Abdominal Pain and Constipation in a DM Patient - Dysmotility Syndrome
Author: V. Dimov, M.D.
Reviewer: S. Randhawa, M.D.
A 58-yo AAF with a PMH of DM2, diabetic gastroparesis, megacolon, autonomic neuropathy, was admitted to the hospital with CC: abdominal pain and constipation x 1 week.
The pain was located in the epigastrium and LLQ, 6/10, constant, non-radiating.
The patient did not complain of N/V/D, CP or SOB. She was was admitted with similar complaints 3 weeks ago, WBC was 15, temperature 37.4 C. At that time, she was diagnosed with diverticulitis and D/C'd home with an antibiotic course and Colace/Miralax.
PMH:
DM2, diabetic gastroparesis, megacolon, autonomic neuropathy, HTN, carpal tunnel syndrome, peripheral neuropathy
She had upper and lower endoscopies 2 months ago. EGD: Gastroparesis, autonomic neuropathy. Colonoscopy: Megacolon, colonic inertia due to DM.
In addition, she also had a water-soluble barium enema and a CT of the abdomen, which did not show any diverticula.
PSH:
Cholecystectomy (laparoscopic), hysterectomy
Medications:
NPH insulin, Prevacid, Clonidine, Colace, Lopressor, Norvasc, Lisinopril, Tramadol, Reglan, Miralax
Physical examination:
Obese lady in NAD
VS 36.9-18-66-168/68
Abdomen: Soft, obese, +BS, epigastric and LLQ tenderness, no rebound
Rectal: hemorrhoids, empty ampulla
What is the most likely diagnosis?
Gastroparesis, megacolon and constipation.
Diverticulitis is unlikely-- she had no diverticula on imaging studies done recently. Pancreatitis is also not very high on the differential diagnosis list -- she is just an occasional drinker and pancreatitis was ruled out just 2-3 weeks ago.
What labs would you order?
CBCD, CMP, INR/PTT, INR
CXR, KUB
UA, urine C&S
Laboratory results:
WBC was increased to 15.4, N 64, L 18
CXR: Mild cardiomegaly, no infiltrates
KUB: Fecal retention
UA and urine culture: negative
What do you think is the reason for the increased WBC?
Diverticulitis - not likely
Is leukocytosis due to an infection?
An empiric therapy wtih Cipro and Flagyl was already started on admission. BCx were negative, she had no fever and the repeated WBC the next day after the admission decreased to 9.
The most likely reason for leukocytosis in this patient is a stress reaction due to pain. She had a similar response during the previous admission, and she had no infectious focus at that time according to the ID consultant.
What happened?
A GI consult was called.
The patient's pain decreased after she moved her bowels. Norvasc was stopped because CCBs have an antimotility effect. Clonidine which can be used as an antimotility agent in DM autonomic diarrhea was also discontinued. Antibiotics and Tramadol were stopped.
Her BP was in the range of 130/80 and she was advised to follow-up with her PCP for a BP check within a week.
The patient had no further complaints and was D/C'd home.
What else can we do?
We started Lactulose instead of Miralax as a prokinetic agent.
Erythromycin can be used as prokinetic but a study (NEJM 10/2004) showed a 2-5-fold increased risk of sudden cardiac death in patients taking erythromycin plus other antihypertensive medications.
A nuclear medicine gastric emptying scan was ordered. This is the "gold standard" for diagnosing gastroparesis.
Final diagnosis:
Abdominal pain and constipation due to DM gastroparesis and megacolon
What did we learn from this case?
Leukocytosis can be due to a variety of reasons and not all of them are of infectious nature.
Autonomic neuropathy and GI dysmotility syndromes are well known complications of DM
Recognize medications with antimotility effects and discontinue them, e.g. Norvasc (and other CCBs), Clonidine and Tramadol.
Twenty years after the diagnosis, 30-60% of DM patients develop signs of visceral neuropathy.
GI symptoms are significantly associated with autonomic and peripheral neuropathy (our patient had peripheral neuropathy with numbness, burning pain and was started on Neurontin during this hospital stay).
Incidence of peripheral neuropathy plus: constipation (29%), GERD (19%), dyspepsia (14%), and frequent abdominal pain (11%).
DM gastroparesis is usually not progressive, does not increase mortality and does not improve with better metabolic control of DM.
References:
UpToDate 12.3.
Published: 03/11/2005
Updated: 08/19/2008
Labels: Endocrinology, Gastroenterology