Sabiston Infections Flashcards
(29 cards)
C. difficile
- anaerobic, spore-forming, gram-positive bacillus.
- Transmission routes include person-to-person spread through the fecal-oral route or through exposure to a contaminated environment by ingestion of spores from other patients and transmission via healthcare personnel’s hands
Toxin A and B
Binding of toxin A or B to colonocyte glycoprotein receptors leads to colonocyte death and release of inflammatory mediators
C. difficile Ribotype 027 strain in the mid-2000s resulted in significant outbreaks and Deaths
RF for C.Diff
Virtually all antibiotics have been associated with C. difficile, but particularly
third and fourth generation cephalosporins,
fluoroquinolones
clindamycin
carbapenems
have been linked to a higher risk of CDI.
Other RF
immunodeficiency (including human immunodeficiency virus infection)
chemotherapy treatment
use of acid suppressing medications such as proton pump inhibitors
GI surgery or manipulation of GI tract including tube feeding
prolonged hospitalization or lengthy stay in nursing homes or rehabilitation units.
Patients with IBD have increased rates of CDI, along with worse outcomes [HIV] and higher rates of colectomy
increased risk for death from CDI include
advanced age
multiple comorbidities
hypoalbuminemia
leukocytosis
acute renal failure
and those infected with Ribotype 027
When it Begins
begin 4 to 9 days after initiation of antibiotics but can commence 10 weeks or more after antibiotic treatment.
Patients presenting with new-onset, unexplained, watery diarrhea (with three or more unformed stools in 24 hours) should be suspected of having CDI.
Patients may also have abdominal pain, fever, and an associated ileus
categorized into
asymptomatic colonization
nonsevere disease
severe disease
fulminant disease
assess clinical severity
Leukocytes of at least 15,000 cells/μL
and/or serum creatinine of at least 1.5 cells/μL are predictors of severe disease according to the Infectious Disease Society of America.
Fulminant or severe CDI is diagnosed in patients demonstrating hypotension or shock, ileus, or megacolon
Diagnosis Test
enzyme-linked immunosorbent assay for toxin detection,
glutamate dehydrogenase immunoassay for C. difficile antigen detection
nucleic acid amplification test
polymerase chain reaction testing
and stool cultures
Other Tests
- Flexible sigmoidoscopy
> not a first-line modality , helpful in cases of inconclusive stool testing or to help exclude other etiologies.
> Classically raised, yellowish-white small (2–10 mm) plaques (pseudomembranes) can be observed in approximately half of patients with CDI
> Histologic findings from the plaques reveal an inflammatory exudate with mucinous debris, fibrin, necrotic epithelial cells, and polymorphonuclear cells.
> In fulminant colitis, colonoscopy may increase the risk of perforation
Imaging is not very useful
> assist in assessing disease severity and response to treatment.
> Typical CT findings include significant colonic wall thickening, bowel dilation, pericolonic fat stranding, high attenuation oral contrast in the colonic lumen alternating with low-attenuation inflamed mucosa (accordion sign), and ascites.
> Ultrasound may also be useful, especially among critically ill patients who cannot be transported to the CT scanner in radiology. Ultrasonography may show bowel wall thickening, narrowing of the lumen, as well as pseudomembranes, which are seen as hyperechoic lines covering the mucosa
Treatment
stopping or minimizing previous antibiotics, parenteral fluids, and correction of electrolytes
Fecal Microbiota Transplant
for patients with recurrent episodes of CDI
Patients with CDI lack protective colonic microbiota to resist replication and colonization
nasogastric, oral (frozen fecal microbial capsules), rectal enema, and colonic per colonoscopy.
A recent comparison between upper and lower methods of delivery demonstrated the lower approaches being more effective.
multiple FMTs needed to achieve a good clinical response.
Current guidelines recommend FMT for patients with multiple recurrences of CDI, in whom antibiotic treatment has failed
Monoclonal Antibodies
Bezlotoxumab and actoxumab directed against C. difficile toxins B and A, respectively.
These antibodies limit colonic damage by neutralization of the toxin and block the binding to host cells.
They can be used as coadjuvant treatment with antimicrobial therapy to help prevent recurrence,
especially among patients infected by Ribotype 027, in severe CDI, and in immunocompromised patients.
abx
Treatment options for recurrent episodes generally include changing antibiotics (from metronidazole to vancomycin or fidaxomicin from vancomycin). In addition, tapered and pulsed regimens are used.
Surgery
a total or subtotal abdominal colectomy with preservation of the rectum has traditionally been performed.
A newer option with similar results for patients without necrosis or perforation is exteriorization of a diverting loop ileostomy with on-table colonic lavage followed by antegrade vancomycin flushes.
CMV Colitis
important etiology to consider in
immunocompromised hosts, particularly in advanced HIV infection, transplant patients, patients with IBD, and in those receiving chemotherapy.
CMV colitis commonly presents with watery or bloody diarrhea, fever, and abdominal pain.
Diagnosis is established by serology and by determining viral load in the blood.
Endoscopy demonstrates patchy mucosal erythema in the colon.
Inclusion bodies seen on biopsy are pathognomonic for CMV.
CMV colitis can progress to sepsis, toxic megacolon and colon perforation.
Treatment is usually supportive with the addition of ganciclovir. Patients with severe, complicated disease may require surgery
ischemic colitis Vs acute mesenteric ischemia
It is important to differentiate ischemic colitis from situations of acute mesenteric ischemia, in which a major vessel of the bowel is obstructed, wherein patients commonly present with severe pain out of proportion to physical findings and require immediate vascular intervention. Ischemic colitis is considered a disease of small blood vessels and typically presents less dramatically, seldom requiring vascular intervention.
Arterial Blood Supply
SMA and the IMA
The SMA gives off the ileocolic, right colic, and middle colic arteries.
The IMA gives rise to the left colic and sigmoid arteries and ends as the superior rectal (hemorrhoidal) artery
There are two well-described collateral networks that aid in preventing colonic ischemia by providing “backup” both within the territories of the two major arteries and between them.
collateral vessel
The main collateral vessel is the marginal artery of Drummond, which runs parallel and close to the mesenteric margin of the colon from the cecocolic junction to the rectosigmoid junction.
The colon can receive collateral blood supply through this artery when one of the larger arteries is obstructed. It is important when resecting a section of colon to preserve this artery since only the vasa recta are located between it and the colon. When it is compromised, ischemia of that section of colon may result.
The second collateral circulation can be found in the proximal region of the large arteries.
The “arc of Riolan” (meandering mesenteric artery) is an infrequent finding, traversing close to the mesenteric root and connecting the SMA or middle colic artery to the IMA or left colic artery. It can have a critical role in situations of SMA or IMA occlusion. The presence of a large arc of Riolan commonly indicates an obstruction of one of the major mesenteric arteries.
watershed areas
two well-described watershed areas where the collateral circulation is classically inconsistent and vulnerable to ischemia.
The first > splenic flexure (Griffiths point). In some studies, up to 50% of specimens were found to lack a marginal artery in the region where the SMA and IMA circulations meet.
> Commonly, surgeons avoid making anastomoses in this area for fear that the impaired blood supply will not be sufficient to permit anastomotic healing, leading to anastomotic leaks.
A second potential watershed area is the rectosigmoid junction (Sudeck’s point). This region receives it blood supply from the superior hemorrhoidal artery and distal sigmoid branches, both terminal branches of the IMA and prone to atherosclerotic changes.
The right colon, although not classically considered a watershed area, it is also vulnerable to ischemia from embolic occlusion because the ileocolic artery is the terminal branch of the SMA. For this reason, the right colon is also particularly prone to low-flow conditions such as heart failure, hemorrhage, and sepsis.
The rectum, which has a good blood supply from both the IMA and the iliac circulation, as well as a strong collateral network, is rarely the victim of ischemic injury.
Drugs causing Ischemic Colitis
Constipation-inducing drugs can cause ischemic colitis, most likely as a result of reduced blood flow and increased intraluminal pressure.
Immunomodulator drugs such as anti-TNF-α inhibitors can affect thrombogenesis,
and illicit drugs such as cocaine and methamphetamines cause ischemia through vasoconstriction, hypercoagulation, and direct endothelial injury
patients present with isolated right-sided ischemic colitis
These patients are more likely to present with abdominal pain without bleeding and more commonly have atrial fibrillation, coronary artery disease, and/or chronic renal failure.
Patients with isolated right-sided ischemic colitis have a higher chance of requiring surgery and have a poorer prognosis.
“thumbprinting,” and The “single-stripe sign,”
- Abdominal plain films may show bowel distension and “thumbprinting,” which are rounded densities along the sides of a gas-filled colon indicative of submucosal edema
- “single-stripe sign,” a single linear ulcer running along the longitudinal axis of the colon is rare but considered specific for ischemic colitis.
Segmental distribution, with abrupt transition between injured and noninjured mucosa, and sparing of the rectum support ischemia over IBD
Why bacterial translocation happens ?
Colonic ischemia can result in failure of the intestinal epithelial barrier with bacterial translocation leading to overt sepsis. For this reason, empiric broad-spectrum antibiotics against both anaerobic and aerobic
