CCB Toxicity

• CCBs are divided into 2 groups:
  • Non-Dihydropyridines (Verapamil and Diltiazem) à cause a pup (heart) problem
  • Dihydropyridines (Amlodipine, Felodipine, Nifedapine, Nimodipine and Lercanidipine)à cause a pipe (vasoplegic) problem
  • However, in large overdoses receptor selectivity can be lost and the dihydropyridines can cause cariogenic shock.

• Ingestion of >10 tablets of verapamil or diltiazem XR can cause life-threatening toxicity.
• Effects are usually seen within 2 hours following standard preparations but can be delayed up to 16 hours with XR preparations.
• Early signs of toxicity includes a rising glucose (patients are in a drug induced hypoinsulinaemic state) and lactate.
• Typical signs include bradycardia, heart blocks and hypotension. If left untreated they can develop refractory shock and die.

Management of CCB overdose:

1. As always, follow ABC. Intubate if the airway is compromised. However, it is important to remember to start at a 10th of your usual induction dose + push dose pressors prior to intubation if the patient is hypotensive
2. High dose insulin is the antidote of choice. Early administration of High Dose Insulin 1unit/kg IV bolus and dextrose 50ml of 50% dextrose (paediatrics 5ml/kg of 10% dextrose to a max of 250ml). Followed by an infusion of insulin at 1 unit/kg/hour IV and a dextrose infusion. Some patients may not require additional dextrose early in the management. This will take 30-45 minutes to start working and therefore you will need other measures to manage the hypotension.
3. Hypotension:
4. Calcium gluconate and atropine. However, both of these agents are unlikely to work.
5. A vasopressor such as norepinephrine will be the most effective. Start it peripherally until you get central access
6. Ventricular pacing rarely works but in severe cases ECMO and intra-aortic ballon pump maybe considered.
7. Decontamination:
8. Charcoal to those who present within 1 hour of standard preparation or 4 hours for XR preparations. Whole bowel irrigation can be considered in patients who present within 4 hours of an XR preparation of 10 or more diltiazem or verapamil tablets.

Sources:

Life in the Fastlane, UpToDate

Epiglottitis

-       Epiglottitis is an acute inflammation of the epiglottis and other supraglottic structures that can lead to airway obstruction -       Is a true airway emergency

-       Haemophilus influenzae used to be the most common pathogen prior to the development of the Hib vaccine. Now, common pathogens include Streptococcus pneumoniae, Staphylococcus aureus, and beta-hemolytic streptococci.

-       Due to immunizations against Haemophilus influenzae serotype b, epiglottitis has decreased in the pediatric population and is now more commonly seen between 30-50 years of age

-       The most common chief complaint is Sore throat

Physical Exam

-       Toxic-appearing, febrile, tachypneic, tachycardic, inspiratory stridor, muffled voice, drooling, anterior neck tenderness (hyoid bone)

Imaging

-       Laryngoscopy is the most accurate method to establish the diagnosis

-       Lateral soft-tissue radiograph of the neck is 88% sensitive. Image findings include a swollen epiglottis termed “thumb sign”. Absence of the “thumb sign” does not exclude the diagnosis

Evaluation and Management

-       Diagnosis is clinical and confirmed with laryngoscopy.

-       Early ENT consultation

-       Patient should remain in a position of comfort. Avoid agitation as it may precipitate airway obstruction

-       If respiratory distress or stridor is present, prepare for intubation.

-       Intubation should be performed in the OR if the patient is stable for transport. For unstable patients, awake fiberoptic intubation is recommended with an anesthesiologist present at bedside.Intubation should be attempted by the most experienced physician.

-       If intubation is unsuccessful, perform emergent cricothyroidotomy

-       Antibiotics: Ceftriaxone (50 mg/kg up to 2 grams IV) and vancomycin (15 mg/kg for concern for MRSA) are a good choice. Trimethoprim- sulfamethoxazole is an acceptable alternative for patients with PCN allergy

-       Decadron (0.1 mg/kg up to 10 mg IV).

-       Disposition: ICU.

Sources:

EM docs, FOAM EM RSS

Wellens' syndrome

Definition:

• Wellens’ syndrome is a pattern of deeply inverted or biphasic T waves in V2-3, which is highly specific for a critical stenosis of the left anterior descending artery (LAD)
• There are two patterns of T-wave abnormality in Wellens’ syndrome:
  • Type A = Biphasic, with initial positivity & terminal negativity (25% of cases)
  • Type B = Deeply and symmetrically inverted (75% of cases)

What happens exactly?

1. Sudden occlusion of the LAD, causing a transient anterior STEMI. The patient has chest pain & diaphoresis.
2. Re-perfusion of the LAD (e.g. due to spontaneous clot lysis or prehospital aspirin). The chest pain resolves. ST elevation improves and T waves become biphasic or inverted.
3. If the artery remains open, the T waves evolve over time from biphasic to deeply inverted.
4. The LAD can re-occlude at any time. If this happens, the first sign on the ECG is an apparent normalisation of the T waves (“pseudo-normalisation”). The T waves switch from biphasic/inverted to upright.
5. If the artery remains occluded, the patient now develops an evolving anterior STEMI.

Diagnostic criteria:

• Deeply inverted or biphasic T waves in V2-3 (may extend to V1-6)
• Isoelectric or minimally-elevated ST segment (< 1mm)
• No precordial Q waves
• Preserved precordial R wave progression
• Recent history of angina
• ECG pattern present in pain-free state
• Normal or slightly elevated serum cardiac markers

Why is this important?

• Myocardial infarction occurs within a mean of 6 – 8.5 days after admission
•  Myocardial infarction occurs within a mean of 21.4 days after symptoms

Management:

• Oxygen, aspirin, nitroglycerin, and heparin are the mainstay medical treatments of unstable angina, which is what Wellens’ Syndrome is, but in this specific case early cardiac revascularization is very important!
• The treatment of choice to improve both morbidity and mortality in Wellens’ Syndrome is early PCI- these patients need to go to the cath lab!
• Stress testing is contraindicated since it can induce a massive anterior myocardial infarction

Sources:

Life in the Fastlane, R.E.B.E.L EM