Bright Red Blood Per … ULCER!!

Dr. Sylvia Cardounell presented a case of H.pylori induced peptic ulcer disease with a few interesting twists.

One atypical feature of this patient’s case was that he presented with bright red bloody bowel movements initially despite having an upper GI bleed. Upper GI bleeds (upper meaning proximal to the ligament of Treitz or 4th portion of the duodenum) classically present with melena, but when brisk and accompanied by other systemic signs and symptoms such as presyncope, tachycardia, and hypotension, can manifest as hematochezia. The BUN:Cr ratio is sometimes used to aid in differentiating between upper and lower GI bleeding. Due to digestion of blood in the stomach, the BUN increases in upper GI bleed, however a significant portion of lower GI bleeds also have increased BUN due to hypovolemia-induced prerenal azotemia. Some authors suggest various ratios 36:1-100:1 as more specific for upper GI bleeds, but our take home message is that the higher the ratio, the more likely it is for your GI bleed to be upper.

The classic presentation of a patient with peptic ulcer disease is epigastric abdominal pain about 2 to 5 hours after a meal when acid is secreted in the absence of a food buffer. Pain may also manifest at night between 11pm and 2am when circadian stimulation of acid secretion is maximal. Other food-provoked symptoms may occur as well including pain worse with eating (due to visceral sensitization and gastroduodenal dysmotility), belching postprandially, early satiety, fatty food intolerance, nausea, and occasional vomiting. Alarm features for dyspepsia that should provoke further testing and looking for alternate diagnoses are unintentional weight loss, dysphagia, odynophagia, unexplained iron deficiency anemia, persistent vomiting, palpable mass or lymphadenopathy, and a family history of upper GI cancer. Our patient’s initial vital signs showed mild tachycardia and hypotension when laying supine, indicating a blood loss of about 40% of total blood volume. Tachycardia typically starts at <15% blood loss, orthostatic hypotension requires a blood loss of at least 15%, and supine hypotension indicates a minimum blood loss of 40%.

The following are good rules of thumb for initially stabilizing your patient bleeding from their upper GI tract:

  • Prioritize access: they should have at least 2 large bore (18 gauge or larger). You can look at the color of your IV catheter to ascertain the gauge. Green is 18g, grey is 16g, and orange is 14g. 14g are not usually used for IV access due to their large size. Smaller IVs are pink, blue, and yellow.
  • Monitor for airway protection, place patient NPO, type and cross, consent for blood transfusion
  • Resuscitate: 
    • Crystalloids should be started for resuscitation if blood products cannot be obtained initially. Be judicious due to the risk of volume overload with subsequent transfusions.
    • Blood products:
      • A transfusion goal of Hgb 7 is appropriate for most patients, but those with unstable coronary artery disease should aim for a hemoglobin of 9. Clinical judgement is necessary in these cases and those who are elderly or with many comorbidities may need a higher transfusion goal.
        • In patients with cirrhosis, overtransfusion has been shown to lead to worse outcomes, likely due to worsening of underlying portal hypertension
      • Transfuse platelets if platelet <50 
        • Platelet transfusion can also be considered in patients on chronic antiplatelet therapy. However, evidence is lacking and given the risks of transfusion, platelet transfusion should not be routine in these patients
      • Goal INR <2. If your patient requires significant PRBC transfusion, you may dilute the concentration of clotting factors in the serum, creating an iatrogenic coagulopathy. Therefore, for every 4u PRBCs transfused, you should give 1u FFP.
  •  Acid suppression: Increasing the gastric pH allows blood to form clots and hopefully stop active hemorrhage. Traditionally, PPI infusion was used for UGIB cases, but more recent evidence has shown no difference in outcomes when comparing continuous PPI infusion and PPI bolusing BID. In fact, there was a trend toward lower rates of rebleeding in the bolusing group. Because of this evidence, the decreased cost, less resource utilization, and increased patient comfort, intermittent bolusing of PPIs is recommended. A loading dose of 80mg IV should still be given before starting 40mg IV BID dosing. Protonix and Nexium are the only PPIs available IV, but there is increasing evidence that oral PPIs may be sufficient.
  • In cirrhotics: octreotide and antibiotics should be added
  • Consider prokinetic agents such as erythromycin or Reglan 30-90 minutes before EGD if your patient has severe bleeding or has recently eaten as these may help your gastroenterologist visualized the stomach

Once you diagnose peptic ulcer disease, your differential remains broad. 

Peptic ulcer disease accounts for >50% of upper GI bleeds. It has myriad causes and risk factors. H.pylori, NSAID-induced, steroid-induced, and stress ulcers are our most commonly considered components on the differential, but ulcers have been associated with other more rare disorders such as gastrinoma, IgG4 related infilrative gastropathy, polycythemia vera, and sarcoidosis. There is also an association with acetaminophen of 2-3g/day or higher, bisphosphonates, Sirolimus, and an increasing body of evidence indicating that SSRIs increase risk of PUD as well. Smoking also increases the risk of peptic ulcer disease through many mechanisms.

Our patient received testing for H.Pylori via stool antigen test, which returned positive. Another atypical aspect of his case was that he received biopsy of his gastric mucosa during his EGD as well, but this came back negative. Typically, biopsy has a sensitivity of 90-95%, but active GI bleeding, antibiotics, PPIs, and bismuth-containing compounds decrease the sensitivity of biopsy, stool antigen test, and urea breath testing. If biopsy is negative for H.Pylori and you are worried about the sensitivity of biopsy in your clinical case, doing noninvasive H.Pylori testing 2 weeks after cessation of PPIs and 4 weeks after cessation of bismuth compounds is indicated. If EGD is indicated for another reason, biopsy is always first line for H.Pylori diagnosis. If no EGD is indicated, stool antigen or urea breath test should be used. 

Serology is not used to diagnose H.pylori because it remains positive after H.pylori treatment or after exposure that is not causing clinical disease.

H.Pylori Treatment:

Triple therapy should be used unless there is significant local resistance to clarithromycin (15% or more) or the patient has risk of macrolide resistance (has received macrolides for any reason). 

Triple therapy: Clarithromycin, amoxicillin, and PPIx14d

Quadruple therapy: Tetracycline, Flagyl, PPI, and Bismuth Subsalicylate x14d

One month after treatment of H.pylori, you should confirm eradication with urea breath test or stool antigen.

Yep..It’s AlcHep

Today we reviewed a case of a  middle aged gentleman with a long history of alcoholism who presented with diffuse abdominal pain and rectal bleeding and was found to have a direct bilirubin of nearly 30. We first went through the differential for direct hyperbilirubinemia, which can be placed in two broad categories, intrahepatic cholestasis & obstruction.

We reviewed the clinical manifestations of alcoholic hepatitis and were reminded that it is typically a patient with long-standing alcoholism who presents with jaundice, abdominal pain, direct hyperbilirubinemia, an AST:ALT typically ~300 or less in a 2:1 pattern, low albumin and sometimes fever/leukocytosis and no infectious etiology.

The diagnosis is a clinical one, and remember..obstruction must be considered. Infection is commonly present initially but can also develop later and one must also be hypervigilant about infection. We discussed the discriminant function score, which estimates the severity of alcoholic hepatitis once the diagnosis is made – a score of >32 predicts a high risk of mortality and steroid therapy may be useful. We reviewed the data briefly and made a case that it is uncertain whether it is useful, but it is certainly harmful in cases in which steroids are contraindicated, such as infectionactive GIB, uncontrolled hyperglycemia, acute pancreatitis and psychosis.

If you and your team decide to use steroids, check a Lille Score at 7 days to determine if steroids are helping, and if you complete a 28 day course, make sure to taper the steroids afterwards.

As our GI fellow stated, what clearly shows a mortality benefit is alcohol cessation…use their admission as an opportunity to counsel them! The remainder of care is supportive, and should include attention to volume status, electrolyte repletion (remember K, Mg, Phos), nutrition (enteral preferred), and monitoring for the usual complications of cirrhosis. Lastly, nonselective beta blockers should be temporarily held in patients with severe AH until it resolves as it increases the risk of acute kidney injury.


We went through a case of an elderly gentleman who presented with productive cough, shortness of breath, leukocytosis, and a large left pleural effusion.

In the evaluation of a pleural effusion in the setting of a suspected pneumonia, pleural fluid sampling is imperative. Parapneumonic effusion is an umbrella term for any type of pleural effusion in the setting of an adjacent pneumonia and can be divided into uncomplicated/simple and complicated effusions.

Uncomplicated effusions are usually small (i.e. costophrenic angle blunting, <10mm on lateral decubitus radiograph, or estimated volume <100mL). If they are sampled, they do not contain evidence of infection (negative gram stain/culture, normal glucose, and pH >7.2). These do not require treatment separate from treatment of the underlying pneumonia. However, they can become infected and if clinical improvement is not observed in 2-4 days, repeat imaging should be performed to check if the effusion has increased in size.

Complicated effusions are any effusions that are infected, including empyemas (pus within the pleural cavity). Typical features of a complicated pleural effusion include loculations, large size (>0.5 hemithorax), thickened pleura, split pleura sign on CT, and sepsis. These effusions have exudative features upon pleural fluid sampling, high WBC count (usually neutrophilic if bacterial), pH <7.2, and glucose <60. They should be promptly treated with antibiotics with coverage of anaerobes as well as Strep species, usually a 3rd generation cephalosporin with Flagyl OR Augmentin. Drainage should also be attempted as soon as possible with chest tube placement.

It was previously thought that large bore chest tubes were the treatment of choice, but according to the MIST1 trial, smaller catheters had much improved pain scores without worse outcomes, although they did have more frequent blockages, which can be alleviated by sterile saline flushes Q6h.

LV Pseudoaneurysm After MI – Bad News Bears

Today we learned about a very uncommon mechanical complication after MI to a patient with subacute pleuritic pain and dyspnea and found to have an inferior MI on EKG. A TTE was concerning for an aneurysm and a left heart cath revealed a large aneurysm on the LV-gram.

We reviewed the common complications after MI (arrhythmia and heart failure) as well as the three major mechanical complications after MI (all of which are exceptionally rare). They all can occur 0-14 days after MI. We did not discuss, Dressler syndrome, which can occur a few weeks to even a year after MI and is fever

Ventricular Septal Defect

  • presents as a holosytolic murmur along left sternal border, often with a thrill
  • EKG findings are non-specific
  • TTE reveals a high velocity L->R shunt

Papillary Muscle Rupture

  • presents as a holosytolic murmur along left sternal border and apex;
  • EKG findings are usually associated with inferior/inferior-posterior wall MI
  • TTE reveals a flail leaflet with severe mitral regurgitation

LV Free Wall Rupture

  • presents as hypotension, JVD, distant heart sounds
  • EKG findings are non-specific
  • TTE reveals a pericardial effusion with tamponade, discrete wall motion abnormality; a defect in the myocardium can sometimes be seen
  • if the rupture is incomplete and contained within the pericardium, this can cause a pseudoaneurysm and is highly prone to rupture. surgical intervention is the treatment of choice


Central Adrenal Insufficiency

We presented a fascinating case of a middle aged woman who presented with fatigue, weakness, and a significant weight loss in the past year who was found to have hypotension refractory to a usual fluid challenge. Her AM cortisol was low and her post-stim cortisol remained <18, confirming the diagnosis of adrenal insufficiency. Her ACTH was inappropriately on the low end of normal, consistent with a central AI (secondary or tertiary). Here are the highlights:

Clinical Manifestations in Primary AI only:

  • Generalized hyperpigmentation of the skin and mucus membranes (exclusively in chronic primary adrenal insufficiency)
  • Hyponatremia/hyperkalemia and hypoglycemia generally occurs in primary AI only

Diagnosing Adrenal Insufficiency

  • An AM cortisol < 3 is sufficient, but a ACTH stimulation test is preferred
  • Check the ACTH level prior to the test!
  • After giving the standard-high dose of 250mcg of synthetic ACTH, a cortisol is checked 1 hour later and if <18, confirms the diagnosis of adrenal insufficiency
  • If the patient has AI, then look at the ACTH (which will take some time to result anyway)
  • If normal (inappropriately so) or low, this is ACTH dependent AI, also known as central AI (in secondary the problem is the pituitary and in tertiary, the problem is in the hypothalamus)
  • If high, then this is ACTH-independent AI, also known as primary AI (AKA the problem is with the adrenal gland)

Causes of Primary AI and Secondary AI

  • The causes for both are lengthy, but remember the most common etiology for each!
  • The most common cause of primary AI in the developed world is autoimmune adrenalitis
  • The most common cause of central AI is discontinuation of glucocorticoids

Cryptococcal Meningitis and a New Diagnosis of AIDS

Today, we presented an interesting case of a young man with no past medical history who presented with two weeks of progressive headache and fever, now with nausea, vomiting, and an episode of transient blurred vision. CSF revealed an elevated white blood cell count with lymphocytic predominance, low glucose, and elevated protein. Serum and CSF CrAg subsequently came back positive and fungal blood cultures showed Cryptococcus Neoformans.

Illness script for Crypto Meningitis:
Epi: AIDS patients with CD4<100
Symptoms: Indolent onset 1-2 weeks for fever, malaise, and headache. Can develop meningeal signs, altered level of consciousness, and focal neuro deficits. Disseminated disease can include pulmonary symptoms and skin findings resembling molluscum contagiosum.
Diagnosis: Serum and CSF CrAg with 93-100% sensitivity and 93-98% specificity. Crypto can be isolated on India Ink stain of CSF 60-80% patients.
Treatment: Induction with 2 weeks of IV amphotericin B and PO flucytosine, consolidation for 8 weeks with high dose fluconazole, and maintenance for one year with low-dose fluconazole. Serial LPs for ICP control. Start ART 2-10 weeks after starting antifungal treatment (delayed due to risk of IRIS).


The Ophthalmologist’s Pulse Examination That Identified a Vasculitis!

Today we discussed an impressive diagnostic mystery of a young woman with chronic neck pain and paresthesias who was later found to have a diminished ipsilateral pulse and a SBP of > 60 points in the affected arm compared to the contralateral arm!

The case highlighted a few, highly important points – first – that the pulse examination is paramount in the patient with paresthesias of an extremity.

A broad differential for diminished/absent radial pulse includes atherosclerosis (i.e PAD), embolism, vasculitis (i.e GCA and TA, less commonly Beurger Disease), anatomic (dissection, thoracic outlet obstruction, thrombosed aneurysm) and iatrogenic (i.e post ABG, vasopressors). When you notice unequal pulses in a patient with symptoms relating to that extremity, you must treat this as an emergency!

We then reviewed the distinguishing characteristics of GCA and TA


The key takeaway to remember is that TA is a chronic disease, filled with relapses and therefore these patients must be diligent about their immunosuppression, which in some cases may be lifelong at very low doses.

For those of you who are still here, a historical treat is your reward. At the 12th Annual Meeting of the Japan Ophthalmology Society held in 1908 in Fukuoka, the young Dr. Mikito Takayasu presented a curious case of vascular malformations of the eye. Two of his colleagues, Drs. Katsutomo Onishi and Tsurukichi Kagoshima also presented similar findings, but noted absence of pulses as well. The findings are impressive, but even more impressive is a subspecialist examining the entire body in a patient they were concerned about, a truly admirable – but increasingly uncommon – practice!