The new 2010 AHA Guidelines no longer recommend the use of atropine in caring for patients with cardiac arrest. While it may be useful in vagally-mediated bradycardias, the evidence does NOT support the use of atropine in patients with asystole or PEA; therefore, it has been removed from the cardiac arrest algorithm.
Transverse Myelitis
A group of inflammatory disorders characterized by acute or subacute motor weakness, sensory abnormalities and autonomic (bowel, bladder, sexual) cord dysfunction.
Symptoms are usually bilateral but both unilateral and asymmetric presentations can occur.
Look for a well-defined truncal sensory level
-below which sensation of pain and temperature is altered or lost.
Causes: Autoimmune after infection or vaccination (60% of cases in children), direct infection, or a demyelinating disease such as MS. No cause is found in 15 – 30% of cases.
Incidence: Bimodal peak at 10-19 years and at 30-39 years.
Diagnostic testing: MRI of the ENTIRE spine to both rule out structural lesions and rule in an intrinsic cord lesion. If MRI is normal reconsider the original diagnosis.
Treatment: Steroids are first-line therapy. Dosing is controversial but generally involves high IV doses for 3-5 days (1000 mg methylprednisolone). Plasma exchange is second line for those who don’t respond to steroids.
French LK, et al. Hydrogen peroxide ingestion associated with portal venous gas and treatment with hyperbaric oxygen: a case series and review of the literature. Clinical Toxicology 2010;48:533–38.
Ocular sonography is a fast, simple, and non-invasive tool to detect elevated intracranial pressure (ICP) by measuring the optic nerve sheath diameter (ONSD). Several studies have shown a positive correlation between increased ONSD (>5.7mm) and elevated ICP (>20mmHg). Although ultrasound may not replace CT or MRI to diagnose the cause of the increased ICP, its use as a triage tool can expedite these tests.
The technique:
Please see the references below for more information and, as with any new technique please consult local experts prior to making clinical decisions.
The new 2010 AHA guidelines have provided greater focus on airway issues in patients suffering from cardiac arrest. Amongst the important areas of new emphasis are: (1) Cricoid pressure is no longer routinely recommended during intubation, and in fact it has been given a Class III rating ("harmful"); and (2) there is now a very strong push to use quantitative end-tidal CO2 monitoring (rather than just qualitative confirmation) of the airway after endotracheal intubation.
Dabigatran
Optimal management of subarachnoid hemorrhage requires prognostic understanding and effective communication with neurology and neurosurgical consultants, as well as the patient and their family members.
It is therefore often helpful to utilize and reference the widely recognized Hunt and Hess Scale in grading symptoms of ruptured cerebral aneurysm and subarachnoid hemorrhage severity:
For your convenience, an online Hunt and Hess Scale calculating tool can be found at:
http://www.mdcalc.com/hunt-and-hess-classification-of-subarachnoid-hemorrhage-sah
Ventilation Pearls in the Post-Cardiac Arrest Patient
In honor of Halloween and candy....
Hyperglycemia (> 140 mg/dl) at the time of admission is an independent risk factor for adverse outcomes and mortality both during the hospital stay and long-term in patients with acute MI. Hyperglycemia is associated with adverse platelet function, thrombolysis, and coagulation. Tight glucose control is recommended to begin as soon as possible after admission in patients with acute MI in order to optimize outcomes.
Risk Factors for Spinal Epidural Abscesses
Building on Dr. Corwell's pearl from last week concerning Spinal Epidural Abscess, risk factors for Spinal Epidural Abscesses other than IV drug abuse are:
The infection can occur via three routes 1) hematogenous spread 2) Direct Extension from a local infection such as osteoomyelitis, and 3) iatrogenic introduction which is thought to be responsible for 14-22% of the cases. A catheter in the epidural space for more than 2 days has a infection rate of 4.3%.
Necrotizing Enterocolitis
When a patient presents to the ED with a recent ingestion of a wild mushroom there are three very specific questions you must ask:
1) Exactly what time did you eat the mushroom?
2) Exactly what time did you begin vomiting/diarrhea/GI Sx in general?
3) Are there are more mushrooms that can be brought to ED for identification?
The reason the first two questions are critically important is it determines the total time of onset of toxicity. As a very general rule of thumb, delayed GI symptoms >6hrs is predictive of a possible lethal ingestion of a cyclopeptide containing mushroom like Amanita Phalloides. Immediate symptoms < 6hrs and even more so if within 2 hrs usually indicates ingestion of a nonlethal mushroom that causes GI distress (many mushrooms like Clitocybe nebularis)
Website with pics of the most poisonous mushrooms:
http://scienceray.com/biology/botany/13-deadliest-mushrooms-on-the-planet/
There is a saying:
"There are old mushroom pickers and wise mushroom pickers but no old and wise mushroom pickers"
Classic Cerebrospinal Fluid Characteristics
Increasing literature demonstrates ICU delirium is bad. Delirium in mechanically ventilated patients is an independent predictor for long-term cognitive defects (e.g., managing money, following detailed instructions, reading maps, and developing dementia). The cited study found 80% of patients with ICU delirium had cognitive dysfunction at three months, and 70% had residual dysfunction at one year (33% had severe dysfunction).
You must be aggressive to prevent delirium:
- Implement daily assessment tools (e.g., CAM-ICU)
- Daily awakening and spontaneous breathing trials
- Early patient mobilization
- Aggressive pharmacological treatment of delirium
- For more information: www.icudelirium.org
Magnesium is considered a mainstay of treatment of prolonged QT syndrome leading to torsade de pointe, including those cases caused by drugs. The exact mechanism of action is unknown, though it is thought to stabilize the myocardium. Interestingly, magnesium infusions will not necessarily change the heart rate or QT interval on ECG.
The dose is 2 g IV followed by an infusion (similar to treatment of eclampsia/preeclampsia). The bolus should be given slowly if the patient is relatively stable, but can be pushed over 1 minute in a patient with ongoing torsade that is not responding to electricity.
Epidural compression syndrome encompasses spinal cord compression, cauda equina syndrome, & conus medullaris syndrome.
Causes include:
Measurement of a post-void bladder residual volume tests for the presence of urinary retention with overflow incontinence (a common, though late finding) (sensitivity of 90%, specificity of 95%). Large post-void residual volumes (>100 mL) indicate a denervated bladder with resultant overflow incontinence and suggest significant neurologic compromise. The probability of cauda equina syndrome in patients without urinary retention is approximately 1 in 10,000.
Use this in your daily practice!!
The administration of glucocorticoids can minimize ongoing neurologic damage from compression & edema until definitive therapy can be initiated. The optimal initial dose and duration of therapy is controversial, with a recommended dose range of dexamethasone anywhere from 10 to 100 mg intravenously. Consider traditional dosing (dexamethasone 10 mg) for those with minimal neurologic dysfunction, & reserve the higher dose (dexamethasone 100 mg) for patients with profound or rapidly progressive symptoms, such as paraparesis or paraplegia.
Colic