UMEM Educational Pearls

Needle Decompression - Are we Teaching the Right Location?

• Tension pneumothorax frequently results in circulatory collapse and may lead to cardiopulmonary arrest.
• In the event that tube thoracostomy cannot be immediately performed, traditional teaching is to perform needle decompression in the second intercostal space, mid-clavicular line using a 5-cm angiocath needle.
• Recent literature, however, has challenged the traditional location for needle decompression.  In fact, researchers found:
  • Needles placed in the second intercostal space often failed to enter the chest cavity and relieve tension physiology.
  • Needles placed in the fifth intercostal space in the anterior axillary line were more likely to enter the chest cavity with a lower failure rate.
• Take Home Point: It may be time to reconsider the optimal position for needle decompression of tension pneumothorax.

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Question

40 year-old male presents with fever, chills, & cough. What’s the diagnosis and the MOST likely cause? 

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• Early CPR performed by laypersons can double the chances of survival in out-of-hospital cardiac arrest (OHCA)
• A retrospective cohort that combined 2 RCT compared the survival effects of dispatcher CPR instruction consisting of chest compression alone or chest compression with rescue breathing
• There was a lower risk of death after adjustment for confounders (adjusted hazard ratio 0.91, 95% confidence interval 0.83-0.99, p=0.02)
• Findings strongly support a long-term mortality benefit of dispatcher CPR instruction strategy consisting of chest compression alone rather than chest compression plus rescue breathing

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Intraosseus (IO) access has become quite popular in critically ill patients requiring immediate resuscitation. In a patient responsive to pain, however, pain and discomfort is associated with the force of high-volume infusion through the established line.

• Before flushing the line, consider administering preservative-free 2% lidocaine (without epinephrine) for patients responsive to pain prior to flush.

• The suggested dose is 20-40 mg (1-2 mL) of the 2% lidocaine, followed by the 10 mL saline flush.

If preservative-free 2% lidocaine is not stocked in your ED, now is the time to consider adding it.

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This winter season has brought a rise in influenza and RSV activity in Maryland and in many parts of the country. It is also important to remember other potentially lethal infections that are prevalent in the winter and early spring months, such as Neisseria meningitidis. In fact, a recent study2 showed a potential increase in meningococcal disease when influenza and RSV activity is high.

What:
Encapsulated, gram-negative diplococcus
Where:
Found in nasopharyngeal secretions, carrier rates 2-30% in normal populations
Who:
Age of incidence has 2 peaks: children < 2 years old, teens 15-19 years old
Young adults who live in shared housing, such as college dorms and military recruits

Clinical Presentation:
Early non-specific symptoms of URI, fever, malaise, myalgias
Meningitis: non-specific prodrome + headache, stiff neck (not found in younger children who often present atypically with irritability and/or vomiting)
Meningococcemia: above symptoms + hypotension + petechial rash (>60% of patients)

Treatment:
Early (!) antibiotics: 3rd generation cephalosporins (<3mo: cefotaxime; older infants, children, and teens: ceftriaxone); PCN G is antibiotic of choice for susceptible isolates
Early and aggressive management of shock

Prevention:
Tetravalent vaccine, MCV4 (Menactra, Menveo), available for serogroups A, C, Y and W-135 is given routinely at age 11-12 years old with an additional booster at 16-17 years old. MCV4 does not protect against serogroup B which accounts for 30% of infections.
 

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There have been many attempts to reduce the incidence of contrast-induced nephropathy. Mechanism usually centers around antioxidant properties or free radical scavengers that prevent the acute kidney injury that may result after intravenous contrast. IV Fluid hydration, sodium bicarbonate and acetycysteine have been studied with only some evidence. There is also some controversial data that is beginning to surface regarding the use of atorvastatin with a recent article in Circulation 2012 that showed high dose atorvastatin (80mg) 24 hrs prior to angiography prevented contrast-induced acute kidney injury in patients with mild to medium risk. Link to article has been provided:

http://circ.ahajournals.org/content/126/25/3008

Case Presentation:

A 43 year old diabetic woman presents with dyspnea and a dry cough. Her vital signs are:  BP 84/42, HR 135 RR 37 T 38.5.  Lobar consolidation is seen on chest xray.  She decompensates and is intubated, a central line is placed, and IV fluids are started.  Her husband reports that they had just returned from  a vacation in Thailand one week earlier.

Clinical Question:

Does the recent travel change your choice of empiric antibiotics?

Answer:

The patient should also be covered for melioidosis, and infection caused by Burkholderia pseudomallei.

• Infection can occur via direct contact with, inhalation of, or ingestion of the bacteria.
• B. pseudomallei is highly endemic in Thailand and Northern Australia, but melioidosis has been contracted in the Americas and other parts of Asia and Australia. (True epidemiology is unknown due to difficulties in culturing the bacteria)
• Clinical presentation most frequently involves pulmonary infection, abscess formation, or bacteremia.
• Labs that don't have experience with this bacteria have difficulty culturing it and it is often misidentified.
• Treatment is 10-14 days of ceftazidime or a carbapenem.
• After recovery, the patient requires TMP-SMX for 3-6 months for bacterial eradication. 

Bottom Line:

Patients presenting with severe infections and recent travel to an endemic area should receive emperic antibiotics with ceftazidime or a carbapenem until another source is identified. 

University of Maryland Section of Global Emergency Health

Author: Jenny Reifel Saltzberg, MD, MPH

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The updated Surviving Sepsis Guidelines have been released (click here) and here are some recommendations as they pertain to hemodynamic management (grades of recommendations in parenthesis).

Fluid therapy

• An initial fluid bolus of at least 30 mL/kg is recommended; crystalloids should be the initial fluids (1B).
• Consider albumin when “substantial” amounts of crystalloid have been given (2C).
• Use of hydroxyethyl starch is not recommended (1B)

Vasopressors (targeting MAP of at least 65 mmHg)

• Norepinephrine (NE) is the vasopressor of choice (1B)
• Epinephrine (EPI) if an additional agent is required; can be added to or substituted for NE (2B)
• Vasopressin (0.03 units/minute) can be added to NE; it should not be titrated or used as a single agent (ungraded).
• In selected patients (e.g., bradycardia or low-risk of tachyarrhythmia), dopamine may be considered (2C). Low-dose dopamine (for renal protection) should not be used (1A).
• Phenylephrine (PE) is not recommended, except if (1C):
  • Serious NE associated arrhythmias
  • Cardiac output can be measured and is increased with low MAP (PE can reduce cardiac output)
  • Other therapies cannot achieve the target MAP

Corticosteroids

• Use if fluids and vasopressors cannot restore adequate perfusion
• Total daily dose of 200 mg (2C) administered by continuous infusion (2D)
• ACTH stimulation test is not recommended (2B)
• Tapering hydrocortisone when vasopressors have been discontinued (2D)

Inotropic Therapy

• Administer dobutamine if it is believed that cardiac filling pressures are elevated, cardiac output is low, or persistent signs of hypoperfusion despite other therapies (1C)

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Question

40 year-old female drove into a ditch. Right sided chest pain and stable vitals. Here's the CT but what do you think the initial CXR showed (Hint: it's a trick)?

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• Many infants w/cyanotic heart disease only survive w/early surgical intervention
• The most rapid & effective first-line therapy for stabilization of the crashing neonate is IV prostaglandin E1 (PGE1)
• PGE1 serves to reopen the ductus arteriosus allowing partially desaturated systemic arterial blood to enter the pulmonary artery and be oxygenated
• The widespread use of this agent has profoundly decreased morbidity & mortality 
• The initial dose of PGE1 is 0.1 mg/kg/min
• ADR for PGE1 include: apnea, hypotension, edema, and low grade fever

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Hematoma Block

Provides good aesthesia for reduction of fractures. Onset in approximately 5 minutes

Benefits:  No need for NPO, simple and easy to perform & can be done without additional personnel (unlike w/ procedural sedation)

Contraindications: Open fractures, dirty or infected overlying skin

1) Identify fracture site with x-ray and palpation

2) Clean skin w/ Betadine

3) Insert needle into the hematoma. * Confirm placement by aspirating blood *

4)  Inject anesthetic (lidocaine 1 or 2%) into the fracture cavity and adjacent periosteum

http://www.youtube.com/watch?v=tjnsdjfwMmY

Cyclophosphamide-induced hemorrhagic cystitis is a well known to oncologists. This unique complication of this chemotherapeutic drug has a defined mechanism and could be seen in your Emergency Department.

- Hemorrhagic cystitis occurs in 46% of patients that receive cyclophosphamide

- Can occur even months after administration

- 5% can actually die from the hemorrhage

- Treatment: Bladder irrigation, hydration, supportive. Oral adminsitration of MESNA (2mercaptoethan sulfonate) and bladder irrigation with prostaglandins and even methylene blue have been attempted.

Question

A 38 year old man is brought in by ambulance for a seizure.  His medical history is not known. On exam he is post-ictal and otherwise has a non-focal neurologic exam.  He has an abrasion above the right eye, a small tongue laceration, and was incontinent of urine. A head CT was done and is shown below.  What was the cause of this man's seizure?

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Attachments

1301231959_neurocysticercosis.jpg (109 Kb)

Postintubation Hypotension

• It is clear that preintubation hypotension is associated with increased mortality in critically ill patients who require mechanical ventilation.
• Unfortunatley, the literature is less clear on the frequency and impact of hypotension that develops after intubation.
• Two recent publications in the Journal of Intensive Care provide valuable information on postintubation hypotension.  Some highlights of the studies include:
  • Retrospective cohorts of over 300 patients who developed postintubation hypotension, defined as a SBP < 90 mm Hg within 60 min of intubation.
  • Postintubation hypotension occurred in almost 25% of patients.
  • Median time to hypotension was 11 minutes.
  • Patients with postintubation hypotension had a higher inhospital mortality (33% vs. 23%).
  • A preintubation Shock Index > 0.8 was the strongest predictor of cardiovascular collapse after intubation.
• Take Home Point: Postintubation hypotension occurs frequently and may be associated with worse outcomes.

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Question

45 year-old male complains of chest pain and cough. He also tells you, "...oh, and by the way doc, I just smoked something." What's the diagnosis?

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·       Cyanosis in the newborn is defined as an arterial saturation <90% and a PO2 <60 torr

·       To help differentiate between cardiogenic and non-cardiogenic causes initially obtain an arterial saturation on room air and obtain a subsequent measurements on 100% oxygen

·       Infants w/neurogenic or pulmonary causes of cyanosis will demonstrate increases in arterial blood saturation on 100% oxygen while infants with congenital heart disease show minimal elevation

·       There are 3 general sources of arterial desaturation in neonates with structural heart disease:

1.) Lesions with decreased pulmonary blood flow (tetralogy of Fallot, severe pulmonary stenosis/atresia, and tricuspid atresia)

2) Admixture lesions, in which desaturated systemic venous blood mixes with intracardiac blood, and then enters the aorta (transposition of great vessels, partial anomalous pulmonary venous drainage)

3) Lesions with increased pulmonary blood flow and pulmonary edema, in which diffusion barriers and intrapulmonary shunting prevent proper oxygenation (truncus arteriosus)

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Question

Patient:  A 10 year old female is brought to the ED after swallowing 2 beads (see image).  Based on the findings, what are your concerns and what is the disposition?

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SSRIs and SNRIs like venlafaxine and sertraline are well known to cause hyponatremia. Usually considered safe, this adverse drug event can lead to weakness, confusion, seizure and even cerebral edema. Elderly are more susceptible to this adverse effect.

ADH is regulated by serotonin and thus the mechanism for the Hyponatremia is SIADH. 

Tolvaptan, a vasopressin receptor antagonist, has been a new treatment that has been used anecdotally in Europe. Waiting for the first US case report. 

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More than 1.2 billion people are infected with at least one species.

Most helminth infections are contracted by ingesting the eggs, except strongyloides and hookworm whose larvae penetrate bare skin when it is contact with the soil.

The roundworm (Ascaris lumbricoides) life cycle involves migration through the lung tissue which can cause pneumonitis.  Patients can present with interstitial infiltrates, wheeze, and blood tinged sputum.  Ascaris than migrates to the intestines where it can cause partial small bowel obstruction. In pediatric patients, the appendix may be invaded causing gangrene with symptoms indistinguishable from appendicitis.  In adults, the worms can invade the biliary tract and cause biliary disease or pancreatitis.  Fever causes this helminth to migrate and it can emerge from the nasopharynx or the anus.

Whipworms (Trichuris trichiura) present as colitis or symptoms similar to inflammatory bowel disease.  Chronic illness can involve anemia and clubbing.  In severe cases, trichuris can cause dysentery and rectal prolapse. 

Hookworms (Necator americanus or Ancylostoma duodenale) also have a pulmonary phase, but with milder symptoms than Ascaris.  Eventually hookworms cause iron deficiency anemia and malnutrition.  They can be a primary cause of anemia in pregnancy in endemic areas.

Threadworm (Strongyloides stercoralis) can cause a wide spectrum of disease presentations.  The infection can start with a rash, larva currens.  The infection may be subclinical or may invade the lung, intestinal wall, or the nervous system.  Eventually hyperinfection may develop which is a very large increase in worm burden and then the infection becomes disseminated. 

Toxocara canis or toxocara cati have affected approximately 14% of the US population.  These helminthes reproduce in dogs or cats, and human infection is not part of the normal life cycle.  Most infections are subclinical but it can produce a mild pneumonitis that is very similar to asthma.  There can be pain and inflammation as the helminthes travel through organs such as the liver or lung and is called visceral larva migrans.  The helminth may also move through the eye and optic never causing an ocular form of the disease, ocular larva migrans. 

Pinworms (Enterobius vermicularis) are the cause of most common helminth infection in US and can present with anal pruritus leading to trouble sleeping.  When an infection is identified, everyone in the household should be treated, regardless of symptoms. 

University of Maryland Section of Global Emergency Health

Author: Jenny Reifel Saltzberg, MD, MPH

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Intra-aortic balloon pumps (IABP) are devices that provide hemodynamic support during cardiogenic shock; the balloon inflates during diastole (improving coronary artery perfusion) and deflates during systole (reducing afterload and improving systemic perfusion). Click here to see a 41 second video illustrating how it works. 

Several guidelines recommend placement of an IABP for patients in cardiogenic shock secondary to acute myocardial infarction (AMI), if early revascularization (e.g., CABG) is planned (Class I recommendation). Data behind this recommendation, however, is limited.

The IABP-SHOCK II trial was a randomized, multi-center, open-label study that enrolled 600 patients (598 in the analysis) with cardiogenic shock secondary to AMI (STEMI or NSTEMI). Patients were randomized to the control group (receiving standard therapy; N=298) or the experimental group (receiving IABP; N=300).

No significant difference was found between groups with respect to 30-day mortality (primary end-point), secondary end-points (e.g., time to hemodynamic stabilization, renal function, lactate levels, etc.), or complications (e.g., major bleeding, peripheral ischemic complications, etc.).

Bottom line: Perhaps it is time to reassess the approach to cardiogenic shock secondary to AMI when early revascularization is planned. At this time consultation with local expertise is recommended.

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