Acute Abdomen

Dr. Andey Rahman

Objective• On completion of this lecture you will be able to:

– Define the acute abdomen. – Describe the cause and pathophysiology of the following acute abdominal

diseases: • Acute appendicitis• Intestinal obstruction• Acute mesentric ischemia• Gastritis, peptic ulcer disease• Peritonitis • Acute pancreatitis• Acute cholangitis• Cholecystitis

– Identify and describe the symptoms, signs, clinical course and laboratory and x-ray findings for the acute abdominal diseases listed under Objective 2.

– Identify the clinical features that help to distinguish the surgical from the non-surgical acute abdomen.

– Construct an approach to evaluation and management of the acute abdomen.

Definition

• Intra-abdominal process causing severe pain and often requiring surgical intervention

• It is a condition that requires a fairly immediate judgement or decision as to management

• Identify, diagnosis

General causes

• Inflammatory– Bacterial – acute appendicitis– Chemical – PGU lead to spillage of gastric content

• Mechanical – obstructive condition such as; intestinal obstruction, intussesception, adhesion

• Vascular - mesenteric arterial thrombosis or embolism. When the blood supply is cut off, necrosis of tissue results, with gangrene of the bowel

Cont…

Acute appendicitis

• Caused by luminal obstruction of the vermiform appendix, typically by a fecalith

• Continuous mucus secretion – increase intraluminal pressure – appendicceal vascular insufficiency – bacterial proliferation/inflammation – perforation – peritonitis

Clinical feature

• Early– Malaise– Indigestion– Bowel irregularity– Anorexia

• Periumbilical pain, nausea, vomitting, flank pain, dysuria

• RIF pain, rebound tenderness, guarding, rovsig sign, psoas sign

Diagnosis

• CLINICAL!!!• Alvarado score – aid in diagnosis• Investigation –

FBC/BUSE/creat/GSH/UFEME/UPT• Xray, US

Management

• Appendicectomy – prompt surgical referral• NBM• Fluid resus/maintainance• Antiemetic• Analgesia• Antibiotics

Acute pancreatitis

• acute inflammatory process of the pancreas that may involve surrounding tissue and remote organ systems

• mild inflammation to severe extensive pancreatic necrosis and multi-organ failure

• The specific mechanism that triggers pancreatic inflammation remains unclear

Causes

• Gallstone• Alcohol• HyperTG• ERCP

Pathophysiology

• Unregulated activation of trypsin – activation of digestive enzymes, complement, kinins – antudigestion of pancreas – pancreas injury, inflammation – acinar cells necrosis- multiorgan failure

Clinical feature• Persistent abdominal pain

– Epigastric area– Radiate to the back– Worse in supine, relieved by sitting up with the trunk flexed and knees

drawn up• Physical findings

– Fever– Tachycardia– Hypotension/shock– Absent bowel sound– Cullen sign, turner sign – uncommon, late indicate retroperitoneal and

intra-abdominal hemorrhage and severe necrotizing pancreatitis– Hypoxemia, ARDS

Cont…

• Cullen sign

• Grey-Turner sign

Diagnosis

• Diagnosis of acute pancreatitis is generally made in the presence of two of the following three features;– characteristic abdominal pain– serum amylase and/or lipase levels three times or

more the upper limit of normal– characteristic findings of acute pancreatitis on US

or CT scan

Amylase vs lipase• The sensitivity and specificity of amylase level as a diagnostic test

depends on the cutoff value• Serum amylase concentrations exceeding three times the normal

upper limit support the diagnosis in the setting of abdominal pain• When the cutoff level is raised to 1000 IU/L (more than three times

the upper limit of normal), specificity approaches 95% but sensitivity remains about 61

• Lipase catalyzes the breakdown of triglycerides into fatty acids and monoglycerides

• Pancreatic inflammation leads to increased enzyme levels• The accuracy of lipase level is better than that of amylase level in

the diagnosis of acute pancreatitis, and it is the preferred test when available

• cutoff activity of 600 IU/L, most studies have reported specificities above 95%, with sensitivities ranging between 55% and 100%

Prediction

• used to determine the severity of acute pancretitis

• Because the Ranson criteria are applied after 48 hours, criteria are less useful for ED assessment

Treatment

Acute Cholangitis• requires the presence of biliary obstruction and an infected

biliary tract• Causes of biliary obstruction include choledocholithiasis,

biliary tract strictures, stricture of a biliary anastomosis, and compression caused by malignant disease

• Charcot triad: fever, jaundice, and right upper quadrant pain

• The Reynolds pentad is altered mental status, shock, fever, jaundice, and abdominal pain

• ED treatment is aggressive volume replacement, administration of broad-spectrum antibiotics, and consultation for emergency surgical or endoscopic decompression of the biliary tract

Cholecystitis

• inflammation of the gallbladder that occurs most commonly because of an obstruction of the cystic duct from cholelithiasis

• Obstruction of cystic duct – distention gallbladder – compromised blood flow and lymphatic drainage – mucosal ischemia and necrosis

Clinical feature

• RUQ pain sometimes radiated to Rt scapula• Fever• Tachycardia• Palpable gallblader• Murphy sign/ US Murphy sign

Management

• Analgesic• Antibiotic• Fluid resus• Surgical consultation

Intestinal obstruction

• inability of the intestinal tract to allow for regular passage of food and bowel contents secondary to mechanical obstruction or adynamic ileus

• Adynamic ileus (paralytic ileus) is more common but is usually self-limiting and does not require surgical intervention.

• Mechanical obstruction can be caused by either intrinsic or extrinsic factors and generally requires definitive intervention

Pathophysiology• Intraluminal accumulation of gastric, biliary, and pancreatic

secretions • the bowel becomes congested and intestinal contents fail

to be absorbed • combination of decreased absorption, vomiting, and

reduced intake leads to volume depletion with hemoconcentration and electrolyte imbalance and ultimately can cause renal failure or shock

• increase in intraluminal pressure • intraluminal pressure exceeds capillary and venous

pressure in the bowel wall, absorption and lymphatic drainage decrease, the bowel becomes ischemic, and septicemia and bowel necrosis can develop

Clinical feature

• Abdominal pain– Crampy– Colicky/intermittent

• Vomitting• No BO, No flatus• Abdominal distention• Bowel sound - active to absent

Management• Investigation– Blood – FBC/BUSE/GSH/VBG– Radiography – AXR, CXR

• Nasogastric tube is often unnecessary, but could be considered in the presence of severe distention and vomiting

• Vigorous IV fluid replacement is needed because of loss of absorptive capacity, decreased oral intake, and vomiting

• Administer preoperative broad-spectrum antibiotics in the ED

• Surgical referral

PUD & Gastritis

• acute or chronic inflammation of the gastric mucosa and has various etiologies

• Dyspepsia is continuous or recurrent upper abdominal pain or discomfort with or without associated symptoms

Pathophysiology• HCL destroy gastric mucosa• Mucus and bicarbonate ion secretions protect

mucosa. Prostaglandins protect mucosa by enhancing mucus and bicarbonate production and by enhancing mucosal blood flow

• The balance between these protective and destructive forces determines whether peptic ulcer disease occurs

• H. pylori infection or NSAIDs are thought to be the causal agents of peptic ulcer disease in almost all cases

Clinical feature

• Burning epigastric pain• pain also may be described as sharp, dull, an

ache, or an "empty" or "hungry" feeling• Pain may be relieved by ingestion of milk,

food, or antacids, presumably due to buffering and/or dilution of acid

• Pain recurs as the gastric contents empty, and the recurrent pain may classically awaken the patient at night

Diagnosis

• Uncomplicated peptic ulcer disease can be strongly suspected in the presence of a "classic" history, including epigastric burning pain; relief of pain with ingestion of milk, food, or antacids; and night pain accompanied by "benign" physical examination findings, including normal vital signs with or without mild epigastric tenderness

• The gold standard for diagnosis of peptic ulcer disease is visualization of an ulcer by upper GI endoscopy

Investigation

• To rule out other emergencies• ECG• CXR• Amylase• FBC

Treatment

• Goal of treatment is to heal the ulcer while relieving pain and preventing complications and recurrence

• PPI, H2 receptor antagonist, antacids• Eradication of H. Pylori• No NSAID

Acute Mesentric Ischemia• Mesenteric artery occlusion can result from

thrombosis or embolism which usually arises from a recent myocardial infarction or atrial fibrillation

• rare but serious cause of an acute abdomen, characterized by sudden onset of severe diffuse abdominal pain associated with nausea, vomiting, progressive distention, and sometimes bloody diarrhea

• pain is out of proportion to the physical findings which are minimal at the onset

Cont…• Initially peristalsis is hyperactive, then gradually

diminishes• When peristalsis is absent, the bowel wall is

usually not viable• Signs of peritonitis develop rapidly with distinctly

elevated white cell count and elevated temperature

• X-ray films of the abdomen may reveal wide-spread gas and fluid filled loops of bowel but negative x-ray findings do not exclude this diagnosis

AAA• An abdominal aortic aneurysm is defined as an

aneurysm 3.0 cm in diameter, and repair is considered for an aneurysm 5.0 cm in diameter

• Clinical feature;– Syncope– flank, back, or abdominal pain – severe, tearing– GI bleeding from an aortoduodenal fistula– extremity ischemia from embolization of a thrombus in

the aneurysm– Shock– sudden death– Pulsatile mass

Cont…

• Investigation– US– AXR – calcified aorta– CT scan with contrast

Treatment