19 year old female with a 24 hour history of abdominal pain. She had noticed the pain during a morning lecture and it had initially been mild and generalised. Early associated features included nausea, malaise and she had had two episodes of loose stool. She was a new student and had been living that lifestyle so she thought that it was probably due to alcohol.
However in the last couple of hours, the pain had significantly worsened. She described it as constant and sharp. She had vomited and didn’t feel like eating or drinking. She had no further diarrhoea, was passing urine although concentrated. She was advised to come to hospital by the 111 service. There was no PV bleeding, no malena or haeamtemasis and no urinary symptoms. Her last menstrual period was 6 weeks ago and normal, she has a very irregular cycle that can vary from 3-8 weeks.
She had well controlled asthma using salbutamol and beclomethasone, no other medications and no drug allergies. Interestingly she had had a couple of previous episodes of right lower abdominal pain before – although not as bad as this, this was when she was diagnosed and treated for pelvic inflammatory disease 18 months ago. She was a non-smoker, denied illicit drugs, being a new student she had been drinking more alcohol than usual.
She was alert and orientated. Her vital signs were stable but she had a HR of 104, BP 104/62, RR 16, Sp02 100% and a temperature of 37.8. The abdomen was soft but was mildly tender in the epigastrium and tender with some guarding in the right lower quadrant. Rovsings positive. Murphy’s negative. Rebound tenderness. Bowel sounds slightly increased.
|Cholecystitis||Tender epigastrium with fever and vomiting
Murphy’s sign negative
Possible diagnosis however appendicitis/ectopic pregnancy more likely given location of worst tenderness
|Pancreatitis||Fever, tender epigastrium and tachycardic, with increased alcohol intake.
Although not classical pain
|Gastritis||Drinking lots – student
Some epigastric tenderness, although doesn’t explain right iliac fossa pain
|Gastroenteritis||Two episodes of loose stool, now resolved but patient still unwell
Vomiting is in-keeping with gastroenteritis
Severe abdominal pain is unusual and makes it less likely
|UTI/Pyelonephritis||No urinary symptoms
Urine dip normal
|Renal Colic||Pain not classical loin to groin
No haematuria (although present in only 90% cases of renal colic)
Venous blood gas – normal, lactate 1.3
Baseline bloods (done at triage) – U&E, LFT, CRP, FBC, Amylase, WCC 11.1, CRP 43
Urine pregnancy test and serum BHCG negative
USS – abdomen and pelvis: Moderately inflamed and oedematous appendix, normal gynaecological anatomy
Pain Management – IV paracetamol, IV morphine, IV buscopan
Screening for and treating for sepsis
NBM – IV fluid
Early involvement of the decision making surgical team for appendicectomy
Royal College of Surgeons estimate 40,000 cases a year in UK. Usually a disease of the young with peak incidence within 20s and 30s.
The appendix is located at the base of the cecum and the appediceal orfiice opens into the cecum directly.
Despite being the most common surgical emergency, its aetiology is poorly understood. Appendiceal obstruction is thought to be the leading cause of appendicitis, although the cause is not always identified. The mechanism of luminal obstruction varies depending upon age. In the young, lymphoid follicular hyperplasia due to infection is thought to be the main cause. In older patients, luminal obstruction is more likely to be caused by fibrosis, fecaliths, or neoplasia. Once obstructed, the lumen becomes filled with mucus and distends, increasing luminal and intramural pressure.
The earliest change is mucosal ulceration which is thought to be caused by increased intrluminal pressure. Inflammation accompanies this. Inflammatory infiltrates spread through the appendiceal wall causing localised peritonitis. These further causes pressure in the appendix to increase. The increased pressure results in thrombosis and occlusion of the small vessels, mucous pooling and stasis of lymphatic flow. As lymphatic and vascular compromise continues the wall of the appendix becomes ischaemic and necrotic.
Bacterial overgrowth occurs within the diseased appendix.
Once significant inflammation and necrosis occur, the appendix is at risk of perforation, which leads to localized abscess formation or diffuse peritonitis.
Of note less common causes of appendices inflammation include, chrons, UC, TB
NICE guidance – ectopic pregnancy
NICE guidance – appendicitis