security. Alleged GI blood loss by its nature is occult initially and management is expectant – it will appear PR eventually. There are those with spurious unconfirmed bleeding and alleged witnessed ‘coffee grounds’ or ‘dark stool’ with no definite physiological or clinical or lab evidence and those with clear evidence of active GI bleeding. Need to have risk assessed and monitored and managed accordingly. Be careful with those on beta-blockers where normal ↑HR response may be muted. Steroids can mask perforation and acute abdominal pathology.
  
• Coagulopathy: warfarin-induced bleed: needs IV VITAMIN K 5–10 mg and prothrombin complex concentrates, e.g. Octaplex/Beriplex. Target INR <1.5. REVERSE WARFARIN EVEN IN THOSE WITH METAL HEART VALVES WITH MAJOR BLEED. Risk of harm from temporary reversal of anticoagulation for several days is likely much less than the risk of exsanguination in those with genuine signs of significant haemorrhage. Upper GI bleeding and stent or metal valves: risk of proven bleeding usually is the more pressing and anticoagulation/antiplatelets should be stopped and reversed acutely. Stent thrombosis is a concern if bleeding occurs soon after PCI and stenting, however, so is anaemia-induced cardiac ischaemia and exsanguination. Liaise closely with cardiologists and gastroenterologists to manage risk.
  
• Severe oesophagitis: OMEPRAZOLE 40 mg OD PO. Manage blood loss. Consider also SUCRALFATE 2 g BD PO.

Oesophageal variceal bleed

• Resuscitate. Consider ITU and intubation: failure to control severe bleeding, encephalopathy, hypoxia, aspiration. Terlipressin and antibiotics may be started pre-endoscopy if varices likely.
  
• Antibiotics: give a broad spectrum antibiotic usually parenteraly when acutely unwell, e.g. IV CO-AMOXICLAV or IV TAZOCIN (unless penicillin allergy) or CEFTRIAXONE to any patient with cirrhosis who presents with an upper GI bleed. Other antibiotics include NORFLOXACIN PO and QUINOLONES.
  
• Bleeding: treat any coagulopathy with FFP. Transfuse platelets if there is continued bleeding and platelet count is <50 000/μL. Consider IV VITAMIN K 10 mg. Consider TRANEXAMIC ACID 1 g tds PO. Give blood products as needed. Target Hb >80 g/L and INR 1.3 with FFP. Platelets >50. Fibrinogen >2 with cryoprecipitate. Consider IV VITAMIN K 5–10 mg slow IV if prolonged PT.
  
• Active management: 40% will not settle conservatively and need active treatment to control bleed. Admit HDU. Target Hb 80 g/L. Over transfusion may increase bleeding. Endoscopic bleeding risk factors: severity of cirrhosis, ↑hepatic vein pressure, variceal size, tense ascites, endoscopic appearance, e.g. haematocystic spots, diffuse erythema, bluish colour, cherry red spots, or white-nipple spots. Large varices >5 mm diameter. Prophylactic treatment to prevent variceal bleeding is recommended with large oesophageal varices irrespective of the presence or absence of red colour signs.
  
• TERLIPRESSIN (GLYPRESSIN) 2 mg IV followed by 1–2 mg 4-hourly for 3 d (C/I if severe IHD or stroke or peripheral vascular disease); mesenteric/splanchnic vasoconstrictor decreases portal venous inflow. 34% reduction in mortality for VB. Give immediately prior to endoscopy if varices likely. Alternative is OCTREOTIDE 50 mcg/h infusion for 3–5 days (can be used in those with IHD) but evidence base poorer.
  
• Laxatives: reduce risk of encephalopathy: LACTULOSE 30–50 ml TDS and PHOSPHATE ENEMAS to get 2+ or more soft bowel motions per day.
  
• Endoscopic management: variceal band ligation: is first choice option for oesophageal varices where a rubber band placed around varix. Sclerotherapy: first choice for gastric varices and may also be used for bleeding from oesophageal varices.
  
• Balloon tamponade: Sengstaken tube with gastric and oesophageal balloons. Placed in intubated patient in Level 3 care by experienced operator. Gastric balloon placed in stomach via mouth and filled with 200–300 ml of water as per instructions. AXR to check position. Gentle retraction pressure on balloon can stop bleeding – usually the weight of a 500 ml or 1 L bag of fluids. Oesophageal balloon rarely needs filling. Sedation, intubation and ventilation will aid airway protection and tolerance of the procedure.
  
• Transjugular intrahepatic porto-systemic shunt (TIPS): if persistent bleeding. Radiological guidance. Guide wire inserted into internal jugular to IVC to hepatic vein into liver. Stent passed over wire to create communication, allows high-pressure portal veins to shunt into systemic veins. This drops portal pressure, reducing bleeding and shunts portal venous blood bypassing liver to IVC, but can worsen encephalopathy. Local gastroenterologists will suggest when appropriate. Usually done at tertiary centre for uncontrolled VB.
  
• Long term: beta-blockers for varices decrease rebleed by 40%. Re-banding for varices until obliterated. Liver transplantation.

Peptic ulcer disease

• Adequately resuscitate and correct clotting and platelets before endoscopy. High risk patients have melena, haemodynamic instability, anaemia and co-morbidities and should be considered for endoscopic therapy once resuscitated.
  
• Urgent endoscopic therapy: visible clot removed and bleeding vessel injected with ADRENALINE which tamponades and vasoconstricts vessels with a second endoscopic treatment such as thermal coagulation or clips improving outcome in high risk bleeding ulcers. Failure to stem bleeding consider angiography or surgery if unstable.
  
• Rebleeding is from large GU over 2 cm and lesser curve and posterior wall DU. Visible clot and visible bleeding increase bleed risk. The risk of rebleeding from a peptic ulcer decreases significantly 72 h after the initial episode of bleeding. Start IV PPI if signs of risk of rebleeding. If there is evidence of high risk ulcers with active bleeding, adherent clot, visible vessel start OMEPRAZOLE 80 mg IV bolus and 8 mg/h for 72 h. PPI raises gastric pH and aids clot stability and haemostasis. Continue for 3 days when rebleeding most common. Reduces bleeding and need for transfusion. For the remainder start an oral PPI, post-endoscopy, which should be used for at least 4 weeks to heal ulcers, e.g. OMEPRAZOLE 20–40 mg OD. H. pylori should be eradicated if present (biopsy result or CLO test). Some consider this to be unnecessary if the patient is going to be on long-term PPI treatment.
  
• Angiography combined with selective vessel embolisation or selective intra-arterial VASOPRESSIN may be used where available if bleeding persists.
  
• Surgery: when endoscopic measures fail and bleeding persists then direct ligation of bleeding vessel needed. Uncommon event nowadays. Declining surgical experience. Liaise quickly if deteriorating. Perforation is rare (rigid abdomen, toxic, masked in those on steroids) but commoner with DU than GU. Needs surgical closure and abdominal drainage.
  
• H. pylori eradication: all should have CLO test and H. pylori eradication if positive. Early pre-endoscopy PPI can reduce sensitivity of H. pylori detection at endoscopy. Eradication is OMEPRAZOLE 20 mg + (METRONIDAZOLE 400 mg OR AMOXICILLIN 1 g) + CLARITHROMYCIN 500 mg ALL given 12 h for 7 days. Follow up: all H. pylori +ve need testing for successful eradication. All gastric ulcers need to be rescoped at 4–6 weeks to ensure healed and no gastric malignancy.
  
• Additional: SSRIs should be used with caution in those at risk of upper GI bleed particularly if on NSAID, clopidogrel or aspirin, Consider switching to non-SSRI.
  
• Repeat OGD for patients with a gastric ulcer at 6–8 weeks. This is because occasionally gastric ulcers are malignant even though at first presentation they appear benign.

Other causes

• Gastritis/duodenitis: oral PPI therapy and H. pylori eradication if CLO test positive.
  
• Gastric/oesophageal cancer: treat much the same as peptic ulcer disease. Argon laser or other comparable interventions may be tried. Some may need surgery.
  
• Dieulafoy’s lesion: cautery or angiographic embolisation. Surgical over-sewing if other management fails.

Reference: NICE (2012) CG141: Acute upper gastrointestinal bleeding: management issued.

• About: bleeding from beyond the ligament of Treitz. May be from small bowel or colorectal. If source unclear do OGD. A torrential upper GI bleed can cause fresh PR bleeding. Always exclude a colorectal cancer.
  
• Causes: diverticular disease (blood, mucus), haemorrhoids (fresh bright blood on toilet paper), colorectal cancer (anaemia, bowel habit, weight loss), ulcerative/Crohn’s colitis (known IBD), ischaemic colitis (AF, atherosclerosis, smoker), pseudomembranous colitis (recent antibiotics + C. difficile). Angiodysplasia, colorectal polyps, Meckel’s diverticulum. Radiation enteropathy, e.g. for gynaecological malignancies. Use of NSAIDs, anticoagulants, antiplatelets. Localised trauma – foreign bodies, sexual assault with anal fissure (severe pain on defecation, tear can be seen).
  
• Clinical: look for signs of shock and volume loss/anaemia. A history of pain and weight loss and altered bowel habit suggests cancer. Check if patient on warfarin, antiplatelet or a DOAC. Evidence of coagulopathy – liver failure. Gynaecological malignancies and bowel irradiation (radiation proctitis). Perform digital rectal examination and proctoscopy. Any local trauma.

Investigation

• FBC, U&E, coagulation if coagulopathy suspected or warfarin. Group and cross-match 2–4 units or more as needed.
  
• Colonoscopy: usually with good bowel can visualise entire colon. Often difficult to see source when bleeding acutely and often deferred to allow bleeding to settle.
  
• OGD: if source unclear. A torrential upper GI bleed can cause fresh PR bleeding. May be multiple sources.
  
• Flexible sigmoidoscopy: for the rectum and left side of the colon. Can be done without full bowel preparation. Proctoscopy to examine anal canal and useful to identify haemorrhoids.
  
• Mesenteric angiography: for angiodysplasia and occult bleeding lesion. The yield is low and therefore usefulness in question. Needs an arterial bleeding rate of at least 0.5 ml/min. It may allow for embolisation to take place.
  
• Technetium-labelled red cell scan: for occult and active bleeding.
  
• CT and CT angiography may localise pathology. CT colonography being used increasingly to look for colonic polyps and cancer.

Markers of poor prognosis

• Age: acute lower GI bleeding occurs most often in the elderly.
  
• Acute haemodynamic disturbance: ↑HR, ↓BP, shock.
  
• Gross rectal bleeding on initial examination (× 2.3–3).
  
• Co-morbidity: 2+ conditions double the chance of a severe bleed.
  
• ASPIRIN or NSAIDs: increased risk of severe lower GI bleeding × 1.8–2.7.
  
• Inpatients: (any cause) who bleed after admission have a mortality rate of 23% compared with 3.6% in those admitted to hospital because of rectal bleeding.

Management

• Supportive: ABC, high flow O2 if shocked and resuscitate. See Haemorrhagic shock, Section 2.22. Correct any coagulopathy and transfuse and replace fluids as required. Most cases settle conservatively. In the acute stage, colonoscopy can be difficult and the usual first lower GI investigation will be a flexible sigmoidoscopy following an enema bowel preparation. If no bleeding cause then consider colonoscopy which may help haemostasis as an effective means of controlling haemorrhage from active diverticular bleeding or post-polypectomy bleeding, when appropriately skilled expertise is available. Other options include CT abdomen, technetium-labelled red cell scanning, angiography and emergency surgery.
  
• Surgery: rarely needed as most bleeding self-limiting and can be managed medically/endoscopically. The exceptions would be massive on-going bleeding (>5 units in 24 h). Involve surgeons early if bleeding does not settle, especially if there is a suspected underlying malignancy, failed medical therapy for ulcerative colitis or ischaemic colitis or ongoing recurrent bleeding from a diverticulum. Localised segmental intestinal resection or subtotal colectomy is recommended.
  
• Catheter mesenteric angiography and embolisation may be attempted (evidence on which this practice is based is limited).

Reference: SIGN (2008) 105: Management of acute upper and lower gastrointestinal bleeding: a national clinical guideline.

• About: rapid onset of abdominal pain, vomiting, pyrexia and possibly ↓BP. This is a surgical emergency potentially requiring operative management. However, may be admitted mistakenly under medical teams or de novo presentation in medical patients.
  
• Atypical ‘understated’ presentations seen in: elderly, immunocompromised, high dose steroids which mask symptoms and signs when gravely ill and septic. Get urgent help if ↑HR, low BP, peritonism, bleeding, pregnant or high NEWS.
  
• Frequency of causes: acute appendicitis 30%, acute cholecystitis 10%, small bowel obstruction 5%, perforated peptic ulcer 3%, pancreatitis 3%, diverticular disease 2%.
  
• Urgent senior review needing resuscitation and possible surgery: (1) severe haemorrhage (↓BP, ↑HR, ↓Hb appears late with bleeding due to AAA or ectopic pregnancy or splenic rupture). (2) Perforation or rupture of a viscus (toxic appearance, rigid abdomen, absent bowel sounds, in extremis, air under diaphragm), ascending cholangitis (jaundice, rigors, RUQ pain). (3) Viscus necrosis, e.g. ischaemic bowel from atherosclerosis, embolism or strangulated hernia, pancreatitis, intussusception, volvulus. (4) Missed ectopic pregnancy can lead to death; is she pregnant?
  
• Historical clues: previous surgery – adhesions suggest causes of obstruction. Known IBD. Peptic ulcer disease and perforation: use of NSAIDs, steroids. Previous appendectomy excludes appendicitis. Warfarin – psoas/retroperitoneal haematoma. Known AAA. Immunosuppression.
  
• Volume status: look for ↑HR, ↓BP on sitting or standing suggests significant hypovolaemia, e.g. acute haemorrhage and blood loss (GI bleed, leaking AAA) or volume loss into obstructed bowel.
  
• Abdominal pain: examine abdomen carefully looking for area of maximum tenderness. Pain tends to come on suddenly or sub-acutely. Mechanism is either peritonitis with well-localised pain that is painful on coughing and movement and patient lies still with guarding and a rigid abdomen. Pain may also be colicky in nature and patient moves about and suggests a more obstructive luminal mechanism, e.g. intestinal obstruction. Associated N&V.
  
• Position: sitting bending forward – chronic pancreatitis; lying still – perforation; restless – renal colic.
  
• Visible peristalsis and distension: suggests obstruction.
  
• Radiation of pain: to shoulder – diaphragmatic irritation; to the back – consider AAA or acute pancreatitis or posterior perforation; to umbilicus – acute appendicitis.
  
• Guarding: reflex contraction of abdominal muscles and discomfort on light abdominal palpation.
  
• Rebound tenderness: increase in severe pain and discomfort when the examining hand abruptly stops pressing on a localised region of the abdomen or on percussion suggests peritonitis (25% don’t have it).
  
• Rigid abdomen: contraction of abdominal muscles. Abdomen feels hard like a wooden board. Suggests perforation.
  
• Fever: >38°C suggests infective or inflammatory process.
  
• Jaundice: common bile duct obstruction, liver failure, gallstones, haemolysis.
  
• Dehydration: peritonitis, small bowel obstruction, DKA, high Ca.
  
• Ascites: bulging flanks, abdominal distension with shifting dullness. Bowel floats and ascites gravitates to lowest point. Consider spontaneous bacterial peritonitis and diagnostic paracentesis in liver disease.
  
• Murphy’s sign: palpation over RUQ causes acute severe pain stopping inspiration. Acute cholecystitis.
  
• Don’t forget: check groin and all hernial orifices as well as scrotal sac and contents.
  
• Per rectum examination – tenderness, induration, mass, frank blood.
  
• Per vaginum examination where indicated – bleeding, discharge, cervical motion tenderness, adnexal masses, and tenderness, uterine size.
  
• Bowel sounds: listen for 2 min to ensure absent. May be high pitched and tinkling.
  
• Check hernial orifices, e.g. strangulated femoral hernia, and the testes of men for a testicular torsion or hernia. Can identify cause of bowel obstruction.

• Cholecystitis: gallstones, RIF pain, Murphy’s sign, fever, jaundice if stone in common bile duct.
  
• Acute appendicitis: pain begins peri-umbilical and moves to RIF as becomes more peritonitis.
  
• Leaking abdominal aortic aneurysm (AAA): midline pulsatile expansile mass, low BP, may have lost a femoral pulse.
  
• Acute pancreatitis: history of gallstones or alcohol and ↑amylase.
  
• Bowel ischaemia: older, ↑lactate, abdominal pain, melena, AF. May need resection of necrotic bowel.
  
• Adhesions causing bowel obstruction: previous surgery, abdominal scars and old incisional wounds.
  
• Incarcerated or strangulated hernia: bowel obstruction and tender hernial orifices.
  
• Pelvic inflammatory pain: may have similar history, vaginal discharge, history of STIs.
  
• Acute diverticulitis: left iliac fossa pain, older patient.
  
• Abdominal wall haematoma: on warfarin or antithrombotics. Coughing. Localised tender.
  
• Gastrointestinal malignancy: stomach, pancreas, small bowel, colonic.
  
• Budd–Chiari: prothrombotic, RIF pain, jaundice.
  
• Inflammatory bowel disease: Crohn’s disease predominantly a small bowel obstruction picture. Ulcerative colitis mainly a colitis picture. Watch for toxic megacolon.
  
• Testicular torsion: acute severe testicular pain.
  
• Ureteric colic/renal stones: renal angle to loin pain, restless, paroxysmal. Stone on CT KUB
  
• Meckel’s diverticulum: pain in RIF. May perforate. Seen in adolescents and young adults. Can mimic appendicitis.
  
• Gynaecological: endometriosis: recurrent pain. Ectopic pregnancy: positive pregnancy test and abdominal pain. Acute salpingitis: on right can mimic appendicitis. Ovarian torsion: on right can mimic appendicitis. Mittelschmerz: ovulation mid-cycle pain. May need urgent gynaecological consult and urgent surgery.

• Gastroenteritis: vomiting and diarrhoea predominate with vague pain and tenderness; gradually settles.
  
• Myocardial infarction (diaphragmatic/inferior): ECG – ST/T changes and troponin.
  
• Lower lobe pneumonia: fever, breathless, chest signs, CXR signs may be delayed.
  
• Pyelonephritis: positive urinalysis, tender renal angle, female.
  
• Addisonian crisis: pale, pigmented creases and scars, ↓BP.
  
• Diabetic ketoacidosis: hyperglycaemic, ketotic.
  
• Sickle cell crisis: Afro-Caribbean origin, similar past history, anaemia. Hyposplenism.
  
• Herpes zoster: rash may not be seen early on – pain affecting abdominal dermatome does not cross midline.
  
• Acute porphyria: variegate and acute intermittent porphyria, hereditary coproporphyria.
  
• Familial Mediterranean fever: Turkish/Middle Eastern. Mesenteric adenitis: viral type illness – younger patients. Mimics appendicitis.
  
• Tabes dorsalis: as part of tertiary syphilis.

Pain and localisation

• Localisation is not an exact science and there is much variability, e.g. late pregnancy.
  
• RUQ: cholecystitis, gallbladder empyema, hepatitis, liver abscess, duodenal ulcer, pneumonia, subphrenic abscess, hepatic flexure of colon.
  
• LUQ: gastroenteritis, splenic disease (infarction/rupture), splenic flexure of colon, subphrenic abscess, perinephritis, acute pancreatitis.
  
• Epigastrium: oesophageal/gastric disease (perforation, gastric ulcer or duodenal ulcer), ruptured AAA, acute pancreatitis, myocardial infarction, PE, pancreatic cancer.
  
• Right flank: ureteric colic (loin to groin), pyelonephritis (renal angle), retrocaecal appendix, muscle strain, perinephric abscess.
  
• Periumbilical: early appendicitis, small bowel disease – obstruction and inflammatory bowel disease, gastroenteritis, pancreatitis, ruptured AAA, ischaemic bowel.
  
• Left flank: ureteric colic (loin to groin), pyelonephritis (renal angle), muscle strain, perinephric abscess.
  
• RIF: appendicitis, mesenteric lymphadenitis, perforated duodenal ulcer, caecal obstruction, Meckel’s diverticulum, ectopic pregnancy, ovarian pathology, terminal ileal disease (Crohn’s/Yersinia pseudotuberculosis) or very rarely RLQ diverticulitis, biliary colic with low lying gallbladder, acute salpingitis.
  
• LIF: sigmoidal diverticulitis, constipation, ectopic pregnancy, ovarian pathology, ischaemic colitis, rectal cancer, IBS, ulcerative colitis.
  
• Suprapubic: cystitis, UTI, acute urinary retention, testicular torsion, pelvic inflammatory disease, ectopic pregnancy, uterine disease, diverticulitis.

Investigations

• Bloods: FBC, CRP, U&E, pancreatic amylase/lipase. LFT and INR if any suggestion of liver disease or gallstones. Group and cross-match if suspected AAA, ectopic pregnancy or laparotomy or frank bleeding. Consider ABG and lactate.
  
• Erect CXR and erect AXR can help exclude pathology. Perforation of viscus with free air visible under the diaphragm or between viscera and subcutaneous tissue on lateral decubitus. Distended small bowel proximal to small bowel obstruction with air–fluid levels. Small bowel more central. Thickened oedematous valvulae conniventes span entire wall of small bowel unlike colonic haustra. Renal stones may be seen best with AXR or CT. Normal AXR does not exclude ileus or many other pathologies. Toxic megacolon if diameter >7 cm in midtransverse colon. Pancreatic calcification may suggest acute or chronic pancreatitis. ‘Thumb printing’ with ischaemic bowel.
  
• CT abdomen: imaging important but does not substitute for good clinical assessment – appendicitis shows inflamed appendix fluid-filled with fat stranding and a hyper attenuated wall with IV contrast. Uncomplicated sigmoid diverticulitis can show fat stranding and focal thickening of the colonic wall in an area with diverticula. Abscess formation or fistulas may or may not be seen. Colonic cancers may be seen. Renal stones. Obstruction with transition zone showing level of blockage.
  
• USS: imaging of choice for cholecystitis with gallstones and thickened wall hydropic gallbladder. A stone may be seen blocking cystic duct. Sludge or stone material may be seen in the gallbladder. Gallstones may also suggest pancreatitis. Collections in the pelvis or subdiaphragmatic. Abscesses.
  
• Urinalysis: blood, protein, stones. Pregnancy test in all fertile women.

General management

• Supportive: ABC, O2 as per BTS guidance. Get good IV access and protect it. Start IV crystalloid fluids with good IV access and monitor physiology. Give 1 L Hartmann’s or IV NS over 1–2 h as needed. Most patients are dry. Analgesia: MORPHINE 5–10 mg IV + CYCLIZINE 50 mg IV. If tachycardic, ↓BP or bleeding then get senior help urgently. Fertile female consider ectopic pregnancy for all acute abdominal pain and/or ↓BP. Full monitoring BP, HR, temperature and urinary output. Catheterise. FBC, U&E, clotting if liver disease, amylase, group and hold/cross-match if haemorrhage or laparotomy. Severe haemorrhage – give O-negative blood. Suspect sepsis then start TAZOCIN 4.5 g 8 h IV and fluid resuscitation (see Sepsis, Section 2.21). Maintain NBM until senior review decides otherwise. Normal important meds can sometimes be given with sip of water. Diabetic patients need to be started on a VRIII and keep CBG 4–12 mmol/L. AXR is helpful and depending on findings may need abdominal CT. Laparoscopy may reduce rate of unnecessary laparotomy and improve diagnostic accuracy.

• About: weight loss, food regurgitation.
  
• Causes: pancreatic cancer (10–20%) or gastric malignancy. Peptic ulcer disease with scarring and oedema of pylorus. Gastric polyps, duodenal malignancy, cholangiocarcinoma.
  
• Clinical: fullness and vomiting (HCl loss) postprandial which is non-bilious. Weight loss, succussion splash if NBM for 2–3 h. Palpable abdominal mass and gastric dilation. Malnutrition is seen late. Aspiration pneumonia. Supraclavicular lymph nodes. Hepatomegaly and jaundice if liver metastases.
  
• Investigations: FBC, U&E, ↑urea and creatinine, low K develops later after 2–3 weeks. LFT: ↑ALP or bilirubin may suggest malignancy. Venous blood gas: vomits HCl loss, increased HCO3 and low Cl. Alkalosis increases serum K. K excreted to preserve Na. Results in hypochloraemic (hypokalaemic) metabolic alkalosis.
  
• Plain AXR: calcification, masses, perforation.
  
• Barium upper GI studies: can be helpful to identify the gastric silhouette and site of obstruction.
  
• USS abdomen: liver metastases, obstructive jaundice. CT abdomen with oral contrast: will define and stage any masses or mets.
  
• Upper GI endoscopy: may still be food residue in stomach and difficulty passing probe. A lesion may be seen and biopsies taken. A stent may be passable.
  
• Management: IV rehydration and fluid and electrolyte replacement and nutrition. Prolonged vomiting causes loss of hydrochloric (HCl) acid and produces an increase of bicarbonate in the plasma to compensate for the lost chloride and sodium. The result is a hypokalaemic hypochloraemic metabolic alkalosis. Alkalosis shifts the intracellular potassium to the extracellular compartment, and the serum potassium is increased factitiously. With continued vomiting, the renal excretion of potassium increases in order to preserve sodium. The adrenocortical response to hypovolaemia intensifies the exchange of potassium for sodium at the distal tubule, with subsequent aggravation of the hypokalaemia. Manage electrolytes and acid–base disturbances. Specific management depends on cause. Stenting may be possible depending on circumstances. Surgical referral in appropriate cases. (Hypovolaemia, Section 2.20).

Related posts:

– Endocrine and diabetic emergencies – Hepatobiliary emergencies – Haematological emergencies – Dermatological emergencies – Emergency drugs (use with BNF) – Ophthalmological emergencies