A 76 y/o female presents with a ‘bellyache’. She notes the pain started 2 days ago, and is progressively getting worse. Pain was gradual in onset, epigastric in location, and radiates through to her back. She describes the pain as an ’ache’ that is constant (“Like a bad toothache”). Food makes it worse, and she has been vomiting for the past 2 days. She vomits all food, and even without eating, she will have dry heaves. No Hemetemesis or Coffee Ground emesis. No hematochezia, melena, or diarrhea. Last BM yesterday and normal. She has never had this type of pain.
ROS: No fevers, cough, chest pain, shortness of breath, rashes, dizziness. Her sugars have been running high.
PMH: Hypertension, Diabetes (NIDDM), Heart Disease (no heart attack, but 2 stents).
PSH: Hysterectomy (total)
SH: No smoking, social drinking
PE: Obese female in some distress but able to articulately describe her symptoms.
VS: BP 105/50, RR=24, P=80, Temp =98F, Sat = 96%
HEENT: Dry mucus membranes, otherwise normal HEENT
Heart: RRR unremarkable
ABD: Obese, soft. There is tenderness and some voluntary guarding to the epigastric area, RUQ and LUQ. BS decreased. No palpable masses, but obesity limits exam. Lower abd scar (from Hysterectomy) is present. Rectal is guiac negative, non-tender exam.
Ext: Unremarkable, equal pulses, no rashes
Neurologic: Non-focal, unremarkable.
1. What life threatening entities do you need to consider?
The EM mantra is: Think Worst First!!
Abd pain (radiating to the back) in a patient over the age of 50, with a history of hypotension, who is relatively hypertensive, means rule out Abdominal Aortic Aneurysm (AAA). Frequently, you can rule this out on the physical exam, but in this era of quick bedside ultrasound, I usually do a quick ultrasound exam. A simple question (Do you have an aneurysm?) is great, because the patient won’t always include it in their medical problems (they often don’t consider it a problem…the doctor is just watching it). Once ruptured, the mortality for repair is about 70%. (1)
Interesting that a recent review found endovascular repair of a ruptured AAA to be as good as (and for 4 year mortality –superior to) the traditional open AAA repair. (1)
Other abdominal (and extra abdominal) catastrophes include:
a. Ruptured viscous (less likely as abd not rigid…but still possible)
b. Gastric process with or without bleeding (PUD, Gastritis, UGI bleed)
c. Cholicystitis/ Cholangitis – but why the LUQ pain then?
d. Pancreatitis – fits in AAA u/s neg
e. Pneumonia (less likely, no cough, fevers, etc)
f. Acute MI (less likely, no chest pain but could still happen, wouldn’t be the first MI to present like this)
g. Bowel obstruction possible she has had prior surgery.
h. Mesenteric Ischemia
i. Hepititis – doubt with LUQ pain
j. Appy – doubt
Non-catastrophic emergencies include:
b. Viral infection
c. Constipation (don’t most older people have this as baseline?)
d. UTI: she may have this (so many older females do), but I doubt this is the cause for her symptoms
e. Kidney Stone
In general, in older individuals with abdominal pain and vomiting I’m looking to find the emergency, instead of assuming its nothing. Usually, there is ‘badness brewing’ in the belly. Older people are more stoic, and if they have pain and vomiting then something is going on and more likely than not its serious.
2. Labs reveal an elevated WBC =19,000, with 90% PMN. Her Lytes are remarkable for a BUN of 30, and a Creatinine of 1.6. Liver tests reveal an elevated Alk Phos of 250, an elevated SGOT and SGPT (in the 300’s). Bilirubin (direct and total) slightly elevated. LDH is 380. Her Lipase is 980. Lactate is 2.1. Cardiac enzymes are normal. An acute abdominal X-Ray series reveals an Ileus, and a small L plural effusion. EKG shows NSSTT changes, no ST elevation. Based on her likely diagnosis, what additional test does she need?
She has pancreatitis, and an evaluation of the biliary tree is necessary to see if it is gallstone related, and if there is any stone in the duct. Alcohol abuse and biliary stone disease are the common causes of pancreatitis. (2)
3. What is the difference between Direct and Total Bilirubin?
Direct is the conjugated bilirubin (I remember CD: Conjugated = Direct), and the Total includes both. For a great review, see reference #3-5. Basically, after Hemoglobin breakdown, the unconjugated bilirubin (attached to albumin, which is water insoluble), is transported to the liver, where it is conjugated (now water soluble) and excreted via the bile ducts to the intestine. In the intestine, bacteria act on it and convert it to urobiligen, and most of this is excreted in the stool (after metabolism to stercobilin, which renders stool brown). Some of this is reabsorbed, and the reabsorbed is either excreted in the kidney (normally a very small amount), or undergoes re-uptake into the liver. (4, 5). In an obstructive process (stone in bile duct), the direct is elevated because it can’t get excreted properly.
4. What common medications can cause this?
Medications can cause pancreatitis, but it’s not very common. Only about 1.2-1.4% of cases are linked to medications. (6) Actually furosemide and hydrochlorothiazide can cause it. Propofol can also cause it. (6) See the list in Reference 6.
5. What is Ranson’s Criteria?
Ranson’s described the criteria to estimate mortality in 1974. There are five admission criteria, and six 48hr criteria. For a great review, see reference 7 (which is completely available on line). This reference also has the mortality estimations, and the criteria. Personally, I don’t have the criteria memorized, but it’s available on line for free. If you use this on line calculator, it will spit out the mortality information. (http://www.mdcalc.com/ransons-criteria-for-pancreatitis-mortality )
Based on this scoring system, her mortality is estimated at 40%!!!
IV fluid resuscitation was started in the ED (she was relatively hypotensive), along with antibiotics for cholicystitis, and she was admitted to the hospital (with surgery on consult). The ultrasound revealed a dilated common bile duct, gallbladder thickening, stones in the gallbladder but no stone in the duct. (Just passed?). She actually did great and was discharged in 8 days.
1. Egorova N, Giacovelli JK, Gaimpaoo G, Gelijns A, Kent CK, McKinsey JF. National Outcomes for the treatment for ruptured abdominal aortic aneurysm. Comparison of open versus endovascular repairs. J Vasc Surg 2008 Nov 48(5):1092-1100. Entire manuscript accessed at: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2622721
2. Khoury G. Pancreatitis Emedicine Jan 26, 2009. Accessed at: http://emedicine.medscape.com/article/775867-overview
3. The Merck Manual: Jaundice. Accessed at: http://www.merck.com/mmpe/sec03/ch022/ch022d.html#sec03-ch022-ch022d-58.
4. The Merck Manual: Laboratory Tests for Liver Injury Accessed at: http://www.merck.com/mmpe/sec03/ch023/ch023b.html
5. Beckett G, Walker S, Rae P, Ashby P. Clinical Biochemistry, Lecture Notes 7th Edition, Blackwell Publishing, pg 109. Accessed at: http://books.google.com/books?id=dFJVtSTaJUUC&pg=PA108&lpg=PA108&dq=bilirubin+production+and+metabolism&source=bl&ots=Kcwm2BPXI3&sig=oEXRU3dV7NmGHiZDsryNCHi7TN0&hl=en&ei=sl8VSuihJIqxmAf_vJHjDA&sa=X&oi=book_result&ct=result&resnum=7#PPA108,M1
6. University of Alabama School of Medicine. Drug Induced Pancreatitis. Accessed at: http://www.mississippicme.uab.edu/courses/Pancreatitis/ID0429M.asp
7. Ojetti V. Migneco A, Manno A, Verbo A, Rizzo G, Gentiloni Silveri N. Management of Acute Pancreatitis in Emergency Eur Pev Med Pharmacol Sci 2005;9:133-140. Entire manuscript available at: http://www.europeanreview.org/pdf/165.pdf