UMEM Educational Pearls

Important things to document in acute ischemic stroke cases from a medicolegal aspect:

-- time of onset
-- time of diagnosis
-- why tPA given or not given (the longer note for NOT giving it; 90% of related litigation cases based on NOT giving tPA.)
-- date and time on each side of note of every page
-- make it legible
 

 

Hypertension and Epistaxis

We commonly encounter patients with epistaxis who are found to be hypertensive. Some have taught over the years that hypertension causes nosebleeds and that some nose bleeds won't stop until the BP is lowered...

Some pearls about HTN/Epistaxis:

• Most patients we see with hypertension are not experiencing epistaxis, casting serious doubt on a causal relationship
• Studies show that the degree of blood pressure elevation does not correlate with risk of nose bleed
• No studies have ever shown that acute BP reduction in the ED for a nose bleed is beneficial or reduces bleeding
• Much of the debate is sparked by our ENT colleagues who swear that hypertension leads to nose bleeds and that bleeding will not stop until the BP is "treated." Much of this is based on experience with patients in the OR or IR suite. These blood pressures tend to be treated with IV antihypertensives by the ENT folks, and they feel pretty strongly about this relationship.

Beta adrenoreceptor agonists administered by nebulization (e.g. albuterol nebulizers) are thought to be rapidly effective for lowering serum potassium levels in hyperkalemic patients. The mechanism is via a transient shift of the potassium intracellularly. It makes sense. But don't count on it. At least not much. The truth is that the beta-agonist nebs work much slower than you might think. Though they are quickly effective for bronchospasm, the potassium-shifting effect takes at least 30 minutes, and there's not much peak effect for perhaps as many as 60 minutes. Also, the "peak effect" is only approximately a 1.0 mmol/L reduction...and that's with a 20 mg dose. That's 8-times the normal dose than a typical albuterol neb (one of those albuterol "bullets" has 2.5 mg in 3 cc of solution, so a 20 mg dose would be 24 cc of the albuterol solution). The bottom line is that albuterol nebs are not really effective treatment, even transient, for patients with severe hyperkalemia. If you want do something while people are trying to gain IV access on a "tough stick," then it's certainly better than nothing. Ask the nurses or respiratory techs to start continuous nebs...but the IV calcium and insulin are still the key early temporizing measures to focus on until you've got elimination measures underway (kaexylate, hemodialysis, etc.). [Weisberg LS. Management of severe hyperkalemia. Crit Care Med 2008;36:3246-3251.]

Just a quick remainder that Thrombotic thrombocytopenia Purpura, TTP, is typically described as a pentad of symptoms:

1. Neurological symptoms such as altered mental status, stroke, or headache
2. Renal failure
3. Fever
4. Thrombocytopenia (low platelets) associated with purpura
5. Microangiopathic hemolytic anemia

Not all symptoms need to be present and it would be rare for you to see the full pentad.  Consider the diagnosis and request that the lab due a manual differentiation or blood smear.  It is there that they will notice schistocytes, fragmented RBCs, that will help clinch the diagnosis.

Most cases of TTP are idiopathic (~60%) but secondary TTP is known to occur with cancer, pregnancy, HIV, bone marrow transplantation, immunospressive drugs like cyclosporin and tacrolimus, and platelet aggregation inhibitors such as cloperidol.

Treatment consists of plasmapheresis, plasma exchange, immunospression with steroids, Rituximab, and other chemotherapies.

CO is formed from the incomplete combustion of carbon materials, eg. fires, stoves, portable heaters CO reversibly binds hemoglobin, producing carboxyhemoglobin (HbCO). This causes oxygen to bind more tightly to hemoglobin, releasing less in the tissues. Because of this, it affects the organs with the highest oxygen requirements most profoundly (eg. brain and heart).

Symptoms are mainly neurological and cardiovascular, but may include a wide variety of non-specific symptoms. The initial symptoms of CO poisoning may include headache and flu-like illness progressing to confusion, agitation, lethargy, seizures and coma.

Place patients on 100% oxygen to decrease the half-life of HbCO. Though controversial, HBO therapy is thought to decrease the incidence of neurologic sequelae. HBO therapy should be considered for patients with a HbCO level above 20%, severely symptomatic patients with lower levels, and pregnant patients. Remember that pulse oximetry will not be accurate.

Show References

** Fosphenytoin (Cerebyx) is a pro-drug of Phenytoin (Dilantin).

** Differences between fosphenytoin and phenytoin are primarily due to fosphenytoin being more water soluble.
 

Fosphenytoin versus Phenytoin:
•     Fosphenytoin  >  less risk for cardiac-related adverse effects (propylene glycol not required for solubilization)
•     Fosphenytoin >  lower risk of local skin and subcutaneous irritation during infusion 
•     Fosphenytoin > can be given intramuscularly
•     Fosphenytoin >  can be infused at a faster rate (20 mg/kg phenytoin equivalents (PE’s) load at a rate of 100 to 150   mg of PE’s/minute) due to its safer side/adverse effects profile.

Hemodialysis Catheters

Two weeks ago, we had a PEA arrest of a patient receiving HD.  A significant delay occurred in administering fluids and medications as a result of "no iv access".  Don't forget that in these situations you can use the hemodialysis catheter.

• Typically these are double-lumen catheters in the IJ or femoral vein; one lumen carries blood to the HD machine and the other returns it to the patient
• Importantly, each lumen is equivalent in diameter to an introducer catheter (8 French) - permitting rapid flow
• Fluids and medications can be rapidly given through these catheters in code situations

Warfarin-Induced Skin Necrosis (WISN)

Some pearls about a rare, but serious side effect of Warfarin...

• WISN Occurs in 0.01-0.1% of patients taking Warfarin
• More common in middle-age, perimenopausal women being treated for DVT/PE
• Symptoms usually begin on days 3-6 of Warfarin treatment
• Underlying pathophysiology is complex but involves thrombosis of superficial dermal capillaries
• Postulated to be associated with deficiencies of protein C, protein S, and antithrombin III
• Rash is most common on the breats, with thighs/buttocks being second most common site (see picture)
• Diagnosis usually made clinically based on appearance of rash
• Treatment is aimed at restoring Vitamin K dependent clotting factors by administering Vit K and FFP
• For patients with the need for anticoagulation (DVT/PE, etc.) Heparin therapy is usually started

 

55 yo female presented to the ED on the day of hospital discharge for evaluation of this rash.

The rash began 4 days after starting Warfarin. Was being treated for a DVT.

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Sodium bicarbonate A recent review of the literature revealed to me something which I never knew about treatment of hyperkalemia: sodium bicarbonate doesn't work the way we thought. In fact, there's no good evidence indicating that it actually produces a substantial shift of plasma K concentration. Our original teaching was based on prolonged (4-6 hour) infusions of bicarbonate, but short-term infusions do not seem to work. Insulin, on the other hand, is effective and works within 20 minutes. [Weisberg LS. Management of severe hyperkalemia. Crit Care Med 2008;36:3246-3251.]

SIDS

Sudden infant death syndrome (SIDS) is defined as the sudden death of an infant younger than 1 year that remains unexplained after a thorough case investigation, including the performance of a complete autopsy, examination of the scene of death, and review of the clinical history.

SIDS is the single most common cause of death in infants aged 1 mo to 1 yr

Education is key for prevention of these tragic events:

Following the "Back to Sleep" campaign, federal SIDS researchers have conducted annual surveys to examine how infant sleep practices and SIDS rates have changed.  The rate of prone sleeping for infants decreased from approximately 75% in 1992 to a low of 11.3% in 2002

Since 1992, SIDS rates have fallen approximately 58%. In 2002, the National Center for Health Statistics reported a total of 2295 SIDS deaths nationwide for a SIDS rate in the United States of 0.51 per 1000 live births.

Bed-sharing may lead to compromise of the infants' airway because the infant may be suffocated by soft, loose bedding or a sleeping adult.

Cosleeping on a couch or sofa is associated with an unusually high risk for SIDS and should be avoided.

Tryptophan - a precursor to melatonin, it is often blamed for the post prandial coma that many go into after a big turkey dinner. Never mind the 5000 kcals that was consumed during the meal. The supplement really doesn't help with sleeping. Interestingly, turkey isn't even in the top 10 or 20 of foods that contain tryptophan. The top five are:

1) Game meat (Elk): 746 mg of tryptophan

2) Seaweed (Spirulina): 736 mg of tryptophan

3) Spinach: 690 mg of tryptophan

4) Egg White: 673 mg of tryptophan

5) Soy protein: 630 mg of tryptophan

Supplements of L-tryptophan have been contaminated with a compound that has been associated with eosinophilia myalgia syndrome.

 

Stress Related Mucosal Injury (SRMI)

• As the length of stay for many of our critically ill patients continues to rise, it is important to think about some preventative therapies
• SRMI is the term used to describe gastric mucosal erosions that occur in the critically ill
• SRMI can be demonstrated in 75 - 100% of critically ill patients within 24 hours and can cause clinically apparent bleeding in up to 25%
• Independent risk factors for SRMI include mechanical ventilation, coagulopathy, and a prior history of gastritis or peptic ulcer disease
• Additional risk factors in our ED patient population include sepsis, hypotensive states, severe head injury, multisystem trauma, and renal failure
• Typically an H₂ antagonist is provided (i.e. ranitidine or famotidine).  Currently there is no evidence of superiority of PPIs over H₂ antagonists in preventing SRMI
• Pearl:  the best agent to give is probably sucralfate - there is a slightly higher incidence of bleeding compared to ranitidine; however, ranitidine is associated with a much higher incidence of nosocomial pneumonia.  The risk and mortality associated with nosocomial pneumonia in these patients outweighs the minimal risk of major hemorrhage associated with SRMI

What Hypertensive Patient Needs a Workup for End-Organ Damage?

Ah, the age old question...which hypertensive patients need an ED workup for end-organ damage? The "workup" for patients includes renal function, urinalysis, CXR, ECG, etc.

Some pearls regarding working patients up: 

1. Asymptomatic patients in general do not need a workup. There is pretty good literature that shows you just won't find much (expecially anything that will change your treatment plan) if you go hunting in this group of patients.
2. If you set asymptomatic patients aside, you won't find much good data on how much of a workup other patients need. Does a 45 yo patient with a BP of 160/110 and a mild HA need a serum creatinine? What if they have had some mild, atypical CP? The answer is...no one knows. Much of what we we do depends on what we were taught and our current mood. 
3. Asymptomatic patients (truly asymptomatic) don't need chest xrays and ECGs as a rule of thumb...what you find won't help you make a decision. If you find LVH on the ECG, so what? 
4. Obtaining a serum creatinine makes sense, especially of you are going to start a BP agent. 
5. There is a pretty good study by Karas, et al. that showed that a urinalysis without protein or blood predicts a normal creatinine. Use caution, however, if you use this as a screen for renal disease, because many patients with HTN spill protein (despite a normal creatinine)

Third Trimester Bleeding:

• Estimated to occur in 4% of Pregnancy
• 50% will have a benign cause, the other 50% will have a life threatening cause
• Life Threatening Causes:
  • Placenta Abruption
  • Placenta Previa
  • Uterine Rupture
  • Vasa Previa (fetal vessels crossing or running in close proximity to the inner cervical os.
    
• Benign or Non-OB Causes
  • Contact Bleeding (local trauma)
  • Cervical Inflammation (i.e. infection)
  • Cervical effacement and dilation
  • Cervical cancer
  • Other sites:
    • rectal bleeding
    • urinary bleeding
• Evaluation:
  • ABC's: Stablilize mother, consider 2 large bore IVs
  • Consult OB/GYN early (most centers with OB/Gyn will have these patients evaluate and treated in Labor and Delivery), if not readily available complete evaluation as listed below:
  • Initially avoid bimanual exam
  • Obtain baseline labs (CBC, Coags, Chemistries, Consider LFTs if suspecting eclampsia or HELLP syndromes). If not known obtain Rh status
  • Fetal Monitioring ideally with continous fetal heart rate and tocometry
  • Sterile Speculum exam for culture and check for active bleeding.
  • Obtain ultrasound.

 

 

Have you seen any elderly patients with altered mental status (AMS) lately? How quickly did you get an ECG on those patients? Elderly patients often present with mental status changes when they develop cardiac ischemia or acute MI, and this is especially common in the oldest of the elder group. Up to one-quarter of patients > 85 yo with myocardial infarction will present to the ED with delirium or confusion. Get the ECG early on these patients...remember, time is muscle! The delay can be deadly.

Local Anesthetic - Bupivacaine (Marcaine) - Sodium channel blocker with duration of action 2-4 hrs (w/epi 3-7 hrs) - Toxic dose is > 2.5 mg/kg or > 175 mg total dose (Infiltrating into SQ) - Bupivacaine 0.25% = 2.5 mg/mL - Inadvertent intravenous injection can result in toxicity - Lethally cardiotoxic with widened QRS, V-tach and neurotoxic with inebriation and seizures - Anesthesia literature reports successful use of Intralipid as an antidote

• Phenytoin (Dilantin) should not be infused at a rate greater than 50 mg/minute, to a total of 20 mg/kg.

• Caution is encouraged while infusing due to the risk of inducing hypotension and cardiac arrhythmias, making cardiac monitoring during infusion mandatory.

• These adverse effects are partly related to the propylene glycol used to solubilize phenytoin.

• Additionally, the risk of local pain and injury, such as venous thrombosis and the purple glove syndrome, increases with rapid infusion rates.

Dopamine in the ED

• Recall that dopamine is an endogenous catecholamine that is a precursor for norepinephrine synthesis
• Despite the popularity of norepinephrine, dopamine is still used by many EPs in the setting of septic shock
• Dopamine produces progressive alpha-receptor stimulation at doses > 10 mcg/kg/min
• Tachyarrhythmias (namely sinus tachycardia) is the predominant adverse effect
• When selecting a vasopressor agent, be sure to check the HR.  If the patient is already tachycardic, the addition of dopamine will only worsen the tachycardia
• Additional important adverse effects are increased intraocular pressure and delayed gastric emptying

Show References

Healthcare Associated Pneumonia (HCAP)....why is this important for the emergency physician?

Most of us are very familiar with the types of pneumonias commonly seen in clinical practice: community-acquired pneumonia (CAP), hospital-acquired pneumonia(HAP), and ventilator-associated pneumonia (VAP). But, some may not be that aware of a relatively newer type of pneumonia that has been well-defined, healthcare-associated pnemonia (HCAP). Experts in infectious disease and critical care now say that we (the ED) should be assessing ALL pneumonia patients for HCAP risk factors.

Why care, you ask?

• Higher mortality than CAP
• May look like CAP
• Treated much differently than CAP

Risk factors: (most are common sense)

• Nursing home or extended care facility resident
• Recently admiited to a hospital for 2 or more days in the preceeding 90 days
• Home wound care or attending a clinic for wound care
• Dialysis patient
• Home infusion therapy (antibiotics)
• Immunosuppresive therapy or disease

Treatment:

• 3 drugs....not like treatment of CAP!
• Usually a combination of a big gun anti-pseudomonal (e.g. Pip/Tazo) combined with a broad spectrum respiratory fluoroquinolone (e.g. Moxi), combined with Vancomycin
• Key difference between treatment of CAP and HCAP is consideration for multi-drug resistant pathogens, pseudomonas, and MRSA.

Death from ruptured aortic aneurysms and thoracic aortic dissection has a few key features that often help in distinguishing these entities from other causes of rapid decompensation and sudden death:
1. These aortic disasters have a tendency to present with hypotension but without necessarily any specific complaints of pain (in contrast to common teaching).
2. These aortic disasters tend usually to produce PEA as the initial arrest rhythm.
3. These aortic disasters are often diagnosable on bedside ultrasound (AAA seen when scanning the abdomen; dissections frequently produce pericardial tamponade as they dissect backwards into the pericardial sack).

ALWAYS take a look at a patient's aorta and pericardium with the ultrasound when that patient presents in extremis or in cardiac arrest. The results can help make some critical diagnostic and therapeutic decisions.

[recent article related to this topic: Pierce LC, Courtney DM. Clinical characteristics of aortic aneurysm and dissection as a cause of sudden death in outpatients. Am J Emerg Med 2008;26:1042-1046.]