Today we presented a case of syncope 2/2 to age-related degeneration of the conducting system leading to complete heart block. We first went through a framework for Syncope (taken from Dr. Eric Strong’s awesome lecture series)
Definition: Syncope is defined as a transient, self-limited loss of consciousness with an inability to maintain postural tone that is followed by spontaneous recovery.
We then emphasized the importance of choosing wisely in the workup of syncope. All patients with syncope should receive the following:
- A spectacular history
- A splendid physical examination
- An EKG
- Orthostatic vital signs
Depending on the above, target your further testing accordingly
Remember, it’s the cardiogenic syncope that is highly concerning and so the San Francisco Syncope Rule can be useful in deciding who is safe to discharge…BUT, as a recent paper reported, the sensitivity of clinical judgement for adverse outcomes secondary to a syncope is higher than decision making rules. Therefore, if something doesn’t feel right, trust your instincts!
Our patient was found to have complete heart block on an EKG and we reviewed the three major classifications for its etiology:
- Known Pathologic
- Myocarditis (i.e lyme)
- Infiltrative cardiomyopathy (amyloidosis, sarcoidosis
- Post-cardiac surgery
- Post catheter ablation
- Post TAVR
- Idiopathic Progressive Cardiac Conduction Disease (>50% of cases)
- thought to be secondary to age-related degeneration of the conduction system
Finally, we discussed management of complete heart block:
- Atropine use should be avoided since it is likely ineffective (since the block is likely below the AV node) and more importantly it delays more effective treatment
- Electrical & Medication options (either epinephrine OR dopamine) should be considered
- Unless the cause is immediately reversible, patients will generally need a transvenous pacemaker and then a permanent pacemaker
If you made it this far in the post, congratulations. As a reward, do note that the framework for syncope actually has a mnemonic embedded within it (ROCS) 🙂
-Use FENa only to differentiate between prerenal AKI and ATN only in oliguric patients without CKD who are not on diuretics
-Vancomycin renal toxicity is more likely when trough levels are >15 and it is administered with Zosyn or nephrotoxins such as aminoglycosides
-Classic triad of AIN: fever, maculopapular rash, and peripheral eosinophilia is only present in 10% of AIN patients
– Eosinophiluria is neither sensitive nor specific for AIN
– AIN is a clinical diagnosis: Elevated Cr temporally correlating with AIN-inducing drug exposure with improvement after discontinuation of the drug. Renal biopsy is the gold standard of diagnosis, but usually not required.
Today we went through a case of WPW Syndrome that manifested as a wide complex tachycardia 2/2 to rapid atrial fibrillation in a pre-excited state.
We first went on a tangent and discussed the differential for sinus tachycardia.
We then discovered that it was a wide complex tachycardia that was irregularly irregular. We emphasized the first step in the pathway.
Check a pulse!
If unstable with a pulse – SHOCK!
If stable with a pulse – THINK!
If in doubt – it’s probably VT and the ACLS algorithm will work in almost every situation (it is safer to incorrectly assume a ventricular tachycardia than supraventricular tachycardia with abberancy).
-If you are skilled in EKGs, look at https://litfl.com/vt-versus-svt-ecg-library/ and become comfortable at distinguishing them before prime time. Remember though, these algorithms are not always correct and so when in doubt, it’s VT
If you have strong reason to suspect that it is NOT TRUE VT and the patient is stable, ASK FOR HELP before giving any medication
We then reviewed the differential for wide complex tachycardia
1.VT (80% of patients)
2.SVT with a bundle branch block (15%)
3.SVT with antegrade conduction via an accessory pathway (pre-excited syndrome)
6.Anti-arrythmic drugs (class 1C, 1A, digoxin, amiodarone)
We then reviewed the three tachyarrhythmias that can occur in patients with a WPW pattern
- Orthodromic AVRT (usually narrow complex, rate usually 200-300)
- Antidromic AVRT (wide complex, rate usually 200-300)
- Afib/flutter (wide complex, irregular rhythm, QRS complexes change in shape and morphology, and axis remains stable unlike polymorphic VT)
Treatment of Antidromic AVRT or Atrial Fibrillation with Pre-excitation:
- If unstable with a pulse, cardioversion
- If stable with a pulse, procainamide is readily available in our hospital
- Definitive treatment is catheter ablation which has a success rate of 80% at 5 years in the prevention of tachyarrhythmias .
Finally, we emphasized: DO NOT treat with AV nodal blocking agents e.g. adenosine, calcium-channel blockers, beta-blockers as this may increase conduction down the accessory pathway. Per UpToDate: “Amiodarone should generally not be used in patients with AF and accessory pathway.” Remember, ventricular tachycardia (far away and the most common wide complex tachycardia) is often used in wide complex tachycardias that are regular and monomorphic per the ACLS protocol. If you’re thinking it could be pre-excitation (very rare), ask for help before administering a medication!
Source: 2015 AHA Algorithm obtained from UpToDate
Today we discussed a case of a patient with chronic constipation who presented with abdominal pain and hematochezia. A CT scan revealed a large fecaloma, which led to stercoral ulceration of the rectum, colitis and eventually perforation.
We first reviewed the etiologies of hematochezia, remembering that in up to 15% of cases, a brisk UGI source is the etiology. When this occurs it is typically in patients who have hemodynamic instability. Some aspects to aid in the diagnosis were put together in an excellent Rational Clinical Examination article in JAMA that Dr. Jacobson referenced. Findings that have a high LR of a brisk UGI are melenic stool on examination, an elevated BUN/Cr ratio 30, an NG lavage with blood or CGE . Findings that have a high LR of the etiology being a LGIB is a history of LGIB and clots in stool.
We then discussed a framework for LGIB:
We discussed the complications of constipation:
- Decreased quality of life
- Anal Fissures/Tears
- Rectal Prolpase
- Stercoral Ulceration
Stercoral Ulceration/Colitis/Perforation 101
- most cases have been reported in elderly, psychiatric, bedridden, or narcotic-dependent patients with a history of constipation
- Fewer than 150 causes of perforation have been described in the literature
- Severe chronic constipation thought to induce the formation of stone-hard fecalomas and maintain a continuous peressure over the bowel wall leading to pressure necrosis
- This ulceration sometimes leads to a state of stercoral colitis (localized ischemia due to increased luminal pressure)
- CT findings of perforation are fecal impaction, colonic dilatation, colonic wall thickening, discontinuity in the enhancement of the bowel wall in relation to focal fecal distension of the colonic lumen, and extraluminar free air
- A mortality rate of ~30% has been mentioned
- Treatment is generally surgical
Erythema Multiforme: Acute immune-mediated reaction characterized by appearance of target-like lesions on skin often accompanied by bullae involving oral, genital, or ocular mucosa.
-Epidemiology: most common in young adults 20-40
-2 forms: Minor (only mild or no mucosal involvement) or major (severe mucosal involvement and may have systemic symptoms like fever and arthralgias)
-Triggers: 90% infectious (most commonly HSV, but can be viral, bacteria, or fungal)
-Cases have been associated with meds (most commonly NSAIDs), malignancy, autoimmune disease, vaccines, radiation, sarcoidosis, and even menstruation
-Treatment: Usually self-limited within a few weeks
Today we learned about a patient who presented with hemoptysis in the setting of latent TB that was diagnosed as TB Bronchiectasis. We discussed the framework for hemoptysis:
We then reviewed the CT and determined it was bronchiectasis:
- Bronchioectasis is defined as “Irreversible dilation and destruction of larger bronchi caused by chronic infection and inflammation”
- Development of bronchiectasis always requires two factors
- An infectious insult
- Impaired drainage, airway obstruction or a defect in host defense
- Any pulmonary Infections
- Childhood infections (bacterial, viral or mycoplasma PNA)
- Mycobacterial infections
- Cystic Fibrosis
- up to 7 percent of patients with cystic fibrosis (CF) are diagnosed at age 18 years or older
- Sinusitis and bronchiectasis are the major respiratory manifestations of CF in adults
- Airway obstruction
- FBA or any other intraluminar obstructing lesion (such as a carcinoid tumor) or extraluminal compression
- Defective host defenses
- Local: Ciliary dyskinesia
- Systemic: hypogammaglobulinemia/prolonged immunosuppression
- Young Syndrome
- Bronchiectasis, sinusitis and obstructive azoospermia who have no evidence of cystic fibrosis
- Rheumatic/Systemic Disease
- Primary Ciliary Dysfunction
- Allergic bronchopulmonary aspergillosis
- should be suspected in patients with a long history of asthma that is resistant to bronchodilator therapy and associated with a cough often productive of sputum that is mucopurulent or contains mucous plugs.
- Alpha-1 antitrypsin deficiencies
- Signs and Symptoms
- cough, mucopurulent sputum production, dyspnea, rhinosinusitis, hemoptysis (27%) and recurrent pleurisy
- on exam crackles and wheezing are common
- Radiographic Findings
- The internal diameter of the bronchus is larger than that of its accompanying vessel
- the bronchus fails to taper in the periphery of the chest
- Treatment of Acute Exacerbation
- Deciding when a patient has an acute exacerbation requires clinical judgement as there is no laboratory features specific for an exacerbation
- Antibiotics decrease the existing bacterial burden and can decrease systemic inflammatory mediators
- 10-14 day treatment course is appropriate (though the ERS 2017 guidelines suggest 14)