UMEM Educational Pearls

• The Dix-Hallpike Maneuver is performed to help diagnose/rule out benign positional vertigo, a condition attributed to floating (canalithiasis) or fixed (cupulolithiasis) otoconial debris within the posterior semicircular canal of the ear.
• To perform, turn the patient's head 45 degrees to one side and then rapidly but carefully recline them backwards to a supine position, preferably with the head hanging partially off the bed (i.e. at a position about 10-20 degrees inferior to that of the rest of the body).  Next, perform the maneuver by turning the patient's head 45 degrees to the other side.
• If nystagmus is induced, the test is positive.  Note the following five characteristics of the nystagmus:  (1)  latency, (2)  direction, (3)  fatigue (i.e. extinguishes with repetitive maneuvers), (4)  habituation (i.e. duration), and (5)  reversal upon sitting upright.
• Note that the Dix-Hallpike Maneuver described here is the diagnostic version, not the one performed therapeutically, the latter of which is also helpful. 

 Medical Regimen for Suspected Variceal Bleed

To review what Dr. Bond and Dr. Winters have already posted:

Three medical therapies have been shown to be effective in patients with severe upper GI bleed thought to be due to esophageal varices:

• Octreatide: 50-100 ug bolus followed by 50 ug/hour. Has been shown to lower the rebleeding rate substantially. Even if varices have not been confirmed by endoscopy, Octreatide has also been shown to be effective in ulcer bleeding as well.
• Antibiotics (3rd generation Cephalosporin): Have been to lower the rebleeding rate in variceal bleeding. 
• Intravenous Proton Pump Inhibitor: Remember that a liver patient is as likely to have a non-variceal source of bleeding (ulcer), so add a PPI drip. Raising the pH stabilizes clot. Without endoscopy, you don't know if they have an ulcer or another etiology.

Most of our gastroenterologists recommend this regimen (all three therapies)

Other things to consider:

• Platelets, FFP
• Intubate EARLY-most endoscopists will want the airway protected prior to the scope.
• Don't be too aggressive with blood replacement/IVF: The gastroenterologist don't want these patients too resuscitated with blood products. Certainly don't aim for a Hct >30.

Coagulopathy and Trauma

• When resuscitating a trauma patient recall that the "lethal triad" consists of acidosis, hypothermia, and coagulopathy
• Coagulopathy is induced by the combination of direct loss of clotting factors, consumption in clot formation, dilutional due to crystalloid administration, acidosis, and hypothermia
• When giving PRBCs in trauma resuscitation, don't forget to give FFP
• The ratio to remember is 1U of FFP for every 2U PRBCs

Post-MI cardiogenic shock, while traditionally thought to carry a mortality > 80%, actually has perhaps half that mortality when patients are treated aggressively with prompt invasive therapy (PCI, possibly CABG). Fibrinolytics have traditionally been discouraged, but authors now indicate that they should be given if all of the following three conditions are present:

1. PCI will take greater than 90 minutes,
2. Less than 3 hours have elapsed since onset of STEMI
3. No contraindications to lytics are present.

Sent on behalf of Dr. Amal Mattu

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 Trigeminal Neuralgia

• A neuropathic disorder of the trigeminal nerve that causes episodes of intense pain.
• Also known as Tic Douloureux
• Many cases are associated with vascular compression and subsequent demyelination of the trigeminal nerve, though other causes include compression by a tumor, and multiple sclerosis.
• Classic Trigeminal Neuralgia is a clinical diagnosis that has the following criteria:
  • Paroxysmal attacks of pain lasting from a fraction of a second to two minutes that affect one or more divisions of the trigeminal nerve
  • Pain has at least one of the following characteristics: intense, sharp, superficial, or stabbing precipitated from trigger areas or by trigger factors
  • Attacks are similar in individual patients
  • No neurological deficit is clinically evident
  • Not attributed to another disorder
• Treatment options include:
  • Medical:
    • Carbamazepine (most common and drug of choice)
    • Gabapentin (lacks evidence in trigeminal neuralgia but widely used for other neuropathic pain)
    • Lamotrigine
    • Baclofen
  • Surgical:
    • Microvascular decompression: posterior fossa is explored and the culprit blood vessel is moved off the trigeminal nerve. Typically the nerve is padded with a teflon sheet in order to provide additional protection. 80-90% successful with little or no facial numbness.
    • Ablative: Attempts are made to just incapacitate the pain fibers but these techniques can result in facial numbness as other sensory fibers can be damaged.  Common methods include:
      • Glycerol or alcohol injection
      • Radiofrequency rhizotomies
      • Stereotactic radiation therapy
      • Complete severing of the nerve.

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Acute Appendicitis – Delayed Surgery option?

• Appendicitis incidence in children = 4/1000
• The traditional emergent surgical intervention has recently been challenged.
• Three RETROSPECTIVE studies investigated delayed/urgent vs emergent surgical interventions
  • 2 of the three found no significant difference in perforation or complication rates between the 2 groups.
  • 1 found that the emergent group had higher rates of perforation.
• What you need to know:
  • surgeons may base their decisions on these studies, which do have limitations (being that their retrospective)
  • despite the time of day, you should still advocate for patients that are “sick” to go to the OR rather than get antibiotics to “cool off” first.

Show References

 Did you know how many toxicities and adverse effects amiodarone has? Many are severe, and many VERY common.

1. CARDIAC: hypotension with rapid infusion, prolonged QT, torsades

2. NEUROLOGIC problems occur in 20-40%, including malaise, ataxia, and peripheral neuropathies

3. ENDOCRINE: hypothyroidism and hyperthyroidism

4. GI problems occur in 25%

5. OPHTHALMOLOGIC disturbances include optic neuropathy, papilledema, and photosensitivity

6. SKIN: blue grey pigmentation

7. PULMONARY: pulmonary fibrosis

• Nystagmus which results from gaze (i.e. extraocular motion) in a particular direction, is detected by asking the patient to look at a target object 20 to 30 degrees to the right or left of their midline (i.e. when looking straight ahead) for 20 seconds.
• If gaze nystagmus is present, the eye will beat towards the intended direction of gaze.
• The ability to maintain eccentric gaze is a function of the brainstem and midline cerebellum, particularly the vestibulocerebellum. 
• Gaze nystagmus is attributable to a central process, typically due to drugs (i.e. sedatives, anti-epileptics), alcohol, CNS tumors, or cerebellar degenerative syndromes.

Aspiration Pneumonitis

• Aspiration pneumonitis is an acute lung injury resulting from the aspiration of gastric contents
• It is an inflammatory condition rather than infectious
• Despite the inflammation, corticosteroids have been shown to have no effect on mortality
• Aspiration pneumonitis is self limited
• Antibiotics are generally held for 24 to 48 hours
• When to consider empiric broad spectrum antibiotics in the ED:  Gastric contents are sterile in most patients.  Patients who may have colonization/contamination of gastric contents are more likely to progress from pneumonitis to pneumonia.  Consider empiric antibiotics for aspiration pneumonitis in the patient with SBO, gastroparesis, those receiving enteral feeds through a G- or J-tube, and those on chronic PPI's/antacids.

Clinical Presentation of SVC Syndrome

SVC syndrome (caused either by tumor or thrombosis of the SVC) classically presents with facial swelling, arm swelling, and dilated chest wall veins. The problem in the real world is that often times the manifestaions are a bit more subtle.

Some SVC syndrome pearls:

• Consider the diagnosis in patients with a generalized complaint of facial swelling or "fullness," particularly if they have an indwelling catheter in place.
• Consider in patients who complain there face is swollen or red (plethoric) in the morning, or who notice this when their arms are raised (Pemberton's sign)
• The diagnosis is usually established by CT.
• Patients with SVC syndrome and the complaint of hoarseness or headache should make you nervous, as these symptoms may indicate laryngeal and cerebral edema.
• The importance of examining the neck and chest in ED patients cannot be overemphasized. Often the one clue that leads to the diagnosis is prominent and asymetric neck, upper chest, or shoulder veins.
• Treatment: For tumor related SVC syndrome-head elevation, possibly steroids, radiation therapy (along with biopsy if no cancer diagnosis established); For thrombotic-related SVC syndrome-anticoagulation, Interventional Radiology consult for lytics/stent

Right ventricular (RV) dysfunction in the setting of acute MI accounts for only 5% of cases of cardiogenic shock but carries nearly the same mortality as LV shock. Shock due to RV dysfunction is usually treated by aggressive volume loading with IVF. However...

In some cases of RV dysfunction, RV end-diastolic pressure can be very high, resulting in shiftng of the invterventricular septum into the LV cavity, which in turn decreases LV filling and cardiac output. Aggressive fluid resuscitation in these patients may actually further worsen RV pressures, leading to further reductions in cardiac output. These patients should instead be treated early with vasopressors.

How do you tell if your patient needs aggressive fluid resuscitation or early vasopressors? Bedside ultrasound can be the answer...if you find marked distension of the RV, go with early vasopressors. If the RV appears normal in size (smaller than LV), go with the IVF.

And of course early revascularization is critical as well.

(adapted from: Reynolds HR, Hochman JS. Cardiogenic shock: current concepts and improving outcomes. Circulation 2008;117:686-697.)

It has become standard that close contacts of individuals being treated for bacterial meningitis be treated prophalacticly with antibiotics to prevent additional cases.  Fluoroquinolones, in particular ciprofloxicin, have been the drug of choice as a single dose provided adequate protection.

Now the CDC is reporting the first cluster of fluoroquinolone-resistant meningococcal disease in North America have been documented along the Minnesota-North Dakota border.  As of now, the CDC still recommends ciprofloxacin for all parts of the country except for a 34-county area in the Minnesota-North Dakota area.  In that area the CDC is recommending rifampin, ceftriaxone or azithromycin be used.

This needs to be followed closely as the resistant organism is extremely likely to spread across the country and it will probably this time next year when nobody can use ciprofloxacin anymore.

Umbilical Cord Problems

• Delayed Umbilical Separation
  • Normal Time for cord separation = 1 – 8 weeks postnatal age.
  • Common Reasons for Delayed Separation:
    • h/o Neonatal Sepsis and antibiotic administration
    • h/o Prematurity
    • h/o C-Section delivery
    • h/o Low Birth Weight
  • Rare, yet most concerning reason for Delayed Separation:
    • Immuno-Deficiency – Leukocyte Adhesion Deficiency type 1 (LAD-1)
      • Life-threatening
• Omphalitis
  • Infection of the remnant of the umbilical cord
  • More common in developing countries
  • Staph. aureus is most common organism cultured
  • Complication from:
    • Spontaneous Evisceration
    • Necrotizing Fasciiis of scrotum and/or penis
    • Peritonitis
    • Intra-abdominal abscesses
  • Early detection is paramount

Since all of us are taking care of critically ill patients for longer periods of time, I think it is important to be familar with current critical care literature.  Often, we are the first "intensivist" a patient sees when they arrive to the hospital.  To keep us up to date, I am going to be sending out critical care literature updates every couple of weeks similar to Amal's cardiology updates.   Please email me with any questions, comments, or feedback.

Mike

Recent Articles from the 2008 Critical Care Literature

Hydrocortisone therapy for patients with septic shock.

Sprung CL, Annane D, Keh D, Moreno R, Singer M, et al. NEJM 2008;358:111-24.

            Corticosteroid therapy for patients with septic shock seems to change favor every couple of years.  In the first publication of the Surviving Sepsis Campaign Guidelines, steroids were given a favorable recommendation based largely upon the results of one multicenter, randomized, controlled trial. (Annane, et al. JAMA 2002;288:862-71) In this study, Annane reported a reduction in the likelihood of death in patients who did not respond to the corticotropin stimulation test and were given steroids (hydrocortisone and fludrocortisone).

            The current study is from the CORTICUS Study Group and is a multicenter, randomized, double-blind, placebo-controlled study conducted in 52 ICUs from March 2002 to November 2005.  Enrolled patients had to have clinical evidence of infection, a systemic response to infection, organ dysfunction attributable to sepsis, and the onset of shock within 72 hours (SBP < 90 mmHg despite fluids or vasopressors).  Patients were randomized to receive either hydrocortisone or placebo for 5 days.  Doses were then tapered over the next 6 days for a total duration of therapy of 11 days.  A lack of response to corticotropin was defined as an increase in cortisol of no more then 9 mcg/dL.  The primary end point of the study was the rate of death from any cause at 28 days in “non-responders”.  Some important secondary end-points included the rate of death at 28 days in “responders”, time to reversal of shock, duration of ICU and hospital stay, and rates of death at 1 year.

            Four-hundred ninety nine patients were enrolled in the study.  Of these, 233 were identified as “non-responders”.  In this group, 125 were randomized to receive hydrocortisone and 108 received placebo.  The demographic and clinical characteristics of patients in each group were similar.  Over 90% of patients in each group were vented and all were receiving vasopressors, the most common being norepinephrine.  With respect to the primary outcome, there was no significant difference in the rate of death at 28 days between the study groups.  For the secondary end points, there was also no significant difference in the rate of death in “responders”, duration of ICU or hospital length of stay, or death at 1 year.  The only difference that was found in those receiving hydrocortisone was a reduction in the time to reversal of shock.  Importantly, this did not translate into improved mortality.  Lastly, the authors reported an increase in new episodes of sepsis and septic shock in those receiving hydrocortisone but the absolute numbers are small.

            Things to Consider:  Investigators had planned to enroll 800 patients but stopped at 499 due to slow recruitment, termination of funding, and expiration of the study drug.  In addition, the mortality rate in the placebo group was lower than what would be expected.  As a result, the study is inadequately powered.  In contrast to the Annane study, enrollment of patients could be up to 72 hours after the onset of shock, raising the question of timing of steroids administration.  Furthermore, the majority of patients in this study were older, Caucasian males who required emergency surgery – not typical of the septic shock population at UMMC.  Importantly, patients who were receiving long-term corticosteroids within the past 6 months, or short-term steroids within the past 4 weeks, were excluded – the patients we would typically give stress dose steroids to during refractory shock. 

            Take Home Point: Although CORTICUS is underpowered, it is one of the largest trials to date on corticosteroids in patients with septic shock.  The results indicate that corticosteroid therapy in this patient population of “non-responders” had no effect on mortality.  Based upon this study, the latest version of the Surviving Sepsis Campaign Guidelines has downgraded their recommendation on corticosteroids.  It appears that the pendulum regarding steroids may now be swinging back in the negative direction.

Intensive insulin therapy and pentastarch resuscitation in severe sepsis.

Brunkhorst FM, Engel C, Bloos R, Meier-Hellmann A, Ragaller M, et al. NEJM 2008;358:125-139.

            The concept of “tight glucose control” in critically ill patients primarily began with the Van de Berghe study in 2001.  In this study, investigators found a reduction in mortality in critically ill patients whose glucose was maintained between 80 – 110 mg/dL. (Van de Berghe G, et al. NEJM 2001;345:1359-67.)  The benefit was primarily seen in cardiac surgery patients who had multiple organ failure from sepsis.  Furthermore, these patients were given a high glucose challenge immediately after surgery – not a common practice.  More recently, the same investigators evaluated MICU patients who had not undergone surgery nor received a glucose challenge.  (Van de Berghe G, et al. NEJM 2006;354-449-61.)  In this latter study there was no benefit to intensive insulin therapy.

            The current study is a multicenter, randomized, open-label study of both intensive insulin therapy and hydroxyethyl starch in patients with severe sepsis.  The study was conducted from April 2003 to June 2005 in 18 multidisciplinary ICUs at academic tertiary hospitals in Germany.  The study was designed to detect a decrease in mortality from 40% to 30% at 28 days.  Enrolled patients had to have the onset of severe sepsis or septic shock either 24 hours before ICU admission or less than 12 hours after ICU admission.  The primary end points were the rate of death from any cause at 28 days and morbidity.  Since we do not use HES in the ED for volume resuscitation, I will focus on intensive insulin therapy.

            The insulin arm of the study compared intensive insulin therapy to conventional insulin therapy.  In the conventional group, insulin was given when glucose values were > 200 mg/dL, with the goal of maintaining glucose between 180 – 200 mg/dL.  In the intensive insulin group, insulin was given when glucose values were > 110 mg/dL, with the goal of maintaining glucose between 80 – 110 mg/dL.  Treatment ended at either discharge from the ICU, death, or a total of 21 days of therapy were reached.

            Five hundred thirty seven patients were enrolled, 290 in the conventional insulin group and 247 in the intensive insulin group.  Baseline patient characteristics including age, pre-existing co-morbidities, sites of infection, lab values, and hemodynamic variables were similar between the groups.  Total nutritional intake, including glucose, was similar in both groups.  Interestingly, the majority of patients had nosocomial acquired infections and over 60% in both groups were given hydrocortisone.  Overall, there was no significant difference in the rate of death between the intensive and conventional insulin therapy groups.  Furthermore, there was no significant difference in morbidity between the two groups.  As one might expect, there was significantly more hypoglycemic episodes in the intensive insulin therapy group (17% vs. 4.1%).  Although no deaths were attributable to hypoglycemia, there were more “life threatening” episodes of hypoglycemia in the intensive insulin group.  As a result of the increase in hypoglycemic episodes the study was stopped early.

            Take Home Point:  In this patient population with severe sepsis, intensive insulin therapy, using a continuous infusion, to maintain glucose between 80 – 110 mg/dL did not improve mortality.  It did, however, result in significantly more hypoglycemic episodes (glucose < 40 mg/dl).  Many EDs across the country are now developing and implementing sepsis protocols primarily based upon the SSC Guidelines.  Based upon this study, intensive insulin therapy may not be a necessary component to the ED management of patients with severe sepsis or septic shock.

Both dealing with the adverse effects from therapeutic administration, like when you order it on the floors or take yourself - to the overdose setting. Here is a brief list of the common sleep aids, MOA and toxicity. (Zolpidem or Ambien gets the award for most entertaining adverse effect of "Sleep Eating")

• "Unisom": there are multiple formulations, most have diphenhydramine or some derivative. Toxicity is anticholinergic and Na channel blockade in overdose. Be aware that some have doxylamine which causes atraumatic rhabdomyolysis.
• Zolpidem (Ambien): Nonbenzodiazepine hypnotic, with sedation as the primary effect though the reports of hallucinations, "sleep eating" and "sleep coitus" have been made famous.
• Eszopiclone(Lunesta): Nonbenzodiazepine hyponitic, mechanism of action unknown. Does not require a controlled substance Rx but is expensive. Toxicity: metallic taste next day, minimal toxicity reported.

Be sure to perform a thorough head and neck examination in the dizzy patient, as the etiologic source is often due to ear, nose, and throat pathology, such as structural abnormalities, some of which may even signal a more widespread process

Such common physical examination findings may include the following:

• cerumen impaction
• otitis media with effusion
• chronic otitis with otorrhea
• chronic sinusitis with nasal airway obstruction
• orophayrngeal findings consistent with sleep apnea
• congenital abnormalities of the pinna, external auditory canal, and face may suggest labyrinthine involvement

D-Dimer in the Critically Ill

• Diagnosis of VTE in the critically ill can be challenging and these patients are at high risk for the disease
• Only 3.6% - 16% of critically ill patients have a negative d-dimer, regardless of the presence or absence of VTE
• Even in patients with low pretest probability, d-dimer in the critically ill is of limited utility

Crowther MA, et al. Neither baseline tests of molecular hypercoagulability nor D-dimer levels predict deep venous thrombosis in critically ill medical-surgical patients. Intensive Care Med 2005;31(1):48-55.

Direct Renin Inhibitor-Aliskiren (Tekturna)

This drug is the 1st in a new class of antihypertensives called direct renin inhibitors-1st approved in 2007. This drug, along with three others being developed, inhibits the entire Renin-Angiotensin-Aldosterone System (RAAS) which has been shown to lead to definitive 24 hour blood pressure control.

Why should emergency physicians care, you ask?

• It is only matter of time before we start seeing patients on this drug. I saw my first just a few weeks ago, and according to some of our nephrologists we can expect to see a whole lot more.  Emergency Physicians should at the very least know about this new class of drug.
• Side effects of the drug are similar to ACE inhibitors (ACE-I), like hyperkalemia.
• The drug can cause angioedema, so development of angioedema on this drug pretty much takes all three angiotensin drugs (ACE inhibitors, angiotensin receptor blockers, and direct renin inhibitors) off the list of potential BP meds for the patient. All three can cause angioedema.

J Hypertension March 2007

Just a reminder, after a recent case of a patient that had a large AMI the day after a negative dobutamine stress test...

Neither stress testing nor coronary angiography are definitive for ruling out unstable/vulnerable plaques. If the HPI for your patient is very concerning, don't obviate your concern just because of a recent negative stress test or angiography. These tests are good at identifying large occlusions, but they tell us nothing about recent rupture or about composition of the plaques, and we now know that it is the composition that determines plaque instability. Size doesn't always matter...

Ultrasound in Pregnancy

1.  A full bladder is needed for Transabdominal Ultrasound and an empty bladder for transvaginal ultrasound.
2. A gestational sac should be visible on transabdominal ultrasound with a quantative HcG of 5000-6000 mIU/ml, and a quant of 1500-2000 mIU/ml on transvaginal.
3. When taking photos, ensure that you show all of the applicable landmarks.  [i.e.: bladder, and uterus]  If you just zoom in on the pregnancy anybody else (i.e.: your expert witness) reading the scan will not be able to confirm that the pregnancy is in the uterus.
4. To confirm an IUP, you must see the yolk sac within the gestational sac.  A double decidual sign is an early sign of pregnancy but it is not always seen and should not be relied upon.
5. If you have a confirmed IUP an additional ectopic pregnancy is extremely unlikely unless the patient was taking medication to stimulate their ovaries (i.e. Infertility treatment).  If on stimulation therapy a very thorough exam needs to be done to look for additional pregnancies.
6. If Quant >2000 mIU/ml and there is no evidence of an IUP, patient needs to be treated as an ectopic pregnancy.