Digestive System
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ESGE recommends offering treatment to all the patients with CBD stones (symptomatic or not) who are fit enough to undergo procedure.
This is true that we should explain always the option of intervention, and we should at least talk about risks of complication from leaving untreated biliary stones (Roughly about 25%  - biliary colic, pancreatitis, cholangitis- vs 12% if we clear the bile stones) this is  based on this  Gallrisk sweddish cohort   where they followed 3969 patients with untreated CBD stones, during follow-up ranging from 0 to 4 years. 

In summary: Explain why there is an indication to treat, which risks ERCP associates, what the alternatives may be  (ie Cholecystectomy plus surgical bile duct exploration in the same setting when approppriate) and their own risks.  And last but not least, explain the alternative of not treating and only monitoring, and the risks of this approach as well.

The majority of pancreatic cancers are due to spontaneous mutations in a complex combination of usually several mutations ((KRAS) mutations are common in 90% of pancreatic cancers, but in combination with different other mutations, DNA damage and usually other risk factors.

There is however a very important percentage (5%-10%) of new PC which associate familial pancreatic cancer (Defined by two first-degree-relatives with pancreatic cancer), There are indeed genes involved such as BRCA2 gene  mutations  ( 3.5-fold increased risk of pancreatic cancer ).  Other inherited mutations in the STK11 gene cause the Peutz-Jeghers syndrome, and individuals with Peutz-Jeghers have a 130-fold increased risk of pancreatic cancer

To put in context,

One degree relative with PC  makes relative having an 80% increased risk of developing pancreatic adenocarcinoma (this is RR: 1.8)

individuals with 2 degree relatives with PC have a nine fold risk , and this rises to thirty-two times greater risk if three or more first degree relatives have been previously diagnosed

Based on this  article of the NEJM

Hb needs to be kept 7-8g/dl at least,  and a target of >9-10g/dl  if significant cardiovascular disease.  Andenaxet is recommended if life threatening or uncontrolled bleeding, like this case which is responding only partially to resucitation with fluids and continues to pass blood, so it could be prescribed.  If not available, 4-F PCC can be used instead.  Urgent sigmoidoscopy in general has no role and it would likely be useless without an adequate bowel preparation as we would expect to have very poor visibility due to stool and blood remains.

Unprepped colonoscopy or any form of sigmoidoscopy is NOT recommended in acute lower GI Bleeding unless very clear that the source is known to be anorectal or very distal colon (see American Guidelines) BSG guidelines also recommneds Colonoscopy as  inpatient with adequate bowel preparation, not urgently but  ideally after stabilising the patient.

If after resucitation and transfusion the patient remains unstable, then a joined plan with intensivist and surgical colleagues should be made (i.e, Interventional radiology, vs quick preparation with movicol, vs enema and salvage lower endoscopy, vs surgical approach)

Delirium tremens is a form of severe withdrawal syndrome in which, long term alcohol has chronically bound to GABA receptors and modified its expression( GABA is the inhibitory neurotransmitter which normally reduces neuronal excitability) . This leads to  GABA downregulation of α1- and α3-containing GABA-A receptors (Liang and Olsen, 2014). GABAA receptor downregulation may contribute to anxiety and shakes of withdrawal once alcohol is not present in the nervous system. Also, chronic hyperestimulation of the GABA system by alcohol leads to brain mechanism of up-regulation of the postsynaptic N-methyl-D-aspartate (NMDA) type of glutamate receptor, which mediates the postsynaptic excitatory effects of glutamate to counteract this inhibitory effect of GABA, and once alcohol is suppressed this excitatory system takes over causing autonomic hyperactivity, tachicardia, cardiovascular collapse, seizures or even comma and death.

Solid pseudopapillary neoplasm account for around 5% of pancreatic neoplasm. They are almost exclusively found in females (f:m ratio 10:1) and usually appear in their 20s.  CT and EUS can show well-encapsulated mass with varying solid and cystic components, caused by hemorrhagic degeneration. Peripheral calcification may occur.  They appearance can vary from solid to purely cystic- therefore even a small cystic lesion in a young female without previous pancreatitis episodes must make us consider this diagnosis

These lesion have a potential for malignant degeneration (Around 15%) therefore surgical removal is recommended . Cytology can show cluster  or sheets of papillary cells, PAS + and Vimentin.

• CLINICAL CASE AND Image: Dr Hajar Adil
• Source: Endosonography, 5th Edition by Shyam Varadarajulu, MD, Paul Fockens, MD, PhD and Robert H. Hawes, MD.
• Learning point brought by Dr Sarto Paquin

Whenever an HCC (Hepatocelullar carcinoma) is resected in an early starge, 5-year recurrence occurs in up to 60-70% of the cases,  either as a result of intrahepatic metastases (true recurrent disease) or de novo cancer in the remaining cirrhotic liver .  However, similar rates of reccurence occurs if we use ablation instead of surgical resection (  between 60% and 85% recurrence with ablation) via the same mechanisms (either incomplete tumor erradication, or new tumor formation)

5-year recurrence after liver transplant is way lower (8-20%) and of course varies depending on the tumoral burden --> potential microvascular invasion at the time of the transplant.

See BSG guidelines

In the guidelines they mention the increasing resistance of  Hpylori strains in the US to Clarithromycin (20-30%)  and Levofloxacin (approaching 40%) , therfore supporting antibiotics with much lower resistance rates (such as amoxicillin, tetracycline, and rifabutin that are all 5%)

That is why this guidelines say Clarithromycin- and levofloxacin-containing treatment regimens should be avoided in the absence of demonstrated macrolide and quinolone susceptibility, respectively.

Clarithromycin- and levofloxacincontaining treatment regimens remain an important option for selected patients, especially treatment-experienced patients with confirmed persistent H. pylori infection with strains that are known to be susceptible to these antibiotics

Vonoprazan is potassium-competitive acid blocker (PCAB) that inhibits the H⁺, K⁺-ATPase enzyme system in a potassium-competitive manner.    This is the same target as PPI but this class  of drugs  are acid-stable and thus do not require enteric coating or optimal dosing administration 30 minutes prior to meals , are more potent acid suppression, rapid onset of action, and long-lasting half-life.   Penicillin dual therapy was superior to lansoprazole-clarithromycin triple therapy among patients with clarithromycin-resistant H. pylori strains (70% vs 32%, P , 0.0001).

When treating with Vonoprazan + Amoxicillin, exceptionally we can add Clarithromycin as first line even in naive patients.

Should be endoscopic ablation (Radiofrequency or similar).  We cannot resect endoscopically a lesion that we cannot see.  Check the guidelines

Difficult question.  This response is based on Waterfall trial that compared moderate resucitation (1.5ml per Kg) vs aggressive (3ml per Kg) and showed no difference in worsening pancreatitis  but a tendency of fluid overload in the aggresive group (20.5% vs. 6.3%).

Ringer lactate or Hartmanns have been proved to have benefit ovver saline due to an anti-inflammatory effect which was attributed to the properties of lactate and to have a higher pH that can help counteract acidosis.

This indeed is a subject of debate. American guidelines still mentions that most patients with acute pancreatitis & hypovolaemia could have a deficit of 3-4 L to replace in 24h (Like it is our patient with vomiting and  mild hypotension and tachycardia) . If patient has no evidence of hypovolemia, an initial resuscitation rate of no more than 1.5 mL/kg of body weight per hour should be administered. However, in patients with hypovolemia, clinicians should administer a bolus of 10 mL/kg which in this case is 750ml per hour (1500ml in 2 hours)

So, the answer is  Goal-directed rehydration with Ringer’s lactate solution (or Hartmann’s).  In this case of Hypovolemia, our first step should be resucitate until volume is stable (normal BP, HR and clinical status) looking closely to avoid overfluid, and once patient is stable, keep her on 1.5ml per Kg per 24 h with clinical re-checking every few hours to ensure she is not hyper or overhydrated.