Surgical

Question 1

Ischemic gut

Answer 1

CAUSES:

Arterial embolism from heart - AF, infective endocarditis - ECG, echo for vegetations

Thrombosis to mesenteric artery - atherosclerosis and plaque rupture

Venous mesenteric infarct - hypercoagulable state i.e. antiphospholipid syndrome - lupus anticoagulant and anti-cardiolipin antibodies

Hypotension shock/reduce gut perfusion - VBG lactic acidosis

Abdominal trauma causing disruption to mesenteric artery

ANATOMY:

Coeliac artery - proximal duodenum

Superior mesenteric artery (SMA) - distal duodenum and remainder of small bowel, right colon from the caecum to the splenic flexure. The SMA most commonly affected (85%) due to embolism from AF.

Inferior mesenteric artery - transverse colon to rectum

MANAGEMENT:

Analgesia
Aggressive fluid resuscitation to improve splachnic flow
Avoid vasoconstrictors
Anticolagulation
Broad spectrum antibiotics - peritonitis
Surgery
Interventional radiology

Question 2

Pancreatitis

Answer 2

Ref: Tintinalli’s

CAUSES: “I GETSMASHED”

Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mupms/Malignancy (head of pancreas tumour)
Autoimmune
Scorpion venom
Hyperlipidemia, hypercalcemia, hyperparathyroidism
ERCP
Drugs - antiretrovirals, chemotherapy agents, immunesuppressants (azathiaprine)

PATHOPHYSIOLOGY:
- Trypsinogen inappropriately activated to trypsin in pancreatic acinar cells.
- Activated trypsin in turn activates other digestive enzymes, complements, and kinins, leading to pancreatic autodigestion, injury, and inflammation.

CLINICAL SIGNS:
Rare physical findings associated with late, severe necrotizing pancreatitis include CULLEN’S SIGN (bluish discoloration around the umbilicus signifying hemoperitoneum), GREY-TURNER SIGN (reddish-brown discoloration along the flanks signifying retroperitoneal blood or extravasation of pancreatic exudate), and erythematous skin nodules from focal subcutaneous fat necrosis.

DIAGNOSIS:

Formal diagnosis is based on at least two of three criteria:
- (1) clinical presentation consistent with acute pancreatitis,
- (2) a serum lipase or amylase value significantly elevated above the upper limit of normal, or
- (3) imaging findings characteristic of acute pancreatitis (IV contrast-enhanced CT, MRI, or transabdominal US).

• elevation of lipase or amylase 3x the upper normal limit
• Amylase is not a good choice for diagnosis. Amylase rises within a few hours after the onset of symptoms, peaks within 48 hours, and normalizes in 3 to 5 days.
• Amylase can be elevated in multiple non–pancreas-related diseases, such as renal insufficiency, salivary gland diseases, acute appendicitis, cholecystitis, intestinal obstruction or ischemia, and gynecologic diseases, lowering its specificity for pancreatitis.
• Lipase is more specific to pancreatic injury and remains elevated for longer after the onset of symptoms than amylase.
• The urine trypsinogen-2 dipstick test is a rapid, noninvasive test with high sensitivity (82%) and specificity (94%).26 However, given its current limited availability, it is not included as part of the diagnostic criteria for pancreatitis
• An alanine aminotransferase of >150 U/L within the first 48 hours of symptoms predicts gallstone pancreatitis with a greater than 85% positive predictive value
• There is no evidence that early CT improves clinical outcoumes.
• Morphological change does not correlate with disease severity
• IV contrast can cause nephrotoxicity and worsen pancreatitis
• If the clinical diagnosis of acute pancreatitis is in doubt, consider further evaluation with IV contrast abdominal CT. Characteristic findings include: (1) pancreatic parenchymal inflammation with or without peripancreatic fat inflammation; (2) pancreatic parenchymal necrosis or peripancreatic necrosis; (3) peripancreatic fluid collection; or (4) pancreatic pseudocyst.

COMPLICATIONS:

Local:
- Pancreatic necrosis (sterile or infected), abscess, pseudocyst

Respiratory:
- Pleural effusions and ARDS

Metabolic:
- hyperglycemia, hypocalcemia, hypomagnesia

Haematological:
- DIC, VTE

Gastrointestinal:
- biliary obstruction with jaundice, splenic or portal vein thrombosis, illeus, gastritis, gastric ulceration, GI bleeding

Cardiac:
- pericardial effusion

Renal:
- renal failure

Chronic pancreatitis

PREDICTION OF DISEASE SEVERITY:
- Ranson criteria,
- Acute Physiology and Chronic Health Examination-II,
- modified Glasgow score,
- Bedside Index for Severity in Acute Pancreatitis,
- Balthazar CT Severity Index
(some data points are collected 48hrs after presentation, limiting utility in ED)

Clinical findings at initial assessment are associated with severe disease
- SIRS with end-organ failure
- age >55
- obesity
- altered mental status
- comorbidities

PROGNOSTIC INDICATORS ON ADMISSION:
Good prognosis with the following:

PaO2 >60mmHg
Age < 55yrs
WCC < 15
Calcium >2
Renal function - Urea < 16mmol/L
Enzymes - LDH < 250, AST <600, ALT <200
Albumin - > 32g/L
Sugars <10mmol/L

MANAGEMENT:

IV fluids - hartmann’s, 5-10ml/kg/hr

End points:
– Hematocrit 35%–44%

– Maintain normal creatinine

– Heart rate <120 beats/min

– Mean arterial pressure 65–85 mm Hg

– Urine output 0.5–1 mL/kg/h (if no renal failure)

NBM only until pain and vomiting under control. Prolonged bowel and pancreas rest increases gut atrophy and bacterial translocation, leading to infection and increasing morbidity and mortality. Start small low fat diet.

Correct electrolytes:
- hypocalcemia
- hypomagnesia
- hyperglycemia

Analgesia

Antiemetics

Oxygen

Antibiotics only if infected pancreatic necrosis, no role for prophylactic antibiotics

Anticoagulation - VTE prevention

ERCP for biliary obstruction

Manage complications