Acute Abdomen (2)

PRESENTED BY:NIXON OMULIMI

Definition: Encompasses a spectrum of surgical, medical and

gynaecological conditions, ranging from trivial to life-threatening, which require hospital admission, investigation and treatment. The primary symptom of the condition is abdominal pain. ‘Abdominal pain of less than 1 week’s duration requiring admission to hospital, which has not been previously investigated or treated’

It has been estimated that at least 50% of general

surgical admissions are emergencies, and of these 50% present with acute abdominal pain. 30-day mortality of 4% among patients admitted with acute abdominal pain, rising to 8% in those who undergo operative treatment. Affect all age groups, either sex & all socio-economic groups. Careful methodical approach required to arrive at

NEUROLOGIC BASIS OF ABDOMINAL PAIN Pain

receptors in the abdomen respond to mechanical and chemical stimuli.  Stretch - principal mechanical stimulus involved in visceral nociception, Others:distention, contraction, traction, compression, and torsion. Visceral receptors responsible for these sensations are located on serosal surfaces, within the mesentery, and within the walls of hollow viscera, in which they exist between the muscularis mucosa and submucosa.

• Mucosal receptors respond primarily to chemical

stimuli, in contrast to other visceral nociceptors that respond to chemical or mechanical stimuli. • Triggers: substance P, bradykinin, serotonin, histamine, and prostaglandins, released in response to inflammation or ischemia

Visceral pain

Dull, deep and aching in character, although it can be colicky; often poorly localized. Associated with symptoms like nausea, vomiting. Due to distention or spasm of a hollow organ. E.g. in I.O or cholecystitis. • Parietal pain Sharp and very well localized. It arises from peritoneal irritation.

The parietal peritoneum - develops from the

somatopleural layer of the lateral plate mesoderm. Nerve supply:- somatic nerves supplying the abdominal wall musculature and the skin (T5–L2). Parietal peritoneum is sensitive to mechanical, thermal or chemical stimulation Referred pain is aching and perceived to be near the surface of the body.

Localization of pain • Most digestive tract pain is perceived in the

midline because of bilaterally symmetric innervation • Visceral pain is perceived in the spinal segment at which the visceral afferent nerves enter the spinal cord • E.g afferent nerves mediating pain arising from the small intestine enter the spinal cord between T8 to L1. Thus, distension of the small intestine is usually perceived in the periumbilical region.

Foregut- pain referred to the epigastrium Midgut- pain referred to the periumbilical

region Hindgut- pain referred to the hypogastrium

Aetiology Right upper quadrant • • • • • • • • • •

Acute Hepatitis Acute Cholecystitis Cholangitis – Pancreatitis Budd-Chiari syndrome Pneumonia/empyema pleurisy Subdiaphragmatic abscess Liver abscess Congestive cardiac failure Hepatic infarction

Right lower quadrant • • • • • • • • • • • •

Appendicitis Inguinal hernia –strangulated, incarcerated Nephrolithiasis Inflammatory bowel disease (UC ,Crohn’s ) Mesenteric adenitis (yersina) Psoas abscess Meckel’s diverticulitis Salpingitis Ectopic pregnancy Tubo ovarian abscess Ovarian cyst- torsion, rupture, bleeding Mittelschmerz

Epigastric • • • • • • • •

Peptic ulcer disease Gastroesophageal reflux disease Gastritis Pancreatitis Myocardial infarction Pericarditis Ruptured aortic aneurysm Perforated oesophagus

Periumbilical • • • • • •

Early appendicitis Gastroenteritis Bowel obstruction Ruptured aortic aneurysm Diverticulitis Mesenteric thrombosis

Left upper quadrant • Splenic abscess • Splenic infarct • Ruptured spleen • Pyelonephritis • Pneumonia • Gastritis • Gastric ulcer • Pancreatitis • Aortic aneurysm Left lower quadrant • Diverticulitis • Inguinal hernia • Nephrolithiasis • Irritable bowel syndrome • Inflammatory bowel disease • Salpingitis • Ectopic pregnancy • Tubo ovarian abscess • Ovarian cyst- torsion, rupture, bleeding • Mittelschmerz

Diffuse • Gastroenteritis • Mesenteric ischemia • Metabolic (eg, DKA, porphyria) • Malaria • Familial Mediterranean fever • Bowel obstruction • Peritonitis • Irritable bowel syndrome • Sickle cell crisis

Pathogenesis Two main underlying pathological processes involved: 2.Inflammation 3.Obstruction. Inflammation >reactive hyperaemia of the injured tissue as a result of capillary and arteriolar dilatation > exudation of fluid into the tissues as a result of an increase in the permeability of the vascular endothelium > increase in filtration pressure. Finally, there is emigration of leukocytes from the vessels into the inflamed tissues.

Obstruction The smooth muscle in the wall of the obstructed viscus will contract reflexly in an effort to overcome the impedance. This reflex contraction produces colicky abdominal pain. The exception to this rule is ‘biliary colic’. The gallbladder and biliary system has little smooth muscle in its wall and attempts at contraction tend to be more continuous than ‘colicky’. If the obstruction is not overcome, there will be an increase in intraluminal presure and proximal dilatation.

Management Careful, methodical approach – necessary for

proper management of acute abdomen Classify the patient: -Operation necessary -Operation not immediately necessary -Operation not necessary Acute abdominal pain frequently requires urgent investigation and management. Initial management = resuscitate before investigating! Do the ABC. acute care facility where more appropriate nursing care and laboratory and radiology facilities are available.

Patient Evaluation Detailed clinical Hx:

Pain:- remember SOCRATES  Site  Time and mode of onset  Severity  Nature -colicky, continous  Progression  Duration  Exacerbating/relieving factors  Radiation  Associated symptoms: including fevers, chills, weight loss or gain,

nausea, vomiting, diarrhea, constipation, hematochezia, melena, jaundice, change in the color of urine or stool.  Past medical and surgical history, including risk factors for cardiovascular disease and details of previous abdominal surgeries.  Family history of bowel disorders. Alcohol intake. Intake of medications including over the counter medications such as

 Physical examination. Need a thorough P/E  Vital signs- really vital  General examination: The general appearance and level

of comfort or discomfort should be noted, clinical evidence of anaemia, jaundice, cyanosis and dehydration  Abdominal exam  Inspection - abdominal contour - movement with respiration -Does the patient lie still or writhe -Scars – relevant previous illness, adhesions causing I.O -Hernia – intestinal obstruction, strangulated -Visible peristalsis – intestinal obstruction -Visible masses

Palpation Is there tenderness, guarding or rigidity? Are there abnormal masses/palpable organs? Rebound tenderness – peritonitis Percussion  Is the percussion note abnormal? Resonance – intestinal obstruction  Loss of liver dullness – gastrointestinal perforation  Dullness – free fluid, full bladder  Shifting dullness – free fluid Auscultation Are bowel sounds present/abnormal? Absent sounds – paralytic ileus Hyperactive sounds – mechanical obstruction, gastroenteritis Bruit – vascular disease Specific signs Murphy’s sign and Boas’s sign-acute cholecystitis Grey-Turner’s and Cullen’s signs- acute pancreatitis Rovsing’s sign, Mcburney’s point tenderness-acute appendicitis Blumberg’s sign-peritoneal irritation

Do not forget to: Examine the groin- check for hernias Do a digital rectal examination Do a vaginal examination when appropriate Examine the chest- lungs need to be

examined for signs of consolidation and the heart for murmurs and rubs.

Resuscitation or emergency surgery may be

needed, so: - Keep the patient Nill by mouth. Intravenous access – large-bore cannulae. - Naso-gastric tube. - Urinary catheter to monitor I/O - Appropriate analgesia. - IV Fluids -Broad spectrum antibiotics

Investigations Laboratory investigations  Complete blood count with differential  Electrolytes, BUN, creatinine, and glucose  Aminotransferases, alkaline phosphatase, and bilirubin  Serum amylase  Lipase  Serum calcium  Urinalysis  Pregnancy test  blood and urine cultures  Arterial BGA.  G & Save or cross-match.

Radiological investigations  Plain X-rays

- Erect CXR.-pneumonia, air under the diaphragm - Supine AXR: Multiple fluid levels, calcification (renal stones, chronic pancreatitis) - Left lateral decubitus AXR. - Ultrasound. -water soluble contrast studies -LGIT - CT Scan. - MRI  Other investigations: - Endoscopy – diagnostic & therapeutic. - Rigid or flexible sigmoidoscopy for sigmoid volvulus. - ERCP for acute biliary obstruction. - Visceral angiography – intestinal ischaemia, angiembolization for GI bleeding. - Laparoscopy.

Diagnostic Peritoneal lavage: in patients

whom you can’t elicit clear signs or with altered consciouness Laparotomy – may be the ultimate diagnostic procedure. Needed for peritonitis or ruptured viscus Definitive management – dependent on specific aetiology. Prognosis: depends on aetiology