Tag Archives: gi

Pancreatitis (quick hits)

1 Nov

submitted by Christina Brown, M.D. 

Definition – Inflammation of pancreas due to activation, interstitial liberation, and digestion of gland by its own enzymes. Gallstones and alcohol abuse most common causes.

Acute – Exocrine and endocrine function of gland impaired for weeks-months. Function will return to b/l.

Chronic – Dysfunction progressive and irreversible.

Signs and Symptoms

  • Abdominal pain: 95–100%
  • Epigastric tenderness: 95–100%
  • Nausea and vomiting: 70–90%
  • Low-grade fever: 70–85%
  • Hypotension: 20–40%
  • Jaundice: 30%
  • Grey Turner/Cullen sign: <5%

 

Ranson Criteria – Indicators of morbidity and mortality:

o 0–2 criteria: 2% mortality
o 3 or 4 criteria: 15% mortality
o 5 or 6 criteria: 40% mortality
o 7 or 8 criteria: 100% mortality

Criteria on admission:

• Age >55 yr
• WBC count >16,000 mm3
• Blood glucose >200 mg/dL
• Serum lactate dehydrogenase >350 IU/L
• AST >250 IU/L

 
Diagnostic Evaluation/Labwork

Lipase: Rises within 4–8 hr of pain onset. More reliable indicator of pancreatitis than amylase

Amylase: Levels >3 times limit of normal suggest pancreatitis.

Calcium: Hypocalcemia indicates significant pancreatic injury.

Imaging
Abdominal Series – Most common finding is isolated dilated bowel loop (sentinel loop) near pancreas.

CXR: Pleural effusion

RUQ U/S: Useful if gallstone pancreatitis is suspected.

Abdominal CT indications:

• High-risk pancreatitis (>3 Ranson criteria)
• Hemorrhagic pancreatitis
• Suspicion for pseudocyst
• Diagnosis in doubt

Endoscopic retrograde cholangiopancreatography (ERCP) – Indicated for severe pancreatitis with cholangitis or biliary obstruction

 

 
ED Treatment
Fluid resuscitation

Correct electrolyte abnormalities

• Hypocalcemia (calcium gluconate)
• Hypokalemia occurs with extensive fluid losses.
• Hypomagnesemia occurs with underlying alcohol abuse.

Analgesia, Antiemetics

Antibiotics: Indicated if pancreatic necrosis >30% on abdominal CT

 

DISPOSITION:
Admission Criteria
• Acute pancreatitis with significant pain, nausea, vomiting
• ICU admission for hemorrhagic/necrotizing pancreatitis

Discharge Criteria
• Mild acute pancreatitis without evidence of biliary tract disease and able to tolerate oral fluids
• Chronic pancreatitis with minimal abdominal pain and able to tolerate oral fluids. All discharged mild pancreatitis should have scheduled follow-up within 24–28 hr.

 

References:
Lewis, T. Schaider, J. & Barkin, R. & Hayden, S. & Wolfe, R. & Barkin, A. & Shayne, P. & Rosen, P. (2011). Pancreatitis. Rosen & Barkin’s 5 minute Emergency Medicine Consult.

Frossard D, Steer M L, and Pastor C M.: Acute pancreatitis. Lancet. 2008; 371:143–152

Heinrich S, Schäfer M, and Rousson V et al.: Evidence-based treatment of acute pancreatitis: A look at established paradigm. Ann Surg. 2006; 243(2):154–168.
Hayerle J, Simon P, and Lerch M M.: Medical treatment of acute pancreatitis. Gastroenterol Clin North Am. 2004; 855–869

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cannabinoid hyperemesis and…capsaicin?

3 Mar

via a couple EM News articles:

CANNABINOID HYPEREMESIS: QUICK PEARLS:

cyclic vomiting, every few weeks or months

resistant to antiemetics

history of regular cannabis use, usually x years

relief of vomiting/abdominal pain with a hot bath or shower (with resulting compulsive bathing)

episodes ceased when refraining from cannabis use

diagnosis of exclusion

 

INTERESTING BIT ON CAPSAICIN TREATMENT:

TRPV1 receptor in peripheral nervous system – activated by heat >109 F and capsaicin

case series of 7

applied 0.075% capsaicin cream to abdomen

symptoms resolved or drastically diminished in 30-45 min

 

Tiny series, but neat idea.

 

References: EM News article on the syndrome; on capsaicin use; uptodate.com; picture

aortoenteric fistula: fear it

13 Oct

QUICK PEARLS:

Aortoenteric fistula: a communication between the aorta and the GI tract

consider in anyone with a GI bleed and a history of aortic surgery.

Can involve any part of the bowel but 75% involve the third part of the duodenum.

Mean time to presentation from surgical date is 32 months, but can run the gamut.

 

Can be primary (from AAA, but this is rare), but often related to aortic graft

 

Herald Bleeds

  • often have self-limited “herald bleeds”, can be intermittent
  • Stops from vasospasm or thrombus formation
  • Followed by massive GI bleed over the next month; 30% of these are within next 6 hours

 

DIAGNOSIS:

  • Conventional CT
  • CTA (most sensitive with “detection rate” of 61%)
  • EGD (25-62.5% or primary fistulas are identified)
  • Laparotomy

 

TREATMENT OPTIONS:

  • Endovascular stent for those than cannot tolerate surgery
  • Graft resection, repair of duodenal wall, and new bypass (mortality rate: 30-40%)
  • Gentle resuscitation: SBP goal 60-100
  • Survival rates with treatment: 30-70%

 

References:  MacDougall, L et al. Aorto-enteric fistulas: a cause of gastrointestinal bleeding not to be missed.  BJMP. 2010; 3(2): 317.   Ranasinghe, W et al. Primary aortoenteric fistulae: the challenges in diagnosis and review of treatment. Ann Vasc Surg. 2011; 25(3): 386; picture

Mesenteric Ischemia: quick review

22 Sep

What is it?

A reduction in intestinal blood flow, due to

arterial occlusion, usually SMA (85-95%)

nonocclusive ischemia/hypoperfusion, usually related to low cardiac output (20-30%)

-venous occlusion, usually SMV (5%)

 

 

What are the risk factors?

Advanced age, atherosclerosis, low cardiac output states, cardiac arrhythmias, cardiac valvular disease, recent MI, and intra-abdominal malignancy

 

In younger patients, mesenteric venous thrombosis is the major cause of ischemia

 

 

How does it present?

Rapid onset of severe periumbilical abdominal pain out of proportion to physical exam findings, +/- associated nausea and vomiting

 

Be cautious of a more insidious presentation for venous thrombosis; pain may be present for several days to weeks

 

 

How is it diagnosed?

Mostly clinical suspicion

 

A personal history of previous embolism is present in 1/3 of patients with acute embolic mesenteric ischemia; a personal or family history of DVT or PE is present in ½ of patients with acute mesenteric venous thrombosis

 

Lactate is 100% sensitive, 42% specific for intestinal ischemia/infarction

 

CT angiography (CTA) should be done without oral contrast (to avoid obscuring mesenteric vessels) shows findings of acute ischemia:

-bowel wall thickening

-intestinal pneumatosis with portal venous gas

-bowel dilation

-mesenteric stranding

-portomesenteric thrombosis

-solid organ infarction

 

What is the treatment?

Systemic anticoagulation +/- surgery (embolectomy, thrombectomy, bowel resection)

 

Anticoagulation alone may be reasonable in patients with good collateral blood flow

 

Consider hypercoaguable workup for venous thrombosis.

 

 

Submitted by K Estes.

 

Source: uptodate.com; picture

more acronyms: MALS (median arcuate ligament syndrome)

30 Jun

RAGING HYPOTHETICAL:

Your next patient is a 63 M with intermittent abdominal pains with this being his worst and longest case.  You’re worried about  vascular pathology such as dissection or ischemia, and end up deciding to order a CTA.  

 

Your patient gets the CTA, and the read comes back as this:

  • median arcuate ligament syndrome (MALS), with high-grade compression/stenosis of the celiac trunk.

 

So what does actually this mean?

 

QUICK PEARLS:

MALS or Celiac Artery Compression (CAC) results from external compression of the celiac artery by the median arcuate ligament

an unusual cause of visceral ischemia.

more common in younger adults and women than men.

usually associated with weight loss

pain is often post-prandial.

Often an epigastric bruit can be heard on exam.

Some compression of the celiac artery is common even in patients without the syndrome, so making a definitive diagnosis can be difficult.

Referral to a vascular surgeon is an appropriate step.

 

Submitted by J. Stone.

 

References: (Rapp, Joseph H. , MacTaggart, Jason. Chapter 34. Arteries – in Current diagnosis and treatment : Surgery 13th ed. 2010); picture

g-tube out?

23 May

Most G/J tubes require 1-2 weeks to form a mature tract.

 

If under that amount of time, non-operative or non-fluoro guided replacement in ED may form an inappropriate tract and place tube in incorrect location.  Ensure it has been adequate amount of time.

 

If so, prompt replacement with largest foley or g tube possible to ensure patency of tract in prompt manner is ideal.

 

If any signs of infection, do not replace either.

 

Submitted by J. Rothstein.

 

References: emedicine, picture

Blakemore tube for upper GI bleed

12 May

Handy how-to from Dr. Weingart on his EMCrit blog (It’s a bit complicated, so the video is worth a watch):

 

SOME QUICK PEARLS:

 

your patient should be intubated (this would not be comfortable)

 

gastric balloon and esophageal balloon, so good to sort (and temporarily stop, hopefully) a bleed there.  

if the bleed is lower (e.g. duodenal), this won’t help.

gastric balloon is volume (50 mL prior to X-ray confirmation, then another 200mL)

esophageal balloon is pressure-based (hook to sphygmomanometer via 3-way stopcock, 30-45 mmHg)

pre-mark the extra NG tube prior to inserting the Blakemore, so you know where you’re suctioning

 

Knowing is half the battle. Check it out.

 

References: EMCrit blog (+ picture)