Causes of severe intra-abdominal sepsis
- Faecal peritonitis, due to
- Perforated diverticulum
- Perforated tumour
- Perforated ischaemic gut
- Secondary - following previous surgery, eg. anastomotic leak
- Acalculous cholecystitis
- Ruptured gall bladder empyema
- Perforated gastric or duodenal ulcer
- Abdominal collection, eg. abscess
- Toxic megacolon
- Spontaneous bacterial peritonitis
- CAPD-associated peritonitis
Pre-operative management of intra-abdominal sepsis
One does not need to deviate from the existing guidelines. In brief, the early administration of antibiotics is critically important, as is resuscitation to certain hemodynamic goals, and one should not be shy with the vasopressors.
Some authors place great faith in the physical examination and history, suggesting that the shocked patient with clinical features of peritonitis should progress to laparotomy without the pansy fuffery of an abdominal CT. One might view this opinion as an artifact of a bygone era when CT scans were slow and difficult to organise in a hurry. These days, CT is fast and easy. Furthermore, in at least one study about 38% of the acute abdomen patients had no clinical features of peritonitis. Examination findings, particularly in the elderly, are unreliable. Few surgical specialists would take a peritonitis patient to theatre without CT imaging.
Antibiotic choices in abdominal catastrophe
The gut flora are a heterogenous bunch of organisms. Broad spectrum beta-lactams are indicated. There are generic guidelines, which typically involve either a carbapenem or Tazocin. The combination of ampicillin metronidazole and gentamicin was the former favourite. Is there a difference between the regimens, is there a point in adding an aminoglycoside? Probably not, concludes a though Cochrane review.
Among the uniformly polymicrobial abdominal sepsis syndromes, several deviations from the norm stand out, and should be mentioned:
- Gastric or duodenal perforation can release S.aureus, and should get some vancomycin
- There might be situations which favour the use of empirical antifungal therapy.
Empirical antifungal agents in abdominal catastrope
Yes, the upper gastrointestinal tract is colonised with Candida. Yes, that GI contents is now sloshing freely in the unprotected abdominal cavity. Is this reason enough to administer broad-spectrum antifungal drugs to any patient with a perforated viscus?
Certainly, some high risk patients seem to benefit. After a broken-down anastomosis leaks into the abdomen, the contents of that bowel cannot be expected to be the standard mix of anerobes and gram negatives, not after a periof of ICU stay. Thus, fluconazole seems to prevent these patients from developing clinically significant candidiasis. However, a retrospective analysis of patients with primary lower GI perforation did not demonstrate any survival benefit.
Who is likely to develop candida infections
A widely cited study from 2008 has identified some risk factors:
|Risk factors for Candida albicans and non-albicans fungaemia|
Thus, there is some argument that these people, when assailed by abdominal sepsis, should receive empirical fluconazole perioperatively. However, this has not percolated into official guidelines. The Surgical Infection Society recommends:
"Empiric antifungal therapy for Candida is not recommended for adult and pediatric patients with community-acquired intra-abdominal infection"
Proven fungal peritonitis
A consensus statement dating back to the carefree 1990s recommends 4 weeks of amphotericin. This, plainly, is insane. These days fluconazole is given if Candida albicans is isolated from abdominal cultures, and caspofungin if the species is non-albicans.
Damage control surgery
This is source control and washout. Even though some seem to have had some good experiences with primary anastomosis, nobody expects a brilliantly elegant surgical repair to take place in that lake of blood and stool. The initial surgical management has some modest goals:
- Wash out the contaminating material
- Drain abscesses
- Debride dead tissue
- Defunction the gut (stoma formation)
If it were me, I would prefer my abdomen left open.
Generally speaking, care for the patient with an open abdomen is non-specific, and rests on one's ability to maintain organ system function between the stages of a staged abdominal closure. Conversely, if the patient returns to ICU with their abdomen closed, one must monitor vigilantly for the development of abdominal compartment syndrome, which is discussed elsewhere.
The only thing to add is that among the various ways of managing the abdominal defect, the vac dressing seems to be the best, as it will remove ascitic fluid and any contaminants that may be spilling out of fistulas and perforated viscera. If a fistula does form, one may consider using octreotide to decrease the output while feeding the patient with TPN.