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What is the diagnosis? (DON'T LOOK DOWN AT THE ANSWER)

50 year-old male prisoner s/p assault, + LOC

CT shows right-sided traumatic subarachnoid hemorrhage

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Therapeutic hypothermia is generally accepted as a useful intervention that should be employed in patients that are resuscitated after cardiac arrest. Many protocols for cooling are relatively complicated, involving endovascular catheters, cooling blankets, cooling helmets, or other devices that are expensive and not widely available. The cooling process can actually be fairly simple, however, with ice and cool IV fluids. The most recent study that demonstrated this used nothing more than application of ice to the groin, neck, and axillae; and administration of 4^o C IVF infused at 30cc/kg at 100ml/min via two peripheral catheters. Sedation or paralysis + intubation was used as per the norm.

Patients receiving this simple intervention were able to achieve goal temperature of 32^o-34^o C within 3-4 hours, and hypothermia was maintained for a full 24 hours before rewarming.

The study shows that expensive equipment and complicated protocols are not necessary for therapeutic hypothermia.

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                Involves an avulsion of the flexor digitorum profundus  (FDP) tendon from its insertion on the distal phalanx.

     Ring finger is most commonly involved.

                Usually occurs from a grabbing attempt (resulting in forced DIP extension during maximal FDP contraction) as would occur while attempting to grab someone’s jersey such as in football or rugby.

Clinically, there is normal passive DIP ROM with loss of active flexion. Examine this by asking the patient to flex the fingertip at the DIP while the PIP joint is held in extension.

*Remember that patients with a 90% full-thickness tendon laceration may still have normal (albeit painful) range of motion. The examiner must evaluation the strength of the tendon against resistance. This injury is commonly missed as it is diagnosed as a “jammed” finger.

Plain films may show a bony avulsion, but are often negative.

Treatment is primary repair especially with large bony fragments. Partial ruptures can be treated nonoperatively at the discretion of the hand surgeon.

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Hyponatremic seizures are a frightening entity.  Anticonvulsants don't work well, and will likely cause apnea well before they halt the seizure.  Hypertonic saline carries with it the fear of inducing central pontine myelinolysis (CPM) with overly rapid correction of the hyponatremia.  

However:

• CPM usually occurs at sodium level corrections of >8 mEq/L/day
• Hyponatremic seizures are usually stopped with a correction of only 3-5 mEq/L

So, you can safely correct hyponatremia rapidly in the setting of seizures. Do it like this:

Give 2-3 mL/kg of 3% NaCl in rapid sequential boluses, until seizures stop.  A theoretical maximum dose is 100mL/kg, but recall that only a relatively small correction is required to stop the seizure.  

After you've stopped the seizure, correct the hyponatremia slowly, as you would otherwise.

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• Vitamin K can be used intravenously for management of the NON bleeding patient with a high INR (>9).
• Although anaphylactoid reactions have been described, most cases occurred with large doses of vitamin K, administered rapidly, and with little dilution.
• It is estimated that the incidence of anaphylaxis is 3:10,000 doses.
• The subcutaneous route of administration is not recommended because of its delayed and unpredictable responses.

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• The National Institute of Health Stroke Scale (NIHSS) is a well-validated, highly reproducible tool that is widely used to measure neurologic deficit and as a scoring system for stroke intervention.
• This scale is heavily weighted toward recognizing deficit due to anterior circulation strokes, however, while that due to posterior circulation strokes receives fewer points.
• One study found that nearly 1% of patients with MRI-confirmed acute ischemic stroke patients scored zero points on the NIHSS, and that the majority of these were posterior strokes.  These types were more likely to present with truncal ataxia (most commonly), headache, vertigo, and nausea.
• Take home points:  (1) The NIHSS should not replace a thorough neurological examination.  (2) Consider posterior stroke as the source of persistent symptoms in patients with an NIHSS score of zero. 

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Posterior reversible encephalopathy syndrome (PRES) is a syndrome of visual loss, headache, altered mental status, and seizures, typically with severe hypertension. PRES usually occurs with hypertensive encephalopathy or ecclampsia, although cyclosporin and tacrolimus use have been implicated. 

PRES is due to a combination of endothelial damage, impaired auto-regulation and increased cerebral perfusion pressure. Classic CT and MRI findings are parietal-occipital, cerebellar, or brainstem cortical and subcortical edema. 

Early recognition and symptomatic treatment is key; IV anti-hypertensives (hypertensive encephalopathy), anti-epileptics (seizures), IV magnesium and emergent delivery (ecclampsia), and discontinuing offending medications (cyclosporin and tacrolimus).  

With treatment, partial to complete recovery is normal, although residual neurological and visual deficits may persist.

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60 year-old male s/p assault. + LOC. Awake and normal neuro examination on arrival. Deteriorates in the ED after about an hour....

Diagnosis: Epidural Hematoma

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Induced hypothermia is associated with a decline in serum potassium levels. The cold myocardium is already mildly predisposed to arrhythmias, and the combination of hypokalemia + hypothermia appears to increase the risk of polymorphic ventricular tachycardia. Two simple measures should be taken during post-arrest therapeutic hypothermia:
1. Correct hypokalemia before and during cooling.
2. Monitor the patient's potassium level and QT interval during cooling, and correct as needed.

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Peroneal Tendon Subluxation: The Other Ankle Sprain

• Peroneal tendon subluxation is an uncommon cause of lateral ankle pain that is often misdiagnosed as a simple ankle sprain.
• It is commonly associated with sports that require cutting such as skiing, basketball, soccer, and football.
• The subluxation occurs when there is a forceful contraction of the peroneal tendon while the foot is dorsiflexed and inverted.
• Patients will often complain of pain at the posterolateral ankle that started as a forceful pop.  They may also complain of snapping or popping around the lateral malleolus as it continues to sublux.
• On clinical exam, the patient will often have pain along the  retrofibular groove. The peroneal tendon can be tested by actively dorsiflexing and everting the ankle from a plantar-flexed and inverted position.  You should be able to see or feel the subluxation. Passive circumduction of the ankle may also recreate the subluxation.
• Conservative management (i.e.: ankle brace, cast or walking boot) is associated with a low success rate; therefore, these patients should be referred to sports medicine or orthopaedics for possible operative repair.

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Naloxone is the epitomy of an antidote with complete reversal of opioid toxicity within 60 seconds of administration. Remember your clinical endpoint should be respiratory effort. If you utilize "the vial" of either 0.4mg or 2mg and there is a higher probability of withdrawal and for acute lung injury. Here are some tips for administration:

1) IV Access: Try 0.1 mg or even 0.05 mg - anesthesiology typically doses naloxone in micrograms. Reversal is slower so you have to be patient. It is also not as dramatic so closely monitor respirations to see if you have improvement, that may be all that you get. These are probably patients that you don't want that awake anyways.

2) No IV Access: advantage of naloxone is it is bioavailable IV, intranasal and even by nebulizer.  Here you want the dose to be 0.4mg to start for intranasal. Nebulizer is difficult to measure and probably safe to start with 2mg in the nebulizer container.

There is a difference when you know it is an opioid overdose and are reversing apnea versus a diagnostic administration to determine if it is opioid toxicity. In the latter instance you can rationalize the large dose - just be ready and be sure you are not in line of the possible projectile vomiting.

• While seizure patients are often treated with common antiepileptics such as phenytoin and levetiracetam, those with severe refractory disorders may be treated with less frequently used medications such as felbamate.
• Felbamate is reserved as monotherapy or adjunctive therapy for refractory, partial seizures in adults with or without secondary generalized seizure, and as adjunctive therapy for children with partial and generalized seizures due to Lennox-Gastaut Syndrome (condition that causes seizures and developmental delay).
• In patients who present to the ED on felbamate, consider checking a CBC with differential and liver function tests, as it can cause aplastic anemia (relatively rare but 30% fatal) and liver damage (rare but 40% fatal), respectively.
• Signs and symptoms of aplastic anemia include:  fever, sore throat, chills, other signs of infection, bleeding, easy bruising, extreme fatigue, weakness, or lack of energy.
• Signs and symptoms of liver failure include: nausea, extreme fatigue, unusual bleeding or bruising, lack of energy, anorexia, right upper quadrant pain, jaundice, or flu-like symptoms.

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Vancomycin Dosing in the Critically Ill Obese Patient

• Obesity related changes to drug metabolism and distribution can significantly impact the critically ill obese patient.
• Many meds can either be underdosed or overdosed depending on which body weight (ideal vs. actual) is used.
• With the increased incidence of MRSA infections, vancomycin is often included in the initial antibiotic selection for most critically ill ED patients.
• Importantly, vancomycin is one of the most studied antibiotics in obese patients.
• Recent guidelines recommend that an initial vancomycin dose of 25-30 mg/kg actual body weight be considered for any critically ill patient, with subsequent dosing dependent upon renal function and trough levels.

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Isoproterenol is a non-selective beta-1 and beta-2 agonist. The beta-1 effect produces an increase in heart rate, and the beta-2 effect produces mild vasodilation. Two times to consider its use are the following:
1. For overdriving pacing in cases of intermittent torsades de pointes when magnesium is ineffective.
2. For intractable bradycardia, this is another option besides dopamine or epinephrine. Because of the vasodilation, isoproterenol might be preferred to these other drugs when the bradycardia is accompanied by severe hypertension or when vasoconstrictors are not desired.

The drug is not commonly used anymore but is effective in treating persistent bradycardia or for overdrive pacing in patients with intermittent torsades de pointes when magnesium is ineffective. Be wary, though, that the beta-2 effect produces vasodilation so there may be a mild reduction in blood pressure when the drug is used.

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Commotio Cordis

Emergency medicine & sports medicine physicians often cover sporting events where athletes are at risk of commotio cordis

• 2nd most common cause of sudden cardiac death in young athletes in the US (HCM #1)
• Young males between 4 and 18 years old are at greatest risk
• 50% of all cases occur during competitive sports (baseball #1)
• Nonpenetrating, blunt trauma to the chest resulting to cardiac arrhythmia and, often, sudden cardiac  death.
• Ventricular fibrillation (VF) is the most common arrhythmia.
• Thought to occur secondary to a precordial impact during an electrically vulnerable portion of ventricular repolarization (10-30 msec before the T-wave peak)
• Treatment:  Immediate chest compressions and early use of an automated external defibrillator (AED) ((effective in only 15% of cases))
• Survival is much improved if resuscitation administered within 3 minutes (25%) than after 3 minutes (3%)
• Differential diagnosis: other causes of sudden cardiac death including HCM, coronary artery anomalies, long QT syndrome, Brugada syndrome, WPW, CAD, myocarditis, arrhythmogenic right ventricular dysplasia

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• syndrome of hematuria at the END of urination
• evidenced by spotting of blood in underwear
• occurs only in boys
• may last up to a year or longer
• symptoms are usually intermittent and recurrent
• physical examination is normal
• renal ultrasound usually helps rule out structural anomalies, but will usually be normal
• self-limited, with no specific therapy other than reassurance
   

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When you think of an acid or base causing a burn, you usually think of the local damage but there is one particular acid that causes systemic illness. Hydrofluoric Acid, found in your local Home Depot in brick/stone cleaning products, can cause severe illness despite a small total body surface area burn and exposure. A recent case report came out that illustrates how deadly HF can be. The reason is that this acid enters the body and chelates cations like calcium and potassium. The abstract is below but essentially hypocalcemia, hypokalemia leading to asystole 16hrs after exposure all from a 3% TBSA Burn - very impressive.

Background. Although hydrofluoric (HF) acid burns may cause extensive tissue damage, severe systemic toxicity is not common after mild dermal exposure. Case. A 36-year-old worker suffered a first-degree burn of 3% of his total body surface area as a result of being splashed on the right thigh with 20% HF acid. Immediate irrigation and topical use of calcium gluconate gel prevented local injury. However, the patient developed hypocalcemia and hypomagnesemia, hypokalemia, bradycardia, and eventually had asystole at 16 h post-exposure, which were unusual findings. He was successfully resuscitated by administration of calcium, magnesium, and potassium. Conclusion. This report highlights a late risk of HF acid dermal exposure.

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• Ischemic strokes often present as lacunar infarcts, wherein flow along the deep penetrating vessels of the middle cerebral artery is compromised.
• These strokes typically present with either purely motor or purely sensory neurologic deficit, in an ipsilateral pattern, often striking parts of the basal ganglia.
• Lacunar infarcts may present in a mild manner and carry the best prognosis for recovery relative to other types of ischemic stroke.

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The incidence and prevalence of thrombocytopenia in the ICU is poorly defined however, it has been found to be an independent predictor of death in the critically-ill. Increased mortality does not appear to be related to bleeding complications. On the other hand, survivors of critical illness tend to recover platelet faster as compared to non-survivors. 

Thrombocytopenia in the critically-ill is a marker for systemic inflammation/infection although the exact mechanisms are unknown. Common risk factors associated with thrombocytopenia in the ICU population are:

Sepsis

Renal failure

High-illness severity

Organ dysfunction

Bottom line:  Thrombocytopenia in the critically-ill is associated with increased mortality. 

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The September 5 2006 issue of Circulation contained a guideline, based on collaboration between the American Heart Assn, the American College of Cardiology, and the European Society of Cardiology, indicating that procainamide was preferable to amiodarone for the treatment of stable monomorphic ventricular tachycardia.

The 2010 AHA Guidelines have now also listed procainamide as the preferred drug for stable monomorphic ventricular tachycardia, giving it a Class IIa ("probably helpful") rating vs. amiodarone which has a Class IIb ("possibly helpful") rating. [thanks to Dr. Mike Abraham for pointing this out]

Procainamide is also the safest drug for use in tachydysrhythmias when an accessory pathway (e.g. Wolff-Parkinson-White syndrome) is present.

The caveat is that neither procainamide nor amiodarone should be used in the presence of a prolonged QTc.

Acute care physicians should (re-)familiarize themselves with the use of procainamide, and emergency departments should maintain quick access to this drug to stay up-to-date with current national and international guidelines.

 

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