Necrotizing Fasciitis: Clinical Suspicion Is your Only Chance

Dr. Glenn Harris discussed a case of an elderly man with diabetes and end stage renal disease who presented with sepsis from a right groin skin infection draining pus.

We used this opportunity to review our Sepsis-3 guidelines and discuss some of the newer evidence around the way we treat our septic patients.

Sepsis-3 guidelines tell us that sepsis should be defined based on the following 3 criteria:

– known or suspected infection

– organ dysfunction

– life-threatening

There are various scores we can use to increase the accuracy of our clinical judgment in our determination of the life-threatening nature of a septic patient’s disease, or in other words, their risk of mortality. The SIRS criteria is the scoring system most of our residents were taught in medical school, but according to Sepsis-3, this score has fallen out of favor. It is thought to be too nonspecific. Regardless of the underlying pathology, too many patients present to the ED meeting SIRS criteria. Sepsis-3 encourages the use of the qSOFA score, with only three binary criteria of RR, SBP, and the presence of altered mental status. However, since the guidelines came out, multiple studies have cast doubt on the utility of the qSOFA score, criticizing it as too insensitive. A large study comparing it with SIRS and the NEWS (National Early Warning Signs) score concluded that it fared worse in predicting outcomes. The NEWS score actually fared the best and we may see this score pop up in future studies or guidelines.

Treatment of sepsis includes fluid administration (30cc/kg) within three hours, cultures before antibiotics, and antibiotics within 1 hour. Fluid choice has been a hotly debated topic in the past. The evidence seems to support the use of crystalloids, but our classic dilemma is whether to us NS or LR. Normal saline carries with it a risk of hyperchloremic nonanion gap metabolic acidosis as well as a chloride load which decreases renal blood flow. These concerns lead many clinicians to resuscitate their septic patients with Lactated Ringers, but some give up to 2L normal saline and then switch to LR.

Antibiotic choice in cellulitis is guided by which type of pathogen you are concerned for. Typically, your first branch point is whether you believe the cellulitis is purulent (fluctuant, aka has a potentially drainable pocket of pus) or nonpurulent.

Purulent cellulitis is most commonly caused by staph, with a                                          high prevalance of MRSA

Nonpurulent cellulitis is most commonly caused by strep

However, if you have any suspicion for a necrotizing infection, you should cover for a polymicrobial infection. The LRINEC scoring system has been used to help guide our clinical suspicion for necrotizing fasciitis, but lacks sensitivity and does not take into account the patient’s physical exam or vital signs. The score should not be used to rule out necrotizing fasciitis. Clinical findings that should push you to consult surgery as soon as possible out of concern for a necrotizing skin or soft tissue infection are rapid progression, septic shock, crepitus, and hemorrhaghic bullae. These patients also frequently have pain out of proportion to exam. Your index of clinical suspicion is your most useful tool and you should treat for necrotizing fasciitis regardless of a LRINEC score if you are concerned. 

Unstable Bradycardia with a side of Sgarbossa

Dr. Soumya Murag presented an exciting case of unstable bradycardia in a hyperkalemic patient who also met Sgarbossa’s criteria and turned out to have a concomitant inferior STEMI from 99% ostial stenosis of the RCA.

Here are some high-yield clinical pearls we discussed today:

  • First line treatment for unstable sinus bradycardia is atropine
    • Atropine will not work in Mobitz II 2nd degree heart block or complete heart block (atropine acts on increasing the frequency of firing at the SA node, but these P waves will not be conducted in these situations)
    • The vagus nerve is not always connected in transplanted hearts so atropine may be ineffective in heart transplant patients
  • U waves can be seen in sinus bradycardia without underlying electrolyte abnormalities
  • Acute myocardial ischemia should always be on your differential diagnosis in unstable bradycardia
  • A new LBBB in a patient with chest pain or any presentation concerning for acute coronary syndrome is not a STEMI equivalent, but should prompt you to apply the Sgarbossa Criteria
    • Sgarbossa criteria: 1mm or more ST elevation in any lead with an upward QRS complex (concordant ST elevations) gives 5 points, 1mm or more ST depression in leads V1-V3 gives 3 points, and ST elevations 5mm or more in any lead with a downward QRS complex (discordant ST elevations) gives 2 points
    • A score of 3 or more should prompt urgent cardiac cath
  • Hyperkalemia causes a specific pattern of EKG abnormalities as potassium levels increase, which goes as follows: peaked T waves –> wide, low amplitude P waves with prolonged PR interval –> widening of the QRS –> sine wave
  • Nitrates should be avoided in inferior STEMI patients because they are preload dependent and nitrates can precipitate hypotension
    • Morphine can act in a similar manner so should be used only with extreme caution in inferior STEMI patients


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