Intra-aortic balloon pump counterpulsation

• It is possible that at some point in your career you may need to place an intra-aortic balloon pump (IABP) to temporarily stabilize a patient wth cardiogenic shock
• Optimal performance of the IABP is dependent upon proper positioning in the thoracic aorta
• Traditional teaching has been to insert the IABP via the femoral artery and advance to the level of the aortic knob (via CXR)
• A recent study suggests that using the aortic knob to position the IABP may result in occlusion of the left subclavian artery in a substantial portion of patients (16% in the study)
• Placing the IABP 2 cm above the carina may be a more reliable landmark that using the aortic knob

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Suspected Acute Leukemia in the ED

 Key ED Interventions for patients with astronomically high WBC counts:

• Usually talking about WBC counts over 200,000 or so (can be lower in lymphocytic leukemia)
• Hydrate aggressively
• Avoid PRBC transfusions as blood products will increase the patient's cytocrit (combination of WBC, platelets, and RBC) and predispose to organ malperfusion. This may lead to WBC (or blast) sludging in the microcirculation and may result in CNS bleeds. 
• Obviously, call for help immediately! Get a hematologist on the line quickly
• Assume the patient already has Tumor Lysis Syndrome and administer Allopurinol in a dose of 300 mg orally.
• Obtain a uric acid level, and if high, give an intravenous infusion of Rasburicase-eliminates preformed uric acid released from leukemia cell lysis. Renal failure results from high uric acid levels. We have this medication at University.
• The treatment of choice is initiation of definitive chemotherapy....clearly not an option for us in the ED. You can also do leukapheresis (where you take out WBC)....also not an option unless you have a special catheter and a perfusionist/nurse. BUT, you can take off a unit or two of blood (phlebotomy). This will potentially lower the patient's cytocrit. 

Infections occur in up to 8-9% of ICD sites. Early infections usually occur within the first 2 months of placement and are associated with typical findings...redness, tenderness, systemic symptoms, etc. Late infections, however, are often associated with nothing more than JUST pain.

Lack of diagnosis of ICD site infections is associated with a mortality > 50%.

When infected, the entire ICD (including wires) must be replaced.

The most commor organisms associated with ICD infections are Staph and Strep. Treat them all with vancomycin.

Turf Toe:

Most commonly seen in atheletes who compete on artificial turf.  Presents as pain over the 1st Metatarsalphalangeal  (MTP) joint. 

• Due to a tear of the Metatarsal phalangeal Joint Capsule
• Results in subluxation or dislocation of the MTP joint
• Occurs due to:
  • Hyperextension (most common)
  • Hyperflexion
  • Valgus stress
• Treatment:
  • NSAIDS
  • Rest
  • Orthosis -- Prevents dorsiflexion during athletic activities

Pediatric Accidental Non-Fatal Injuries

• Every 1.5 minutes an infant 0-12 months is evaluated in an ED for nonfatal unintentional injuries
• “Falls” are the leading cause of injuries in all age groups (0-12mos)
  • account for ~51% of ED visits in this group
  • Only 2.6% required hospitalization
• “Drowning” was the least common cause of ED visit (0.2%), but
  • accounts for ~47% of the hospitalizations in this group
• “Poisoning” had a bimodal distribution between 0-12 months
  • more commonly seen in 1-3 mos (likely due to parents or siblings) and
  • also in 7mos to 12 mos (likely because of the kids – age when they put things in mouth)

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 How to recognize a truly toxic mushroom ingestion (remember one mushroom can be lethal!):

1) Onset of GI symptoms within 3 hours from time of ingestion: USUALLY NONTOXIC

- Control nausea and  vomiting

- Look for toxidrome: hallucinations, muscarinic symptoms, lethargy

2) Onset of GI symptoms greater than 5 hrs is associated with more toxic mushrooms

- High degree of suspicion for a cyclopeptide mushroom (Amanita phylloides)

- Follow liver enzymes and consier referral to liver transplant center

Bedside Glucometry in the Critically Ill

• Hyperglycemia is common in critically ill patients
• Depending on the underlying condition (e.g. DKA), you may be instituting an insulin drip and following frequent fingersticks in the ED
• A recent study indicates that bedside glucose values may not accurately reflect serum values in approximately 15% of critically ill patients
• This is more likely to occur in patients with poor peripheral perfusion
• Take Home Point: Interpret bedside glucose readings with caution especially in hypotensive critically ill patients

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Hemorrhage Volume on Head CT 

Ever wanted to speak the same language as our neurosurgical colleagues? Ever wonder what they are doing, calculating, or thinking about as they look at the head CT of the large intracranial hemorrhage? 

Most of the neurosurgeons want to know basic information about patients with head bleeds. One thing they always calculate is the hemorrhage volume...i.e. how many mLs of blood are in the bleed? This can be easily done in the ED by using the following formula: called the ABC formula. 

A X B X C/2 X 0.6= mL of blood

A= largest width of the bleed (in cm)

B=largest width perpindicular to A

C=number of cuts you see blood on

So, if A=2cm, B=2cm and the bleed is seen on 3 cuts.....

2 X 2 X 3/2 X 0.6=3.6 mL of blood (not very much in the opinion of a neurosurgeon)

Most of the big bleeds that neurosurgeons drain or take to the OR are 50 cc or so. So, when you call a neurosurgeon and tell them that the patient has 60 mLs of blood, you will definitely get their attention. 

Patients with ICDs presenting to the ED reporting that their ICD fired once do not need mandatory ICD interrogation, admission or an extensive ED workup purely based on the single shock. A workup should be initiated purely based on any other associated symptoms...chest pain, dyspnea, etc. If the patient was doing well and had no other symptoms prior to the shock, the patient should simply have close follow up with cardiology.

Patients presenting after multiple shocks, on the other hand, do need a workup and emergent ICD interrogation (most of these cases also are later deemed inappropriate shocks).

Achilles Tendon Rupture

• Most commonly occurs in males age 30-50 years that participate in occasional high intensity sports that are associated with jumping or quick starts.  [i.e.: Basketball, racquetball, tennis, squash, etc].
  • Exact mechanism is a sudden eccentric force that is applied to a dorsiflexed foot.
• Rupture is also associated with fluoroquinolone and glucocorticoid use.
• Patient will often hear or feel a sudden snap in the back of the ankle or calf.
• Typically ruptures 2-6cm proximal to its insertion on to the calcaneous where its blood supply is the least.
• On physical exam:
  • the patient is unable to plantar flex the foot, raise up on toes, and may have calf swelling. 
  • You may be able to palpate a gap in the achilles tendon.
  • Two specific tests for achilles tendon rupture.
    • Thompson test:  with the leg extended and the foot in neutral position, squeeze the calf muscles.  A positive test is when the foot does not plantar flex when the muscles are squeezed.
    • O’Brien needle test:  Insert a small gauge needle perpendicular to the skin into the proximal (about 10 cm from the calcaneous) achilles tendon. Passively dorsiflex and plantar flex the ankle and foot. If the needle moves in the opposite direction of the movement then the achilles tendon is intact.
• Treatment
  • Refer to orthopedics
  •  Place the patient in a posterior splint with the foot and ankle in slight plantar flexion. 
    • Ideally this will bring the two tendon ends together and speed healing.

This addition was sent in my Dr. Andrew Milstein:

Thanks for the Orthopedics update.  A few pearls for Achilles Tendon Rupture --> often these patients may present like a typical ankle sprain patient and are placed in a hallway chair.  You can't do an adequate Thompson Test while someone is sitting in a chair.  If you're concerned, lay them down on a stretcher to do the test.

Acute Chest Syndrome

• ACS is the leading cause of morbidity and mortality in children and adults with Sickle Cell Disease.
• Definition: ==> A new infiltrate on CXR (excluding atelectasis) PLUS one or more of the following:
  • Tachpnea
  • Fever (>101 degrees F)
  • Chest Pain
  • Cough
  • Wheezing
  • Hypoxemia
• Treatment
  • Bronchodilators
    • Trial of beta-agonists for clinical response is advocated even in those without wheezing.
  • Antibiotics
    • Broad Spectrum: Ceftriaxone PLUS Azithromycin
    • Evidence demonstrates a significant amount of these patients have atypical bacterial infections
    • Vanco is warranted for severe disease unresponsive to therapy
  • Steroids
    • Use for patients with Reactive Airway Disease or severe distress
    • They may cause a rebound of Vaso-occlusive Crisis and need to be tapered.
    • Prednisone 2mg/kg/Day x 5 then taper
  • Pain Control
    • Need to optimize pulmonary toilet by providing adequate pain management, but avoid over-sedation leading to hypoventilation.
    • NSAIDs have proven to be useful in conjunction opiods.
  • Transfusion of PRBCs
    • Simple
      • For pts who have a >10-20% drop from their baseline Hgb
      • For pts who are symptomatic, but not in impending respiratory failure
      • Try not to EXCEED Hgb of 10g/dL post transfusion
    • Exchange
      • For pts with impending respiratory failure
      • For pts with Hgb > 10g/dL and significant symptoms (to avoid hyperviscosity)
    • The decision to transfuse these patients needs to be made in conjunction with the consulting Hematologist.

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 Hemodialysis

• Ethylene Glycol
• Methanol
• Lithium
• Salicylate
• Theophylline (Hemoperfusion)
• Ethanol (rarely needed but can be done)
• Isopropanol (rarely done)

CAVH or CVVH: Lithium, Procainamide, Aminoglycosides, Methotrexate

Exchange Transfusion (pediatrics mostly): Salicylate and Theophylline

• Intracranial hemorrhage (ICH) can expand for the first 24 hours after onset.
• Peak ICH expansion occurs at 6 hours.
• REMEMBER:  The heads of patients with ICH should be elevated (~30 degrees) for at least 24 hours after the onset of bleeding to decrease the extent of expansion.  This is a simple, but too often neglected, clinical measure that potentially offers great benefit to the patient.

 PEA Arrest...Look for AAA rupture and Cardiac Tamponade

If a patient presents in cardiac arrest (particularly PEA), consider the following diagnoses in addition to the causes commonly taught in ACLS:

• AAA with rupture
• Aortic Dissection complicated by tamponade

A 2004 study in Resuscitation by Meron et al. showed the following:

• Approximately 50% of the patients who presented in PEA arrest from a AAA rupture did NOT have abdominal or flank pain prior to arrest
• Approximately 50% of the patients who presented in PEA arrest from cardiac tamponade (from aortic dissection) did NOT have chest pain prior to arrest
• Bedside US was diagnostic in all cases in this subset of patients with PEA arrest of unknown cause

Take home point for the emergency physician:

• Pull the US machine out very early on in the resuscitation of the PEA arrest patient....get the probe on as soon as you can. 

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Vasopressin for Sepsis

• The VASST trial was recently published in NEJM comparing vasopressin vs. norepinephrine for septic shock
• Unfortunately, there are some issues with the study which I will clarify/expand upon in the next Critical Care Literature Update
• There was a trend towards improved mortality in the vasopressin group receiving low doses of norepinephrine (5 - 14 mcg/min)
• Take Home Point: If you are thinking about adding vasopressin to norepinephrine in patients wtih refractory septic shock, do it early.  In other words, add vasopressin when you find yourself titrating norepinephrine doses to 6, 7, 8 mcg/min

ICD shocks are often associated with ST segment elevation and even positive troponin levels that can simulate acute MI. So how do you know if the patient experienced an acute MI with VF that triggered the ICD shock? Or if there simply was an aberrant ICD shock that triggered STE with positive troponins?

STE that is due purely to the ICD shock generally resolves after only 15-20 minutes. Persistent STE beyond that time should be assumed to be true ischemia.

Troponin elevations that are due purely to an ICD shock are usually mild and normalize within 24 hours. Huge troponin elevations and those that last beyond 24 hours should be assumed to be caused by true infarction.

Some simple facts about Pancreatitis:

1. Causes (First two are the most common in the United States)
   1. Gallstones
   2. Alcohol
   3. Hyperlipidemia
   4. Medications [azathioprine, corticosteroids, sulfonamides, thiazides, furosemides, NSAIDs, mercaptopurine, methyldopa, and tetracyclines]
   5. Peptic Ulcer Disease
   6. Scorpion and Snake Bites
   7. Trauma
   8. Infections [ ascaris, mumps, coxsackie virus, cytomegalovirus, Epstein Barr Virus, mycoplasma]
2. Chronic Pancreatitis may not be associated with an elevation of lipase or amylase.
3. Lipase is more specific for pancreatitis
4. Amylase can be elevated in:
   1. pancreatitits
   2. salivary gland injury/disease
   3. ruptured ectopic pregnancy
   4. ovarian cysts
   5. salpingitis
   6. inflammation of the bowel [appendicitis, obstruction]
   7. end stage renal and liver disease [due to decreased clearance]
5. Treatment:  mild cases can be discharged home with clear liquid diet and pain medications, more severe cases needed to be admitted for IV fluids and pain control.  Maintain NPO status.
6. Complications:
   1. Pseudocyst
   2. Phlegmon
   3. Necrosis of the pancreas
   4. Hemorrhage
   5. Intestional obstruction
   6. fistula formation.

Consider HSV

• Consider HSV as an etiology of fever in a neonate (0-30days) even without a maternal history of HSV or h/o active lesions.
  • In one study, only 12% of neonates dx’d with HSV infections had mothers with a known h/o HSV or active lesions.
• Start Acyclovir empirically in these neonates, especially if the Gram Stain is negative.  Send appropriate HSV PCR and Cx.
  • Only 29% of patients (pediatric and adult) ultimately diagnosed with HSV encephalitis were started on acyclovir in the ED. 
  • Those who were not started on acyclovir in the ED, had a significant delay of appropriate therapy.
  • If you don’t think of it… the admitting team might not either.
     

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1) No IV - Try naloxone in a nebulizer - Dose: 2-4 mg  and saline in your nebulizer container.

2) When using naloxone IV, use following dose: 0.05 mg IV - you will find it reverses the respiratory depression without inducing withdrawal. Anesthesia doses naloxone in micrograms, we often overdose our patients. The effect is delayed and not as pronounced as the 0.4 mg blast that causes nausea, vomiting, diarrhea, agitation - all not desirable in the ED.

• A recent retrospecitve study of over 830 patients with suspected or confirmed benzodiazepine overdose from the Florida State Poison Center Database showed that only 0.7% experienced subsequent seizure or seizure-like acitivity (i.e. dystonia, muscle rigidity) after flumazenil administration.
• This study was conducted by emergency physicians from the University of Florida at Jacksonville where flumazenil is apparently often used as an antidote for benzodiazepine overdoses.
  

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