Showing posts with label gastroenterology. Show all posts
Showing posts with label gastroenterology. Show all posts

Saturday, September 13, 2014

Non-surgical management of appendicitis?

From a recent study:

Method
During this 4-year study, we enrolled 26 elderly patients who initially received antibiotic therapy. Of these, 3 were suspected to have complicated appendicitis. Antibiotic therapy consisted of second-generation cephalosporin and metronidazole that was administered for 4 days with a 24 h fasting period. We evaluated the rates of treatment failure and recurrence.

Results
Mean age was 83.5 years and 57.7% (15/26) of patients had comorbidities. One patient (4.8%) failed to respond to antibiotic therapy and underwent subsequent appendectomy. During the median follow-up period of 17 months, 5 patients (20%) experienced recurrence; 3 underwent appendectomy and two received a new course of antibiotics.

Conclusion
Antibiotic therapy without surgery may be a safe and an effective treatment for appendicitis in selective patients aged greater than or equal to 80 years. This is a good treatment option in patients with high operative risk.

Via Hospital Medicine Virtual Journal Club.

Friday, August 22, 2014

Proton pump inhibitors and the risk of spontaneous bacterial peritonitis

From a recent study:

Aim
To determine whether PPI use increases the risk of SBP using a large cohort.

Methods
This retrospective cohort study included 1965 cirrhotic patients with ascites diagnosed between January 2005 and December 2009. The SBP incidence rate was compared between the PPI and non-PPI groups before and after propensity score matching to reduce the effect of selection bias and potential confounders. Multivariate analysis was conducted to confirm the association of PPI use with SBP.

Results
After excluding 411 patients, 1554 were analysed. Among them, 512 patients (32.9%) were included in the PPI group. The annual SBP incidence rate was higher in the PPI group than in the non-PPI group (10.6% and 5.8%, P = 0.002) before matching. Indications for PPI use and dose of PPI were similar between patients with and without SBP. In the propensity score matched cohort (402 pairs), the SBP incidence rate was also higher in the PPI group than in the non-PPI group (10.8% vs. 6.0%, P = 0.038). Multivariate analysis revealed that PPI use (Hazard ratio 1.396; 95% confidence interval, 1.057–1.843; P = 0.019) was the independent risk factor for SBP.

Conclusions
Proton pump inhibitor use significantly increases the risk of spontaneous bacterial peritonitis in cirrhotic patients with ascites. Proton pump inhibitor use should be undertaken with greater caution and appropriately in patients with cirrhosis.

Via Hospital Medicine Virtual Journal Club.

Saturday, June 21, 2014

Practice variation in fluid therapy for acute pancreatitis

–-was widespread in this study from New Zealand.

There are fluid therapy recommendations in pancreatitis guidelines but there is little evidence to back them up. That said, there is an emerging literature on this topic about which I have blogged extensively before.

Via Hospital Medicine Virtual Journal Club.

Thursday, June 12, 2014

Gallstone pancreatitis

A review on this topic recently appeared in NEJM's Clinical Therapeutics series. Key points below.


ERCP indications

Urgent intervention (within 24 hours) is favored in the presence of cholangitis or early intervention (within 72 hours) if suspicion of common duct obstruction exists (e.g. persistent elevation or worsening of LFTs) without cholangitis. The authors cite relevant guidelines and note that increasingly (and since much of the guideline informing research was done) MRCP and EUS have been used to help inform more precise use of ERCP.


Pathophysiology

The pathophysiology is not completely understood, but septal compression by a distended common bile duct or pancreatic duct obstruction and/or bile reflux due to obstruction of a common channel are suspected mechanisms. An unusually long common channel seen in some patients may explain severity of disease in a minority of patients with gallstone pancreatitis. All that being said it is well known, note the authors, that severe pancreatitis can occur with only microlithiasis.


Practical aspects of ERCP

In the presence of obstruction vitamin K absorption may be impaired putting the patient at risk for impaired coagulation, hence the importance of checking an INR, which should preferably be below 1.5 prior to ERCP. In addition the authors recommend that the platelet count exceed 75K. They recommend antibiotics (a quinolone or cephalosporin) pre-procedure.


Cholecystectomy timing

If a sphincterotomy was done the patient is not likely to have recurrent pancreatitis but remains at high short term risk for other biliary events. Thus the authors recommend, if the patient can be stabilized, cholecystectomy that same admission.


Sunday, February 23, 2014

Update on acute liver failure

Here is a recent NEJM review.

There is a paucity of high level evidence to guide clinicians due to the rarity of the condition. However advances in critical care and transplantation have improved the outlook. The authors' recommendations are based largely on expert opinion and lower level evidence.


Definition

The designation acute liver failure (ALF) has largely replaced the old phrase fulminant hepatic failure. The general definition remains the same:

..defined as “a severe liver injury, potentially reversible in nature and with onset of hepatic encephalopathy within 8 weeks of the first symptoms in the absence of pre-existing liver disease..

Subcategories have been proposed, listed in the article, based on time from symptom onset to fully developed ALF. These time intervals provide clues as to etiology.


Etiology

Viral---mainly hep A and E. In addition hep B can be a sleeping giant awakened by immunosuppressive drugs.

Drugs---account for about half of cases in the U.S. Acetaminophen is the most common of these and indeed the most common cause of ALF overall in the U.S. For acetaminophen it's dose related toxicity (subacute worse than a single overdose) but for the other drugs it's idiosyncratic (rare).

Other---ischemic, Budd-Chiari, pregnancy related, miscellaneous, unknown.


Management aspects

Acetylcysteine may be helpful even in patients with non-acetaminophen induced ALF.

Avoidance of hypoglycemia.

Avoidance of hyponatremia (the article recommends maintaining Na on the high side and specifies an optimal range).

Aggressive indications for intubation and mechanical ventilation in patients with encephalopathy (the article specifies an optimal PCO2 range). This is mainly for neuro and airway management though aspiration and ARDS are known complications of ALF.

Preemptive antibiotics (the patients are at high infection risk, and manifestations of ALF often mimic, mask or overlap those of sepsis).



A different profile of encephalopathy compared to that of end stage chronic liver disease

---in which cerebral edema dominates the picture to a greater extent. This is due in large part to the rapidity of ammonia rise in ALF as compared to end stage chronic liver disease. This outpaces the brain's ability to marshal its defenses against swelling.



Dialysis for the liver???

For now extracorporeal treatment modalities are restricted to the setting of clinical trials.


Saturday, November 30, 2013

Gastric antral vascular ectasia (GAVE)

Here is a case report and mini-review.

Disease associations include cirrhosis and rheumatic diseases particularly systemic sclerosis. The terminology surrounding GAVE tends to be confusing. Watermelon stomach is a subtype of GAVE associated more with the rheumatic diseases. Portal hypertensive gastropathy, with which GAVE may be confused, is a separate entity.

Tuesday, October 08, 2013

Management of acute pancreatitis: can we be evidence based?

Evolving concepts and controversies are addressed in a recent review published in the Cleveland Clinic Journal of Medicine. The article is available as free full text. A few take home points will be mentioned here.

The optimal timing of CT scanning is based on the fact that the yield for detecting necrosis is relatively poor until 72 hours or so after presentation. Earlier scanning may be indicated in certain clinical circumstances suggestive of complications. Scanning at the time of presentation is justified if the diagnosis is unclear. That is to say that CT scanning provides just one of the three diagnostic criteria, the other two being clinical and laboratory. If those two are present CT is not necessary to make the diagnosis.

There has been a gradual shift in thinking about severity assessment. While prognostic assessment may be helpful in anticipating complications, advising patients and assembling resources it may not be as useful in an algorithmic approach to management as once thought. For example, a clinical determination of severe pancreatitis defines the patient as having pancreatic necrosis. In the traditional view that would be an indication for antibiotic therapy. But that thinking is not supported by evidence and no longer holds sway. In addition, the role of severity assessment as a target for fluid resuscitation is unclear. Traditional thinking held that assessment of pancreatitis as severe targeted patients for more aggressive initial fluid administration. A study form 2011 by Warndorf and colleagues, however, found the opposite: it was the patients with milder (so called “interstitial”) pancreatitis who benefited most, suggesting that the window of opportunity is lost once pancreatitis progresses to severe.

There are many clinical tools available for severity assessment. Traditional tools (e.g. Ranson) are falling out of favor because they require observation over time and cannot classify patients within the first 24 hours. Some more recently validated methods, particularly the SIRS determination, are simpler to use and enable severity assessment on the front end.

Current concepts in fluid resuscitation have become more nuanced. The traditional view of “more is better” was based mainly on theory, animal data and low level human studies. Despite those limitations it held sway until challenged a couple of years ago by a study I cited here. According to that study fluids in excess of 4.1L in the first 24 hours were associated with harm. The thinking is shifting from “the more the better” to “shoot for the optimum.” Under resuscitation may lead to pancreatic ischemia at the microcirculatory level triggering necrosis, mediator release, SIRS, vascular collapse and distant organ failure. Too much fluid on the other hand may lead to organ congestion and compartment syndrome.

In addition, fluid resuscitation should be front loaded. The Warndorf paper reported that patients given greater than one third the 72 hour total volume in the first 24 hours had better outcomes. Of note, that group also had lower total 72 hour volumes.

As to the actual amount to give, the CCJM review says:

Optimum resuscitation is controlled fluid expansion averaging 5 to 10 mL/kg per hour, with 2,500 to 4,000 mL given in the first 24 hours.

The way to accomplish this in an average sized individual is to front load in the first several hours. Such a protocol was described in a 2011 paper by Wu and colleagues. It is based on an aggressive initial bolus followed by high volume maintenance fluid rates for the first few hours but then calls for a sharp reduction in IV rate if the BUN comes down a bit at either of two lab checkpoints starting around 8 hours following presentation. Patients treated according to that protocol received less total fluid than those who were not and the total amount received came fairly close to the upper range recommended in the CCJM review. Outcomes were not improved with use of the protocol but the patient numbers were small. What was found was that patients treated with lactated Ringer's did better than those treated with saline whether on or off protocol. Again the numbers were small and the outcomes were soft: SIRS and CRP.

Though based only on physiologic rationale (lower microcirculatory pH in the pancreas is believed to activate enzymes and promote inflammation) and the one small study with soft endpoints the CCJM review recommends LR over saline.

Additional discussions in the review focus on nutrition (enteral is better than parenteral, NG is as good as jejunal, and enteral nutrition reduces infection), compartment syndrome (an emerging concern in pancreatitis) and the management of walled off necrosis and fluid collections.


Wednesday, September 18, 2013

When and if to restart warfarin after a GI bleed

From a study in JAMA Internal Medicine:

Background Patients who not only survive a warfarin-associated gastrointestinal tract bleeding (GIB) event but also have an ongoing risk for thromboembolism present 2 clinical dilemmas: whether and when to resume anticoagulation. The objective of this study was to determine the incidence of thrombosis, recurrent GIB, and death, as well as the time to resumption of anticoagulant therapy, during the 90 days following a GIB event.
Methods In this retrospective, cohort study using administrative and clinical databases, patients experiencing GIB during warfarin therapy were categorized according to whether they resumed warfarin therapy after GIB and followed up for 90 days...
Results..Warfarin therapy resumption after the index GIB was associated with a lower adjusted risk for thrombosis (hazard ratio [HR], 0.05; 95% CI, 0.01-0.58) and death (HR, 0.31; 95% CI, 0.15-0.62), without significantly increasing the risk for recurrent GIB (HR, 1.32; 95% CI, 0.50-3.57).
Conclusions The decision to not resume warfarin therapy in the 90 days following a GIB event is associated with increased risk for thrombosis and death.

The median time to resumption of warfarin was 4 days.

Friday, August 23, 2013

Mesenteric vein thrombosis

A free full text review is available from Mayo Clinic Proceedings.

Just a few points of interest:

Think of it when the patient's pain “seems real” and is out of proportion to physical findings.

Pain reaches maximum intensity relatively slowly whereas in acute mesenteric arterial occlusion maximum intensity occurs within minutes or even seconds.

Risk factors for arterial occlusion are cardiovascular---atrial fibrillation and atherosclerosis, whereas for MVT a structural or inflammatory abdominal process is often the underlying cause. Absent that, and in many cases, MVT is a disease of thrombophilia, We are taught to think thrombophilia when clots occur in unusual places. In MVT myeloproliferative disorders, with JAK2 mutation as a marker, stand out.

More about the JAK2 mutation can be found here.

Early anticoagulation improves outcomes. The degree of GI bleeding typically associated with MVT is seldom a contraindication.

Indications for surgical intervention are discussed.

Sunday, June 23, 2013

More evidence of harm related to proton pump inhibitors

This study found a 1 year increase in mortality in discharged elders, attributable mainly to high dose PPI use. PPIs are great drugs but they must be used discriminately. Overuse may be driven by the belief that these drugs are benign, consumer demand and poorly conceived care bundles resulting in inappropriate prescribing for “GI prophylaxis.” The mechanisms of harm are gradually being discovered. See here.  

Tuesday, June 04, 2013

Kayexalate and GI injury

According to a recent systematic review:

Results
Thirty reports describing 58 cases (41 preparations containing sorbitol and 17 preparations without sorbitol) of adverse events were identified. The colon was the most common site of injury (n=44; 76%), and transmural necrosis (n=36; 62%) was the most common histopathologic lesion reported. Mortality was reported in 33% of these cases due to gastrointestinal injury.
Conclusions
Sodium polystyrene sulfonate use, both with and without sorbitol, may be associated with fatal gastrointestinal injury. Physicians must be cognizant of the risk of these adverse events when prescribing this therapy for the management of hyperkalemia.

Sunday, May 12, 2013

Shigatoxin associated hemolytic uremic syndrome (D+ HUS)

As pointed out in this review, the classic form is a pediatric entity. When cases arise in adults they are less typical and the distinction from TTP is blurred. These cases are probably best termed TTP-HUS and should not argue against plasma exchange therapy.