Anorectal Disorders with Dr. Harmon

Rectal prolapse–typically painless presentation, requires reduction. If edematous, can use sugar to improve swelling prior to reduction. 

Anal fissures–painful rectal pain with small bright red blood with BMs. Symptomatic management. 

Hemorrhoids–external can be painful, internal can be painless. Symptomatic management.  Referral to CRS.

Abscesses–Beware the anorectal abscess. Requires DRE looking for any disproportionate tenderness or fluctuance.  If exam concerning for deeper abscess, obtain CT. Treatment of choice is I&D.  If simple perianal, can do bedside I&D.  Any other abscess should be operatively managed.    

Cirrhosis with Dr. Cook:

Path: Progresssive hepatic fibrosis and subsequent liver dysfunction 2/2 hep C and/or alcohol.

Clinical presentation: Encephalopathy, asterixis, hepatorenal syndrome, jaundice, ascites, varices (+/- bleed), +/- SBP, HCC

Work up: Basic labs, +/- sepsis evaluation, +/- CT head, ammonia level if no history 

Treatment: Airway management and BP management PRN, beta blockers, lactulose, +/- antibiotics if concern for SBP or GI bleed.

Gallbladder Pathology with Dr. Carter:

Most gallbladder pathology related to stone–cholesterol vs pigment–formation.  Ultrasound continues to be imaging of choice.

Cholelithiasis: relenting RUQ pain after eating without systemic signs.  Should see normal labs.   Typically managed outpatient.  Can refer for outpatient HIDA. 

Cholecystitis (cal vs acalc):  Elevated WBC, +/- elevated AST/ALT, less likely to have bili elevation, + Murphy’s Sign.  Requires surgical consult. 

Ascending Cholangitis: SICK. WBC, AST/ALT and bili elevation, alk phos elevation. Charcoat’s Triad and Reynold’s Pentad aren’t present in most patients.  Focus on resuscitation, antibiotics, and surgery consult. 

Start with ultrasound (evaluating for GB wall thickening, sonographic Murphy’s, pericholecystic fluid). If ultrasound is non-diagnostic, alternative imaging includes CT w contrast (Fast) or MRI (does not require contrast, safer in pregnancy)

Room 9 Follow-up with Dr. Davenport:

Elderly female presents to resus bay with concern for fall vs ?anaphylactic reaction, per EMS.  Intubated prior to arrival for airway protection.  Given epi, benadryl, steroids PTA.

Arrives HDS.

Initial physical exam with concern for profound facial edema and upper body subcutaneous emphysema. 

Access obtained, labs drawn, CXR not super helpful given subQ air and habitus.  FAST limited 2/2 subQ emphysema. 

BP progressively starts dropping and Radiology calls with concern for tension pneumothorax.  Chest tube subsequently placed with clinical improvement. Panscan obtained with multiple rib fractures, lung contusions, pneumomediastinum, chest tube in place with small residual pneumothorax. 

Family arrives and states patient had significant fall.  No history of anaphylaxis or angioedema. EMS concern for anaphylaxis was likely related to traumatic facial swelling.  This report led to some early diagnostic anchoring, which could have caused a harm event.

Patient was admitted to trauma service, had improvement over hospital course, eventually discharged to SAR.

Learning Points:

* Epi elevates BP, which can make a hypotensive patient look falsely HDS.

* Resus bay CXRs can be difficult to read in resus bay 2/2 body habitus, as well as small screen and bright lights.

* Pneumomediastinum: typically treated with symptomatic support and observation unless injury to great vessels.

* Pulm contusions: hypoxia and hypercarbia–>respiratory acidosis.  High risk for developing ARDS. 

* Cognitive bias: beware anchoring and overconfidence.  These can be natural digressions into energy-sparing cognitive shortcuts in our high acuity in our work environment.  It is easy to develop cognitive biases.  Recognition, mindfulness, and discussion can help prevent cognitive bias.

IR PE Management with Dr. Glaenzer:

Tool for IR-directed treatment of major pulmonary embolism via aspiration of clot.  Presents an alternative to traditional EKOS (directed lytic therapy)

PE–>RV dilatation–>Increased RV wall tension–>Myocardial Tension and Inflammation–>Increased myocardial demand–>Decreased RV output–>Decreased LA preload–>Hypotension–>Death

Inari can be considered in patients with both intermediate and high mortality PE

Upper GI Bleed with Dr. Shah:

Causes:  PUD, H pylori, anticoagulation, hepatic pathology

Physical exam:   DRE, look for signs of cirrhosis (Ascites, jaundice, angioma, hepatosplenomegaly), abdominal scars? (consider aortic enteric fistula), cardiac murmurs? (consider anticoagulation status)

Workup:  CBC, CMP, PT/PTT/INR, type and cross, lactic, trop (in elderly), ammonia (if AMS)

Scoring systems:  Glasgow Blatchford Score (most useful in ED), Clinical Rockall SCore, AIMS65

MGMT:  Blood for Hbg<7.  Platelets for active bleeding and plt<50k.  PCC for INR>2 and life-threatening bleeds on warfarin.  TXA for severe upper GI bleed.  Pantoprazole 80mg IV bolus. Octreotide 25-50mcg IV bolus.  Antibiotics–typically Ceftriaxone 1g IV if concern for variceal bleed. Blakemore tube as last line for unstable patients. Endoscopy>IR>Surgery.