RUQ, Epigastric pain - Lecture notes RUQ pain PDF

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Epigastric / RUQ pain Most Common Life-threatening  investigate Other and rule out quickly Non-specific abdominal pain Acute Coronary Syndrome Peptic ulcer disease Pancreatitis Diabetic Ketoacidosis Irritable Bowel Syndrome Biliary Colic Bowel obstruction Pneumonia Cholecystitis Ascending cholangit...

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Epigastric / RUQ pain

Other Life-threatening  investigate and rule out quickly Peptic ulcer disease Non-specific abdominal pain Acute Coronary Syndrome Irritable Bowel Syndrome Pancreatitis Diabetic Ketoacidosis Pneumonia Biliary Colic Bowel obstruction Cholecystitis Ascending cholangitis Gastritis/oesophagitis/duodenitis PTE Ruptured AAA / Aortic dissection Mesenteric ischaemia Perforated peptic ulcer Oesophageal perforation (Boerhaave’s Syndrome) Abdominal pain account for 5-10% of ED admissions. RUQ/epigastric pain is common, with differential diagnosis forming the following: Most Common

Types of Pain Visceral pain is poorly localised and presents in the midline. It occurs due to visceral afferent nerves sensing organ wall stretching / visceral peritoneum inflammation; - Ache/cramp in Epigastrium regionForegut (Stomach/Duodenum/HPB/spleen) - Ache/cramp in Umbilical region  Midgut (3rd duodenum – 2/3rd Trans colon) - Ache/cram in suprapubic region  Hindgut (rest of Trans colon – Anus) Parietal/Somatic pain is sharper in character and is well localised. The is caused b irritation of somatic nerves on parietal peritoneal wall, which can also cause referred pain felt some distance away from its origin Peritonism This is inflammation of the peritoneum, and can be identified through following signs: - Involuntary guarding - Tenderness on percussion / rebound tenderness - Abdominal rigidity - Lying still - Absent bowel sound  ileus due to inflammation Causes are split into widespread and more localised: - Widespread o Perforated viscous  oesophagus, stomach, duodenum, colon o Spontaneous bacterial peritonitis  associated with ascites o Peritoneal dialysis - Localised o Pancreatitis o Cholecystitis o Appendicitis o Salpingitis Clinical Advice  Physical findings can be masked in patients on steroids/NSAIDs  Shock can be masked in patients on beta-blockers  If abdominal pain is out of proportion to physical findings, don’t rule out but consider  Mesenteric infarction  Aortic rupture / dissection  Acute pancreatitis  Torsion of ovarian cyst  If there is trauma involved, always suspect a splenic rupture  If woman is of child-bearing age, consider gynaecological causes of Abdo pain

Initial investigations in Acute abdominal pain Simple (Bedside) Urinalysis  glycosuria, ketones, leucocytes/nitrites bHCG  pregnancy Blood sugar  ?hyperglycaemia VBG/ABG

Complex (Go away and return with result) Bloods FBC  infection / anaemia CRP  infection / inflammation U&Es  assoc. real function LFTs  biliary problems? Amylase  pancreatitis CXR  basal pneumonia / pneumoperitoneum AXR  Free air / obstruction / volvulus USS  FAST Scan *

*FAST (Focussed Assessment with Sonography for Trauma) Scan looks for free fluid, usually blood, around the heart of abdominal organs after trauma, focussing on 4 main areas: i. Perihepatic space (AKA Morison’s pouch or hepatorenal recess) is a longitudinal view of the RUQ  right liver and kidney injuries ii. Perisplenic space is a longitudinal view of the LUQ  splenic and left kidney injury iii. Pericardium is the subxiphoid transverse view  Pericardial effusion and left lobe liver injuries iv. Pelvis/Transverse and longitudinal views of suprapubic regions  Bladder /Pouch of Douglas

Pancreatitis  Causes  I GET SMASHED o Idiopathic o Gallstones o Ethanol o Trauma o Steroids o Mumps / Malignancy o Autoimmune o Scorpion Sting o Hyperlipidaemia / Hypercalcaemia / Hypothermia o ERCP o Drugs  azathioprine, Mesalazine, Bendroflumethiazide, Furosemide, Sodium Valproate  Signs/Symptoms o Symptoms  Severe epigastric pain radiating to back  relieved by sitting forward  Nausea / Vomiting  Sweating o Signs  Cullen’s sign (belly button) / Grey Turner’s sign (flank)  These are both signs of intraperitoneal haemorrhage  Diagnosis o Bloods  FBC  increased WCC  CRP  increased  Amylase  diagnostic is >3x upper limit of normal, but can be negative, especially if late presentation after onset  Lipase  more sensitive and specific than amylase o Other  CT   AXR  Sentinel loop due to ileus of small bowel where pancreas lies

 Classification o The modified Glasgow Criteria (PANCREAS) predicts the severity of pancreatitis, with a score of 3 or more in 48 hours predicting severe pancreatitis, and needing HDU assessment:  PaO2 55  Neutrophils >15  Calcium 16mmol/l  Enzymes  LDH >600iu/l / AST >200iu/l  Albumin 10mmol/l  Management o NBM +/- NG tube  always good for surgical patient in case needing surgery o IV fluids o Analgesia  morphine o Treat cause  US Abdomen for gallstones/CBD dilatation / check lipids etc.  Complications o Early  Shock / ARDS / Sepsis / Multiorgan failure  Renal failure  DIC / coagulopathy  Hypocalcaemia  Hyperglycaemia o Late (>1 week)  Pancreatic necrosis – cell death of parenchyma/fat  sterile vs infected (gas on CT)  Acute peripancreatic fluid collections (first 4 weeks: non-encapsulated)  Pancreatic pseudocyst (>4 weeks, encapsulated)  pseudocyst is a non-epithelised wall consisting of fibrous and granulation tissue  Pancreatic abscess  Haemorrhage  most likely of splenic artery  Thrombosissplenic/gastroduodenal/colic SMA branches, resulting in bowel infarct  Fistulae  Diabetes Mellitus  Pancreatic insufficiency  malnutrition  Surgical indications  relatively rare, unless treating cause, such as gallstones o Pancreatic pseudocyst  Mass effect  Biliary or GI obstruction/hydronephrosis  Infection  Treatment  Cystogastromy / Aspiration o Infected pancreatic necrosis  Treatment  Debridement and drain replacement

Biliary Disease Cholecystitis  Causes o Types  Calculous (Gallstones)  90%  Acalculous  10% o Bacterial culprits  E. Coli / Klebsiella most often  Signs/Symptoms o Symptoms  RUQ/epigastric pain  referred to shoulder and subscapular, pain worse on eating

 Nausea / vomiting  Not eating due to pain o Signs  Percussion tenderness and Involuntary guarding  Murphy’s Sign  Arrest in inhalation on palpitation of RUQ, which is absent on LUQ  Boas sign  referred pain to subscapular  Diagnosis o Bloods  FBC  raised WCC  o USS is more or less diagnostic  Thickened gallbladder wall  Also look for presence of gallstones within gallbladder or dilated CBD  Management o NBM  Surgical patient o Possible Sepsis 6 protocol:  IV antibiotics  Amoxicillin / Metronidazole / Gentamicin o IV analgesia o Surgical options:  Cholecystectomy  argued whether beneficial to do this at time or wait  Cholecystostomy  drained if worsening cholecystitis / poor surgical candidate  Complications o Gangrene o Perforation o Empyema o Fistulae  cholecystoduodenal, which could lead to gallstone ileus o Cholangitis o Pancreatitis Cholelithiasis This is gallst9ones, and affects 10-15% of the population, with 80% of these being asymptomatic.  Risk Factors (4 Fs)  Female, Fat, Forty, foetus + (OCP, Pregnancy, Diabetes, Family History) Biliary cholic  Pain secondary to gallstone in cystic duct  Presenting features  Postprandial RUQ pain + absence of features of cholangitis/choledocholithiasis o No Jaundice o USS Abdomen o LFTs Deranged o Laparoscopic Cholecystectomy Choledocholithiasis this is gallstones within the Common Bile Duct o Jaundice o Raised LFTS  Alk Phosphate o No Leukocytosis o Increased total bilirubin Ascending Cholangitis  This is presence of obstructive CD stone with superimposed infection o Charcot’s triad in 80-85%  RUQ pain, Fever, Jaundice o Reynold’ Pentad  RUQ pain, Fever, Jaundice, confusion, Hypotension o Leukocytosis, Increased LFTS (Increase Alk Phos) o USS (CBD diameter/stones), MRCP o Treatment:  IV fluids + IV antibiotics (GAM)  Endoscopic Retrograde Cholangiopancreatography (ERCP)  Diagnostic uses  confirm gallstones, intermediate biliary lesion, bile duct injury  Therapeutic options:

Gallstone in CBD  Sphincterotomy / Stone or debris removal / Dilatation / Stent insertion o Bile duct injury repair Risks  pancreatitis, cholangitis, bleeding (melaena), duodenal perforation o

 Mirizzi’s Syndrome  This is extrinsic compression of an extrahepatic biliary duct secondary to: o Impacted stone in cystic duct o Inflammation and fibrosis of the cystic duct o +/- fistulae  Present with  recurrent jaundice / cholangitis

Cholangiocarcinoma  This is a cancer of the biliary ducts, with 80% being extrahepatic  Presenting features: o Jaundice o Systemic upset  anorexia / weight loss / fevers / night sweats etc o Palpable mass in RUQ o Possible RUQ pain, although can be painless o Left Supraclavicular Lymph node  Virchow’s node  Risk factors: o Primary Sclerosing Cholangitis  chronic liver disease characterised by progressive course of cholestasis with inflammation and fibrosis of intrahepatic and extrahepatic bile ducts o Typhoid and Liver fluke  Third world problems  Investigations: o Obstructive LFTs o Elevated CA19-9, CEA, CA125 o MRCP/CT  Treatment o Presents late  often palliation, with 5-year survival only being 5-10% o Surgical resection if possible o ERCP and stent placement for jaundice Courvoisier’s Law  presence of a palpably enlarged gallbladder, which is non-tender and accompanied by painless jaundice, is unlikely to be gallstone  most common causes are malignancies...