Aseptic meningitis is meningitis with negative bacterial cultures. Overall, viral infections are the most common etiology, however medications can also cause this illness.
Well known causes of aseptic meningitis include: antimicrobials (particularly sulfamethoxazole/trimethoprim), NSAIDS, antivirals (valacyclovir), and antiepileptics.
Recently an abstract was published that suggests that patients on levetiracetam have a higher risk of developing aseptic meningitis than those on topiramate and gabapentin. Lamotrigine has also been implicated, but appears to have a lower risk than levetiracetam, topiramate and gabapentin.
Tranexamic Acid (TXA) topically applied was compared to anterior nasal packing in 216 patients with acute anterior epistaxis. Cotton pledgets (15 cm) soaked in injectable TXA (500 mg/5 ml) were inserted into the bleeding nostril and removed after bleeding had arrested. This was compared to standard anterior packing.
RESULTS
| TXA Anterior packing |
| % pts bleeding stopped in 10 min: 71% 31.2% |
| Discharge after 2 hours 95.3% 6.4% |
| Rebleeding in 24 h hours 4.7% 11% |
| Satisfaction scores 8.5 4.4 |
Bottom line: topical tranexamic acid looks promising for control of uncomplicated anterior epistaxis.
Tranexamic acid (TXA) is an antifibrinolytic that prevents clot breakdown by inhibiting plasminogen activation and plasmin activity
The CRASH-2 trial enrolled 20,211 adult trauma patients with significant hemorrhage (SBP <90 or HR 110) or at significant risk of hemorrhage
Patients were randomized to 1 gram TXA over 10 minutes followed by an infusion of 1 gm over 8 hours vs placebo
There was a significant reduction in the relative risk off all cause mortality of 9% (14.5% vs 16%, RR 0.91, CI 0.85-0.97, p = 0.0035)
The patients that benefited most were those most severely injured, and in those treated in less than 3 hours of injury.
It has linear, predictable pharmacokinetics, achieves maximal concentration within 1-2 hours, is 50% renally excreted, and has a half life is 9-11 hours.
Edoxaban was evaluated in a recent trial comparing warfarin in patients with atrial fibrillation.
The primary end point or first stroke or systemic pulmonary embolic event occurred in 1.5% with warfarin, compared with 1.18% in the high dose edoxaban (HR 0.79; 97.5% CI 0.63-0.99, P<0.001). In the intention to treat there were trends favoring high dose edoxaban and unfavorable trends with the lower dose.
The principal safety end point of major bleeding occurred in 3.43% with warfarin versus 2.75% with high dose edoxaban (HR 0.86; 95% CI 0.71-0.91, P<0.001).
Bottom line: Both high dose (60 mg) and low dose (30 mg) edoxaban were non-inferior to warfarin with prevention of stroke or systemic emboli, and were associated with significantly lower rates of bleeding and death from cardiovascular causes.
Currently it is approved for use in Japan.
When patients with severe allergies to penicillin (urticarial, bronchospasm, anaphylaxis, angioedema) are excluded, the cross reactivity to cephalosporins is very low (approximately 0.1%)
The reaction is related to structures in the side chain, not the cyclical structure as thought in the past.
There are several cephalosporins with IDENTICAL side chains that should not be given to patients with allergies to specific penicillins, namely:
ACLS recommendation for procainamide in tachycardic rhythms is:
Loading dose 20 mg/minute (up to 50 mg/minute for more urgent situations) until:
Maintenance infusion is 1 to 4 mg/min.
An easier method for dosing acute onset atrial fibrillation in stable patients was used in the Ottawa Aggressive Protocol, in which they administered 1 gm over 60 min, which was interrupted if BP < 100 mmHg; if corrected by a 250 ml IV bolus, the infusion was resumed. This was not used, however if the patient was to be admitted.
A strategy for treating stable monomorphic VT with procainamide used:
100 mg IV over 1-2 minutes, repeat as necessary until an endpoint of
If no slowing of the tachycardia occurred with a dose of 400 mg, the administration was ceased.
NMS is most often seen with the typical high potency neuroleptic agents (e.g haldol, fluphenazine)
All classes of antipsychotics can cause NMS, including low potency and newer atypical agents; antiemetics can cause this as well.
Symptoms usually occur after the first 2 weeks of therapy, but may occur after years of use
Signs and symptoms include:
mental status changes
muscular rigidity (“lead pipe”)
hyperthermia (>38 - 40 degrees).
Autonomic instability (tachycardia, tachycardia and diaphoresis)
Treatment includes discontinuation of the offending agent and providing supportive care.
While no clinical trials have ever been undertaken, dantrolene (muscle relaxant) is commonly used.
Bromocriptine (dopamine agonist) may also be used, and amantadine (dopaminergic and anticholinergic agent) is used as an alternative to bromocriptone
Recently, several case reports have documented the successful use of diazepam as a sole pharmacologic agent. This may be an alternative or a supplement to the above agents
A recent article was published in the Journal of Medical Toxicology reviewing the use of sodium acetate for treatment of overdoses and poisonings.
Acetate is metabolized to bicarbonate, causing a net increase in cations; this increased strong anion difference leads to alkalemia.
It has been used to treat acidosis in uremia, diarrhea, and in trauma patients.
Although no studies have been conducted using sodium acetate as an antidote, if bicarbonate is unavailable this is a viable option for management of salicylate overdose, and for qrs widening or arrhythmias due to overdoses.
Sodium acetate, if given rapidly (in animals and hemodialysis patients), causes myocardial depression, hypotension, and hypopnea.
The bolus dose should be given as 1-2 mEq/L given over 15-20 minutes. For the maintenance infusion, dilute 150 mEq diluted to 1 L in dextrose 5%, infuse at 2X the maintenance rate.
It must be diluted in dextrose 5% and NOT normal saline.
Approval of Kcentra™ may open the door for studying treatment of the bleeding patient on newer oral anticoagulants.
Creatine
Adverse effects: weight gain, edema, GI cramping, fatigue and diarrhea