UMEM Educational Pearls

• Apart from time and rehabilitation, there is currently no effective treatment for reversing brain damage caused by stroke.

• Clinical recovery after a stroke results from neuro-restorative processes such as neurogenesis, angiogenesis, synaptic plasticity, and/or re-modeled and strengthened connections between neurons. 

• Stem cell therapy for stroke is a novel, but progressive area of research which would potentially facilitate the neuro-restorative processes required for recovery. 

• Despite the extremely complex nature of brain function and central nervous system networks, successful stem cell therapy for brain infarct could become the wave of the future for optimal stroke management.

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Patients in the Critical Care setting may develop HIT as a result of chronic pre-existing risk factors (malignancy, obesity, hypertension, diabetes or medications) or acquired factors secondary to their ICU stay (post-operative state, trauma, central lines or medications such as heparin).

Diagnosis of HIT:

• platelet count<150,000 or relative decrease of 50% or more from baseline
• documentation of antibodies binding platelet factor 4 and heparin, as well as a confirmation test
• typically occurs 5-14 days after initiation of heparin therapy
• can have a rapid (usually a result of previous exposure) or delayed onset
• thrombotic complications develop in 20-50 percent of patients

Treatment of HIT:

• Remove all sources of heparin (including heparin-bonded catheters)
• initiate a non-heparin anticoagulant
• Direct thrombin inhibitors:
  • Lepirudin (cleared by kidney)
  • Argatroban (cleared by liver)
  • Bivalirudin (cleared by proteolysis 80% and kidney 20%)
• Other agents used include:
  • Danaparoid (antifactor Xa activity - not available in North America)
  • Fondaparinux (synthetic selective inhibitor of Xa)

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Can you use a serum d-dimer to rule out aortic dissection?

The answer to the question, in 2010, is no.  

There has been a flurry of recent literature about the use of serum d-dimer to rule out aortic dissection. Some studies have shown a sensitivity of nearly 100%, but other studies have shown sensitivities of only 60-70%....pretty abysmal sensitivities. And despite some of the authorities on the subject touting how good the test is, there is not firm literature to support it. Better yet, there are some active medical malpractice cases I am aware of in which the diagnosis of aortic dissection was missed based on a "negative d-dimer."

My suggestion, and the vascular pearl for the day, is to avoid using d-dimer as a aortic dissection rule out strategy until good evidence (if it ever becomes available) exists. I know that people are using this test to rule out the disease, just realize that EVERY time I have ever given a talk on acute aortic disasters, 2-3 people from the audience always share that they had a case of a "d-dimer negative dissection." 

Be careful....

Women are more likely to be misdiagnosed than men when they present with acute coronary syndromes. There are several possible reasons for this:
1. Women are more often older and more often have diabetes, both of which are factors involved in atypical presentations.
2. Women present with chest pain less often than men. On the other hand, women are more likely to present with nausea, vomiting, indigestion, malaise, loss of appetitie, or syncope than men.
3. When women do have chest pain, they are more likely to report pain that has atypical features, such as radation to the right arm or shoulder, front neck, or back; and the pain is more often described as sharp, stabbing, or tansient.

The bottom line is something that I've believed since high school: women are confusing...!

[the references for this ACS information comes from many different sources, but if anyone needs a good review on this topic, just email me: amattu@smail.umaryland.edu]

Uveitis and Iritis Treatment:

• Once the diagnosis is suspected or made ensure that the patient has ophthamology followup.
• Antibiotics are not needed as this is not an infectious process.
• Pain control is the painstay of therapy (no not narcoletics) but cycloplegics like:
  • Cyclopentolate 0.5-2% 1 gtt TID
  • Homatropine 2-5% 1 gtt TID
  • This will relieve pain and photophobia symptoms
• Topical steroid can be initiated to decrease inflammation but should be done in consultation with the ophthamologist
  • Prednisolone 1% 1 gtt every 1-6 hours.

Quinolone Induced Deliurim

Just to give you another reason NOT to give a quinolone - aside from the C. diff. This adverse effect occurs with quinolones unlike many other antibiotics. It can prolong hospital stay, cause falls and further medical work ups. Some risk factors are:

• Elderly
• Renal Insufficiency
• Benzodiazepine dependence (will actually precipitate withdrawal since quinolones displace the BDZ from the receptor - you have probably done this to a patient if you think about it, that may be why they went crazy)
• Epilepsy - can cause seizures especially with NSAIDs

-- While we typically associate seizures within the context of alcoholism with physiologic withdrawal, studies have shown that there is a dose-dependent relationship between the consumed amount of alcohol and the onset of seizure activity, independent of alcohol withdrawal.

-- Specifically, Ng and colleagues found a 3-fold increase in seizure occurance with 50 to 100 grams of ethanol per day, compared to an 8-fold increase with 101 to 200 grams of ethanol per day.

-- This study further found that ex-drinkers (abstention for >= 1 yr.) were not at any increased risk of seizure and that drinkers who had seizures did so well outside of the conventional window of withdrawal.  

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Defining Acute Kidney Injury (AKI)

• In the pearl from 1/5/10, I highlighted the association of AKI with increased morbidity and mortality in the critically ill along with the avoidance of nephrotoxic medications.
• Currently, two sets of criteria (RIFLE and AKIN) can be used to identify patients with AKI
• According to AKIN, the current diagnostic criteria for AKI is:
  • an absolute increase in serum creatinine > 0.3 mg/dL OR
  • a > 50% increase in serum creatinine from patient baseline OR
  • urine output < 0.5 ml/kg/hr for > 6 hours
• For the critically ill ED patient, the most common causes of AKI include sepsis, hypovolemia, medications, trauma, rhabdomyolysis, obstruction and abdominal compartment syndrome

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Evaluation of the acutely ischemic limb

Some considerations when evaluating/treating patients with acute limb ischemia:

• Strongly consider anticoagulation (usually with Heparin) early
• Consider the source of the ischemia (LV/LA thrombus, AAA mural thrombus, in situ limb thrombosis)
• Always consider aortic dissection as an etiology of acute limb ischemia (chest pain and leg ischemia)
• Early vascular consult and/or transfer
• Obtain bedside ABIs on suspected cases and remember that diabetics may have normal to falsely elevated ABIs secondary to calcified vessels.
• Common theme in laws suits for missed or delayed cases of limb ischemia: failure to perform and document ABIs

Most people know that the ECG is only diagnostic of ACS approximately in 50% of cases, and in fact patients presenting with ACS can have an initially completely normal ECG in up to 10% of cases. However, traditional teaching is that if the patient is actively having chest pain or other concerning symptoms, the patient with ACS will nearly always have ECG abnormalities. NOT SO, according to a recent study. Researchers from Davis medical center evaluated patients with presumed ACS and normal ECGs, comparing the prevalence of ACS in patients with active symptoms (e.g. chest pain) during the normal ECG vs. patients that were asymptomatic at the time of the ECG. Cutting to the chase, they found no difference in ther rule-in rate between the two groups. In other words, don't be reassured at all if a patients has a normal ECG during symptoms.

This study supports other studies which continually show that an abnormal ECG is excellent at ruling-in disease, but a normal ECG is poor at ruling-out disease. In the absence of a diagnostic ECG, it's all about the HPI, the HPI, and the HPI. And also...the HPI.

[Turnipsee SD, Trythall WS, Diercks DB, et al. Frequency of acute coronary syndrome in patients with normal electrocardiogram performed during presence or absence of chest pain. Acad Emerg Med 2009;16:495-499.]


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Iritis is a common diagnosis in the ED, but did you know it was actually a subset of Uveitis.

Uveitis is an inflammation of one or all parts of the uveal tract which consists of the iris, the ciliary body, and the choroid.
 
The subsets of uveitis are:

1. anterior
2. confined to the iris and anterior chamber -- iritis
3. confined to the iris, anterior chamber, and ciliary body -- iridocyclitis.
4. Posterior uveitis -- choroiditis and chorioretinitis, is uncommon, with the exception of cytomegalovirus (CMV) retinitis in patients with AIDS.

Treatment of iritis and uveitis next week.

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Pediatric Constipation is a common presentation to PED and large percentage of GI clinic patient volume

Defined as less than 2 stools per week for two weeks with hard, large pellet like stools

Broad Differential includes functional constipation (most common), stricture, obstruction, celiac disease, Hirschsprung, hypothyroid, Cow's milk protein allergy, CF and spina bifida.  Always inspect the spine and perform rectal

Success of treatment is based on the aggressive nature of treatment and timing of treatment.  Ttreatment is longer and more difficult if patient has to wait on referral to GI specialist.

• Clean out with enema and stool softener (miralax BID for two days, followed by daily maintenance regimen is most common)
• Cheaper and effective regimens include mineral oil, kondremul or lactulose
• Encourage behavioral therapy with routine toilet time and rewards
• Increase fiber in diet to 8-10 grams for toddlers, 12-14 preschool and 14-16 for school age
• Initial treatment is safe and does not require electrolyte monitoring.
• Failed treatment and bounceback may require GI consult, inpatient Golytely therapy with electrolyte monitoring

As we are now into the winter months, exposures to ethylene glycol (antifreeze) and methanol (windshield washer fluid) increase.  Here is a good mnemonic for sorting through an anion gap metabolic acidosis:

C – cyanide, carbon monoxide
A – alcoholic ketoacidosis, acetaminophen (massive OD)
T – toluene (chronic from glue sniffing)
M – methanol, metformin
U – uremia
D – diabetic ketoacidosis
P – propofol infusion syndrome, propylene glycol, paraldehyde
I – iron, isoniazid, ibuprofen (massive OD)
L – lactic acidosis
E – ethylene glycol
S – salicylates, starvation ketoacidosis

• While seizure is rarely associated with stroke during its hyperacute phase, Arboix found that the development of epileptic strokes within the first 48 hours post-stroke occurs about 2.4% of the time and portends a higher degree of in-patient mortality.
• Seizure activity in the setting of acute stroke is more commonly associated with hemorrhagic types (4.3 % of cases), compared to just 2% with ischemic strokes.
• Younger age, acute confusional states, hemorrhagic strokes, cortical strokes, and strokes affecting the frontal, parietal, occipital, and temporal lobes were found to be risk factors for stroke-related seizures.
• The use of prophylactic anti-epileptic medication in the acute phase of stroke varies and, some say, requires further research; such treatment is more commonly reserved for use in hemorrhagic stroke patients, however, if at all.

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The term Sepsis is frequently and colloquially used to describe "sick" patients; but accuracy requires understanding the specific criteria of Sepsis and its associated syndromes.  Following are the defining criteria for SIRS and Sepsis:

SIRS

at least 2 of the following:

Temp >38C or <36C

Heart rate >90

RR> 20 or pCO2<32mm Hg

WBC>12,000, <4,000 or >10% bands

Sepsis:

Systemic response to infection, manifested by 2 or more SIRS criteria with a source of infection confirmed by culture or a clinical syndrome pathognomic for infection.

Severe Sepsis:

Sepsis associated with acute organ dysfunction, hypoperfusion or hypotension; including lactic acidosis, oliguria or altered mental status.

Septic Shock:

Sepsis-induced hypotension not responsive to fluid resuscitation.

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Altered Mental Status-Three Diagnoses That Can "Bite You On The Buttocks"

When evaluating the patient who is altered, consider the following diagnoses:

1. DTs-seems simple enough, right? Remember that some altered patients will not be able to give a history of alcoholism. And this is definitely a diagnosis that can sneak up on you. Bottom line: consider DTs in ALL patients with a delirium.

2. Wernicke's encephalopathy-can also be very difficult to detect. Consider in ALL alcoholic patients with altered mental status and give Thiamine. 

3. Herpes encephalitis-speaking from personal experience, this diagnosis can be extremely tough to diagnose. Consider giving emperic Acyclovir in patients with WBCs in their CSF and a negative gram stain. And don't forget to send off a Herpes PCR. As far as clinical presentations, CNS Herpes can present with a wide spectrum of findings, from isolated headache, to new psychobehavioral changes, to severe depression of consciousness and coma. Be aware that this diagnosis isn't common but failure to initiate Acyclovir may be a fatal mistake. 

Though most people know that therapeutic hypothermia is indicated in resuscitated victims of cardiac arrest, is it safe if that cardiac arrest victim is also being treated for STEMI? Do you need to worry about increased bleeding complications in these patients that are receiving anticoagulants, lytics, PCI, or other standard "bleeding" medications? Are these patients at increased risk for hemodynamic instability with therapeutic hypothermia?

Recent studies have demonstrated that therapeutic hypothermia in acute MI patients receiving other standard treatments (i.e., anticoagulants, etc.) is SAFE: it is associated with no increase in bleeding complications (1), no increase in time to balloon inflation (2), and no increase in hemodynamic instability or malignant arrhythmias (3).

1. Schefold JC, et al. Mild therapeutic hypothermia after cardiac arrest and the risk of bleeding in patients with acute myocardial infarction. Int J Cardiol 2009;132:387-391.
2. Knafelj R, Radsel P, Ploj T, et al. Primary percutaneous coronary intervention and mild induced hypothermia in comatose survivors of ventricular fibrillation with ST-elevation acute myocardial infarction. Resuscitaiton 2007;74:227-234.
3. Wolfrum S, Pierau C, Radke PW, et al. Mild therapeutic hypothermia in patients after out-of-hospital cardiac arrest due to acute ST-segment elevation myocardial infarction undergoing immediate percutaneous coronary intervention. Crit Care Med 2008;36:1780-1786.

Acute paronychia

• Usually result from minor trauma of the skin around the fingernail such as biting, manicures, picking a hangnail or finger sucking.
• Staphylococcus aureus is the most common infecting organism. However other mouth flora such as Streptococcus and Pseudomonas species, gram-negative bacteria, and anaerobic bacteria can also be a cause.
• Recommended treatement consists of incision and drainage and placing the patient on  amoxicillin /  clavulanic acid or clindamycin to cover all the organisms noted above.

Hyperleukocytosis is often seen in acute presentations childhood leukemias, and is defined as a WBC count of greater than 30-50K.  Complications usually arise at counts greater than 300, however, keep in mind that automated cell counters may underestimate very high white counts.

Complications include:

• Hyperviscosity Syndrome / Leukostasis
  • Risk of CVA, PE, Mesenteric Ischemia, etc.
• Tumor Lysis Syndrome (TLS)
  • Risk of fatal arrhythmia, may monitor with K, LDH, Uric Acid
• Disseminated Intravascular Coagultion (DIC)

Treatment:

• EMERGENT LEUKOREDUCTION APHERESIS, aka Leukopheresis
• This is a true emergency - if you are at a facility without leukopheresis capability, the fastest transport mode possible is indicated - fly, don't drive
• Temporizing measures include fluids, fluids, and fluids
• Allopurinol / Rasburicase may be considered, but not if this will delay transport, especially if there is no evidence of TLS - this decision may be made in consultation with the pediatric heme/onc specialist who is helping to arrange for leukopheresis

SUCCIMER (DMSA)

• An oral agent used for the chelation of heavy metals, such as LEAD, ARSENIC and MERCURY
• Forms a water soluble agent that chelates the heavy metal, which are renally excreted
• Most common side effects are rashes, urticaria and GI
• A serious adverse effect is neutropenia, which is rare