   Endotracheal Tube Size Selection for Neonatal Intubation
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   Anaphylaxis :
Up to 40% of anaphylaxis cases may have no clearly identifiable trigger. Diagnosis is based on the acute onset of symptoms involving two or more of the following body systems:
The first-line and most important treatment for anaphylaxis is the prompt administration of epinephrine. For adults, the recommended dose is 0.5 milligrams given as an intramuscular injection in the anterolateral thigh. For pediatric patients, the epinephrine dose is 0.01 milligrams per kilogram of body weight. If hypotension persists after two doses of epinephrine, intravenous epinephrine or vasopressin may be considered as the next step.   Medications That Might Impair Neuromuscular Transmission
Myasthenia gravis is an autoimmune disorder characterized by fluctuating muscle weakness and fatigue due to impaired neuromuscular transmission. Certain medications can exacerbate or induce a myasthenic crisis by further impairing neuromuscular junction function. Healthcare professionals must be aware of these medications and exercise appropriate caution when prescribing them to patients with myasthenia gravis. Macrolide Antibiotics: Macrolides like azithromycin, clarithromycin, and erythromycin should be avoided if possible in myasthenia gravis patients. These antibiotics can cause a rapid onset of weakness, often within one hour of exposure, by inhibiting the release of acetylcholine at the neuromuscular junction. Fluoroquinolones: Fluoroquinolone antibiotics such as levofloxacin, moxifloxacin, and ciprofloxacin are best avoided in myasthenia gravis patients. The FDA has issued a boxed warning due to their similarity to quinine compounds that directly affect the acetylcholine receptor channel, potentially aggravating myasthenic symptoms. Aminoglycosides: Aminoglycosides like gentamicin, tobramycin, and amikacin should be avoided if possible in myasthenia gravis, especially in cases of critical illness, high dosing, or renal failure, as they pose a higher risk of exacerbating muscle weakness. Intravenous Magnesium: Intravenous magnesium should be avoided if possible in myasthenia gravis patients, as it decreases the sensitivity of the postsynaptic membrane to acetylcholine. If supplementation is necessary, oral administration is preferred to minimize the risk of a myasthenic crisis. Beta Blockers: While beta blockers like metoprolol and labetalol can be used cautiously if the benefits outweigh the risks, they have been associated with respiratory failure in myasthenia gravis patients, particularly those with other contributing factors. Close monitoring and use of the lowest effective dose are recommended. Calcium Channel Blockers: Calcium channel blockers such as diltiazem and clevidipine may be used cautiously in myasthenia gravis if the benefits exceed the risks. However, they have also been associated with respiratory failure, even in patients without prior respiratory symptoms. Antiarrhythmics: Class 1A antiarrhythmic agents like quinidine, disopyramide, and procainamide should be used with caution in myasthenia gravis patients, as they inhibit acetylcholine release at the neuromuscular junction and can lead to respiratory failure. Corticosteroids: While corticosteroids like dexamethasone and prednisone are a standard treatment for myasthenia gravis, they may cause a transient worsening of symptoms in the first two weeks of treatment at high doses. Close monitoring is recommended during this period. Neuromuscular Blocking Agents: Myasthenia gravis patients are more sensitive to nondepolarizing neuromuscular blocking agents like rocuronium and vecuronium, while showing increased resistance to depolarizing agents like succinylcholine. Succinylcholine is generally avoided due to its unpredictability, and dosing for non-depolarizing neuromuscular blocking agents should be reduced by 50%. Summary: Healthcare professionals must exercise vigilance when prescribing medications to patients with myasthenia gravis, as certain classes of drugs can impair neuromuscular transmission and potentially precipitate a myasthenic crisis. By adhering to the recommendations outlined above and carefully weighing the risks and benefits, adverse outcomes can be mitigated for this vulnerable patient population.  Transient Ischemic Attacks
A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by focal cerebral ischemia without acute infarction. TIAs are often called "ministrokes" or "warning strokes" as they confer a high short-term risk of subsequent ischemic stroke, with 10-20% of patients suffering a stroke within 90 days. Around 50% of strokes occur within 48 hours after a TIA. Pathophysiology: TIAs arise from a transient disruption of blood flow to a region of the brain, most commonly due to emboli or local thrombosis from atherosclerotic plaque rupture. Less frequent causes include vasospasm, venous thrombosis, or hemodynamic factors like artery dissection or severe stenosis. The topography of symptoms reflects the vascular territory affected. Clinical Presentation: TIA symptoms are negative (loss of function) rather than positive phenomena like headaches or visual auras seen in migraines. Typical TIA symptoms include unilateral motor weakness, dysarthria, monocular blindness, or sensory deficits corresponding to the area of transiently disrupted blood flow. By definition, symptoms completely resolve within 24 hours. Diagnostic Workup: The diagnostic workup aims to determine the underlying etiology, assess future stroke risk, and guide preventative therapy. Essentials include brain imaging such as CT or MRI, neurovascular imaging such as CT or MR angiography or carotid ultrasound, cardiac monitoring for atrial fibrillation, echocardiography for left heart thrombus or patent foramen ovale, and routine blood tests. Emergent Vascular Imaging: Patients with high-risk TIAs (ABCD2 score greater or equal to 4) or crescendo symptoms should undergo immediate vascular imaging (CT or MR angiography) to identify carotid stenosis or intracranial thrombus amenable to urgent intervention. This can significantly reduce stroke risk if done within 24 hours. The ABCD2 Score considers age, blood pressure, clinical features, duration, and diabetes mellitus, to predict stroke risk accurately at 2, 7, and 90 days post-TIA. Antiplatelet Therapy: Patients with TIA should receive dual antiplatelet therapy (aspirin plus clopidogrel) for the first 21 days, as this confers the greatest stroke risk reduction during the highest risk period. After 21 days, monotherapy is recommended to mitigate bleeding risk. TIA Mimics: Clinicians must distinguish true TIAs from other transient neurological events like migraines, seizures, or metabolic encephalopathies that may resemble TIAs. TIA symptoms are negative (loss of function) rather than positive phenomena like headaches or visual auras seen in migraines. The history, tempo of symptom evolution, and presence of positive phenomena like headaches can help differentiate mimics. Visual Symptoms: Particular attention should be paid to patients presenting with visual field deficits or monocular blindness, which are often wrongly attributed to ophthalmological causes. These may represent retinal TIAs or strokes, carrying high future stroke risk if not properly investigated. Cardiac Evaluation: All TIA patients require screening for atrial fibrillation via ECG, prolonged cardiac monitoring, and echocardiography if indicated. The presence of atrial fibrillation is a major risk factor for embolic stroke, necessitating long-term anticoagulation. Secondary Stroke Prevention: Following a TIA, patients require aggressive medical therapy to prevent future strokes. This includes antiplatelet or anticoagulant therapy, treatment of hypertension, hyperlipidemia, diabetes, smoking cessation, and lifestyle modifications. Summary TIAs mandate urgent evaluation and management to mitigate the high short-term risk of disabling ischemic stroke. Thorough diagnostic workup, emergent vascular imaging, appropriate antithrombotic therapy, and rapid implementation of secondary prevention measures are essential to optimize patient outcomes.  Inborn Errors of Metabolism: Pearls and Pitfalls:
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