Grand Rounds Recap - 8/27/2014

Photo Credit: Jason Wilson.  Source: http://www.flickr.com/photos/hive/2962297451/in/photostream/ Accessed 8/29/14

Photo Credit: Jason Wilson.  Source: http://www.flickr.com/photos/hive/2962297451/in/photostream/ Accessed 8/29/14

Botulism

  • Caused by neurotoxin produced by Clostridium bacteria
  • 3 types: food borne, infant and wound
  • Pathophysiology: toxin binds to cholinergic cells and prevents release of acetylcholine
  • Symptoms
    • Foodborne illness starts with N, V and D. Similar to gastroenteritis
    • Neurologic symptoms: fixed and dilated pupils, ophthalmoplegia, ptosis,       bilateral and symmetric facial paralysis that progresses to limbs and trunk, respiratory muscle weakness
    • Patients frequently complain of dysphagia, dry mouth and other anticholinegric symptoms
  • Infant botulism = floppy baby who is weak, has a weak cry, constipation and does not feed well
  • Botulism is easily confused with myasthenia gravis and Miller Fischer variant of Guillan Barre
  • Diagnosis: clinical in the ED
    • Tensilon test is normal but is helpful in diagnosing myasthenia
    • EMG may be abnormal
  • Management
    • Respiratory support: monitor NIF and FVC and intubate if NIF less than -30 or FVC less than 30% predicted
    • Antitoxin is available from health department. It is made out of horse serum, so there is a high incidence of anaphylaxis
    • If you suspect botulism, alert CDC early as these cases are reportable and antitoxin takes a while to arrive
    • Antitoxin should be given ASAP in order to prevent neurologic deterioration

Radiographic Imaging of pregnant patients

  • Fetal exposure to less than 5 rad is not teratogenic
  • Most of the imaging studies that we order, if performed once during pregnancy, are not harmful
  • MRI is likely safe, but avoid gadolinium (category C)
  • If you need to rule out PE, get a CTPA as it is less damaging to the fetus
  • If you suspect appendicitis in a pregnant patient, start with an US and an early OB/surgery consult

Hyponatremia

Classification: tonicity (isotonic vs hypotonic vs hypertonic)

  • Hypotonic can further be classified based on volume status
    • Hypovolemic hypotonic hypoNa = loss of Na exceeds loss of water
      • Urine Na < 20: GI loss, sweating or third spacing
      • Urine Na > 20: renal loss
    • Euvolemic hypotonic hypoNa = excess of free water
      • Urine Na is always > 20
      • Urine osmolality < 100: psychogenic polydipsia
      • Urine osmolality > 100: SIADH, hypothyroidism, adrenal insufficiency
    • Hypervolemic hypotonic hypoNa = disorder of water excretion
      • Urine Na < 20: CHF, cirrhosis
      • Urine Na > 20: intrinsic renal disorder
  • Isotonic hypoNa = pseudohyponatremia.
    • Multiple myeloma or hyperlipidemia
    • True Na is normal
  • Hypertonic hypoNa = hyperglycemia
    • Will correct once hyperglycemia is resolved

SIADH: syndrome of inappropriate ADH secretion

  • Criteria for diagnosis (need to have all 6) 
  1. Hypotonic hyponatremia
  2. Euvolemia
  3. Urine Na > 20
  4. High urine osmolality
  5. Normal renal, liver, thyroid, adrenal, heart function
  6. Corrects with water restriction
  • Work up in the ED: the most important thing you can do is to get UA, urine electrolyte, urine and serum osmolality
  • Urine studies are less valid after fluid resuscitation, so get them before giving fluids if possible

Treatment

  • Hypovolemic hypoNa = give volume
  • Euvolemic = fluid restrict
  • Hypervolemic = fluid restrict + diuretic
  • Acute hyponatremia
    • Hypertonic at 2-3 ml/kg if seizing or in a coma
    • 4-6 mmol/L increase should be enough to reverse symptoms
    • Goal is to reverse symptoms, not restore normonatremia
  • Chronic hyponatremia: correct slowly (6-8 mmol/L/d) in order to avoid osmotic demyelination

Hyponatremia is associated with significantly worse mortality compared to normonatremic patients

Necrotizing Fasciitis

  • Relatively rare with high mortality (25-35%)
  • Most sensitive symptoms are pain out of proportion to exam and tachycardia out of proportion to fever
  • Skin findings and crepitus are late findings
  • Clinical diagnosis in the ED
  • Can get an US or MRI/CT to help diagnose
  • Management
    • Prompt surgical consultation
    • Aggressive volume resuscitation
    • Triple antibiotic therapy: vancomycin, zosyn, clindamycin
    • Hyperbaric oxygen has not been proven to improve outcomes

Pericarditis

  • Pericardial rub heard in 85% of patients. Listen at the apex while patient is leaning forward
  • ECG findings: diffuse ST segment elevations, diffuse PR depressions, PR elevation in aVR, small volage QRS
  • Treatment: NSAIDS + colchicine
    • Colchicine decreases incidence of recurrent disease

Medication Comparisons with Dr. Bryant.

Acetaminophen vs Ibuprofen

  • There are multiple adult and pediatric studies that have shown that ibuprofen is better at fever and pain reduction. 
  • What about combination tylenol/ibuprofen therapy? This is effective, however there are more instances of inadvertent drug overdose. 
  • Ibuprofen is safe to use in children starting at 6 months of age. 
  • What about using ibuprofen in orthopedic injuries? There is no evidence to show that it is detrimental to bone healing.

PPI vs H2 blocker in GERD

  • PPI is a pro-drug and takes 2-3 days before it is effective. 
  • H2 blocker is a competitive inhibior and works within 1 hour
  • It appears that long term, PPI is better at healing peptic ulcers as well as at improving symptoms
  • What about a patient who comes in to the ED with acute pain secondary to GERD? Give them pepcid and a GI cocktail in the ED and send them home on a short course (a few days) of pepcid and a prescription for a PPI. 

Meclizine vs benzodiazepine for vertigo

  • There are no big studies, only consensus guidelines
  • Meclizine seems to work better
  • BPPV: there is no role for medication/ Do the Epley maneuver. 
  • Acute peripheral vertigo: can try meclizine however do not give for more than 48 hours as it delays central compensation

Beta  blocker vs Ca channel blocker for atrial fibrillation?

  • In acute atrial fibrillation, Ca channel blockers are more effective at rate control

Abdominal X-ray with Dr. Teuber

Approach to reading an AXR:

  1. Initial impression: is this an adequate film?
  2. Technique: what is the patient position
  3. Bones
  4. Solid organs: should be able to see liver, bladder, kidneys, ?spleen and psoas muscles bilaterally
  5. Hollow organs
  6. Calcifications
  • Chest x-ray may be better at evaluating for free air under diaphragm
  • SBO vs Ileus may be a difficult diagnosis to make based on AXR alone
  • Rigler sign: air on both sides of the intestine, concerning for perforation
  • Necrotizing enterocolitis: pneumatosis intestinalis is a pathognomonic finding
    • May also see dilated bowel loops
    • Treat patients with NG tube, NPO, IV fluids, antibiotics and prompt surgical consult
  • Intussusception
    • Crescent sign: longitudinal appearance of intussuscepted bowel
    • Target sign: transverse appearance of intussuscepted bowl
    • More common in males, age 3-12 months
    • Classic presentation: intermittent crampy pain, vomiting and bloody stools
  • X-ray rules to live by:
    • Symmetry: R and L sides should look the same
    • There are no straight lines in human body, so you should not see any straight lines on an x-ray
    • Most important film is an old film

Evidence Based Medicine on Hemoptysis with Drs. Winders and Boyer

Lungs have dual blood supply from bronchial arteries and pulmonary veins

Most bleeding comes from bronchial arteries

Hemoptysis = bleeding from below the vocal cords

The first question to ask yourself is if this is truly hemoptysis, as up to 10% of patients will either have a GI bleed, an upper airway or oropharyngeal bleed

  • Hemoptysis = alkaline
  • Hematemesis = acidic

Etiology: bronchitis, neoplasm, bronchiectasis, TB, pneumonia, diffuse alveolar hemorrhage

  • Bronchitis is the most common cause in patients with normal CXR

Massive hemoptysis is defined as hemoptysis that causes impaired gas exchange and/or hemodynamic compromise

  • Work up: CBC, renal, PT/PTT, TEG, EKG, CXR

Lung cancer frequently presents as hemoptysis while there is a 10-24% false negative rate on CXR

Who needs additional work up if their CXR is negative? Anybody who has 2 or more risk factors:

  • Age > 40
  • > 30 pack year history of smoking
  • > 1 week of symptoms OR > 30 mL of hemoptysis in 24 hours

Preferred imaging approach: CT without contrast followed by bronchoscopy

Management in the ED

Right Mainstem Intubation

Right Mainstem Intubation

  • ABCs. Intubate with a large ET tube in order to facilitate bronchoscopy
    • Can consider main stem intubation (right or left depending on where the blood is coming from).
    • No role for a double lumen ET tube - >50% failure rate even when placed by those familiar with the device.  And, it is not possible to perform a bronchoscopy through a double lumen ET tube
  • Put the patient with their bad lung down in order to prevent blood from going into the good lung
  • Consider giving TXA if this is a massive hemoptysis situation
  • Consults for massive hemoptysis
    • Interventional pulmonology fellow and attending
    • MICU fellow, usually same as interventional pulmonology fellow
    • CT surgery
    • Interventional Radiology
  • If you have a patient with massive hemoptysis, get a CT angio of their chest. This helps with plans for embolization. If the patient is too unstable for a CT, can do a flex bronch
  • BAE: bronchial arterial embolization
    • Coiling of the bronchial artery that is the culprit of bleeding
    • Achieves immediate bleeding control in over 70% of patients
    • High rebleeding risk
  • Indications for surgery:
    • Failed BAW
    • Trauma
    • Aspergilloma

Case Follow Up with Dr. Grosso

pH Indicator Roll. Source: http://fi.wikipedia.org/wiki/PH-indikaattori#mediaviewer/Tiedosto:PH_indicator_paper_roll.jpg

pH Indicator Roll. Source: http://fi.wikipedia.org/wiki/PH-indikaattori#mediaviewer/Tiedosto:PH_indicator_paper_roll.jpg

This is a 19 mo male who is brought in by parents after apparent "aftershave" ingestion. He has not tolerated PO since ingestion. He is acting normal but drooling. On exam he is drooling excessively and has an edematous and erythematous soft palate and posterior oropharynx with erosions. He has a normal lung exam and normal CXR.

Aftershave should only cause intoxication as it is mainly alcohol.

This "aftershave" was from Cameroon and made by local "medicine man". pH testing showed very high pH

Alkali ingestions are very damaging if pH of ingested solution is > 11

  • Liquid ingestion causes distal esophageal injuries
  • Solid ingestion causes injuries of the mouth and proximal throat
  • Powder/granular ingestion causes upper airway injuries

Management: ABCs

  • Airway compromise is more common in acid ingestion
  • Lack of oral injury does not mean that they do not have more distal injury
  • Do not induce vomiting as this leads to double exposure and risk of aspiration
  • Do not dilute by pushing fluids as it can cause vomiting
  • Do not give H2 blockers

Indications for endoscopy: perform in 12-24 hours post ingestion if 2 or more of the following:

  • Vomiting
  • Drooling
  • Stridor
  • Dysphagia
  • Odynophagia
  • Abdominal pain

Case Follow Up with Dr. Nelson

"Chickenpox blister" by F malan - Own work. Licensed under Creative Commons Attribution-Share Alike 3.0 via Wikimedia Commons - http://commons.wikimedia.org/wiki/File:Chickenpox_blister.jpg#mediaviewer/File:Chickenpox_blister.jpg

"Chickenpox blister" by F malan - Own work. Licensed under Creative Commons Attribution-Share Alike 3.0 via Wikimedia Commons - http://commons.wikimedia.org/wiki/File:Chickenpox_blister.jpg#mediaviewer/File:Chickenpox_blister.jpg

The patient is a 24 yo male who comes in with a painful and pruritic rash. Started on neck and spread to the entire body. Vaccination status is unknown. On exam he has ulcerations of his buccal mucosa and a diffuse maculopapular rash with some vesicles. Na is 123. Platelets 127. CXR is normal. VZV studies positive and pt gets treated with IV acyclovir

VZV is transmitted via respiratory secretions. Virus is transmissible 24-48 hours prior to rash eruption.

  • Typical illness course is 5-7 days but it can develop into viremia with disseminated symptoms
  • Adults do worse than children

Clinical clues: lesions in various stages and lesions on the scalp

Testing

  • IgG and IgM are not sensitive or specific
  • PCR from unroofed vesicles is very sensitive and specific

Treatment:

  • Acyclovir vs valacyclovir vs famcyclovir
  • Immunosuppressed patients should get VZV immunoglobulin for post-exposure prophylaxis

Complications: secondary bacterial infection, hepatitis, pneumonia, encephalitis


Case Follow Up with Dr. Niziolek: Left Bundle Branch Block and ACS

2% of patients with ACS present with LBBB and these patients tend to do worse

Old guidelines called for cath lab activation for a new LBBB on EKG

2013 guidelines say that this "new" LBBB is actually rarely new so cath lab does not always need to be activated

  • If the patient has a new LBBB in content of AMI, they are having a large anterior or septal MI
  • Most cath lab cases that are activated for a new LBBB show nonobstructive or clean coronary arteries

Sgarbossa criteria: how to tell if the pt with LBBB has an acute MI

  • ST elevations > 1 mm concordant with QRS complex
  • ST depressions > 1 mm in V1, V2 or V3
  • ST elevation > 5 mm discordant with QRS complex

Sgarbossa criteria is very specific but not very sensitive (20%).