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.

1. Check a pulse! 

2. If unstable with a pulse – SHOCK!

3. If stable with a pulse – THINK!

4. 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

5. 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)

4.Pacemaker

5.Hyperkalemia

6.Anti-arrythmic drugs (class 1C, 1A, digoxin, amiodarone)

We then reviewed the three tachyarrhythmias that can occur in patients with a WPW pattern

1. Orthodromic AVRT (usually narrow complex, rate usually 200-300)
2. Antidromic AVRT (wide complex, rate usually 200-300)
3. 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:

1. If unstable with a pulse, cardioversion
2. If stable with a pulse, procainamide is readily available in our hospital
3. 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

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

Diverticulitis:

• Mean age of diagnosis 63 years old, but 16% of cases occur <age 45
• Most common symptom is abdominal pain: 95% LLQ pain, 5% is RLQ pain (more common in Asian patients)
  • 10-15% of diverticulitis patients have dysuria, urgency, or frequency
• In an otherwise healthy patients under the age of 70, uncomplicated diverticulitis without sepsis, significant leukocytosis, diffuse peritoneal signs, or fever >102.5 can be treated outpatient as long as the patient has access to close follow-up (3 days)
  • If symptoms and infectious markers have not improved in 3 days, abscess should be suspected and patient should be admitted and reimaged
• Outpatient treatment of diverticulitis:
  • Antibiotics: Cipro and flagyl first line
  • No evidence for dietary restrictions, but most providers recommend clear liquid diet until symptoms improve
  • Colonoscopy 6-8w after symptoms resolved to screen for colorectal cancer
  • Prevention of recurrences:
    • High-fiber diet
    • No evidence for avoidance of nuts, seeds, or corn as was previously thought
• Complications of acute diverticulitis: abscess, perforation, obstruction, and fistula (usually colovesicular)

Pyogenic Liver Abscess:

• usually polymicrobial
  • EColi most common in Western world
  • Klebsiella most common in Asia (beware of hypermucoid variant)
  • Strep milleri group is common (anginosus, constellatus, intermedius)
  • Staph and strep pyogenes can occur after procedures such as embolization
• Most common symptoms is fever 90%
  • Abdominal pain 50-75%
  • N/v, anorexia, weight loss, malaise
• LFTs are no necessary elevated
• Mainstays of treatment are percutaneous drainage vs. surgical drainage and prolonged course of antibiotics (4-6 weeks)

Today’s case was a middle-aged man with a history of stage 4 pancreatic adenocarcinoma who presented with somnolence and severe thrombocytopenia.

Diagnosis:

TTP should be suspected in any patient with thrombocytopenia and microangiopathic hemolytic anemia (MAHA) with schistocytes on peripheral blood smear. The classic pentad of fever, anemia, thrombocytopenia, renal failure, and neurological findings only occurs in 5% of TTP patients so a high index of suspicion is required for prompt treatment. GI symptoms, which are not included in the classic pentad of TTP, are relatively common so we suggest the following mnemonic.

Fever (10% of patients)

Anemia 

Renal involvement

Thrombocytopenia

Involvement of skin (purpura)

Neurological symptoms

GI distress

Today’s case was a young man with alcohol use disorder who presented with delirium tremens refractory to high dose benzodiazepines and severe anion gap metabolic acidosis.

In the differential diagnosis for hyperthermia, tachycardia, and hypertension in a patient with alcohol use disorder and psychiatric comorbidities, it is essential to consider serotonin syndrome and neuroleptic malignant syndrome in your differential.

The differential diagnosis for anion gap metabolic acidosis in an alcoholic patient is also wide, including alcoholic ketoacidosis, type A lactic acidosis from concurrent shock due to severe alcoholic pancreatitis, hepatitis, or aspiration pneumonia among other infections, type B lactic acidosis from ethanol itself, or coingestion of other toxic alcohols such as methanol or ethylene glycol.

It is important to rule out toxic coingestion in all patients with alcohol use disorder, altered mental status, and severe anion gap metabolic acidosis. Do this by calculating your serum osmolar gap with a formula that includes ethanol.

Serum osm= 2Na + BUN/2.8 + glucose/18 + ethanol/4.7

If the osmolar gap >10, coingestion should be high on your differential.