CCFP Topic: Chest Pain – Part 2

  • Written and Researched By: Caleb Dusdal
  • Peer Review By: Chris Cochrane

Objective Four:
Given an appropriate history of chest pain suggestive of herpes zoster infection, hiatal hernia, reflux, esophageal spasm, infections, or peptic ulcer disease:
a)    Propose the diagnosis.
b)    Do an appropriate work-up/follow-up to confirm the suspected diagnosis.

Herpes Zoster

This is one key reason why it is important to fully inspect your patient presenting with chest pain. It would be embarrassing to miss this as a cause.

As you know this is due to reactivation of laten varicella-zoster from childhood chicken pox that has been lying in wait in the ganglion of the spinal nerve.

  • Presentation
    usually pain or dysthesia precedes visual evidence by 3-5 days.
    This is followed by erythematous papules, which progress to clusters of vesicle with erythematous base

And remember the pathophysiology, these will always present in a dermatomal area. Most often thoracic, but can also be in the trigeminal branches of the face.
This vesicles turn to pustules, and then crust over in about one week.

This is going to be a clinical diagnosis based on history of chicken pox or previous shingles flares, and the appearance of the lesions.

Any benefit requires this be started within 72 hours of symptom onset.

  • Acyclovir 800mg PO five times daily x 7 days
  • Valcyclovir 1 gram PO tid for 7 days


  • Acyclovir 10mg/kg IV q8h for 7-10 days
  • (Valcyclovir should not be Rx due to risk of HUS)

Te zoster vaccine markedly reduces morbidity from herpes zoster and post-herpetic neuralgia among older adults.

The benefits we might get from acute treatment are:

  • Shortens healing time
    • Decreases new lesion formation
    • Reduces risk of post-herpetic neuralgia
Hiatal Hernia

This is a protrusion of the stomach up through the diaphragm. Most are asymptomatic, but may increase incidence of acid reflux.

Sliding hiatal hernia is the most common, with a paraoesophageal variety being less common.

The connection between symptoms and the hernia are not entirely clear. In fact, ove 40% of cases are discovered incidentally on x-ray.
– large hiatal hernias can be discovered incidentall on CXR

  • Definitive diagnosis, particularly for smaller ones, is with barium swallow.

Clinical Presentation
most are asyptomatic.
But retrosternal chest pain can occur.
Occult or massive GI haemorrhage can occur with either type.
Paraoesophageal type can incarcerate and strangulate as a rare complication.


PPI or H2 blocker can be trialed

  • Asymptomatic sliding hiatal hernia requires no intervention aside from symptom management for GERD
    • A paraoesophageal hernia should be reduced surgically because of the risk for strangulation
Gastro-oesophageal Reflux

Commonly accredited to incompetence of the lower oesophageal sphincter, allowing gastric contents into the oesophagus causing the burning retrosternal pain.

Prolonged exposure of the oesophagus to gastric acidic contents can lead to oesophagitis, strictures, or even metaplasia or cancers.

              Clinical in vast majority of cases

Clinical Presentation
– ‘heartburn’ retrosternal burning pain with or without regurgitation of contents into the mout.

  • if an oesophagitis develops may see: odynophagia or even oesophageal haemorrhage
  • resulting strictures can cause progressive dysphagia for solids
  • PUD is usually localized to xiphoid region
  • Infants with this present with vomiting, irritability, anorexia

Most often a trial of PPI or H2 blockers is used, and if they respond, the diagnosis is presumed.

If symptoms are irregular or only in specific contexts, they can first trial antacids prn.

  • Lifestyle measures should always be used:
    • Elevate head of bed, no meals before lying down or going to sleep.
    • Cessation of: alcohol, fats, chocolate, anticholinergic meds, smoking, spicy foods
    • Weight loss

For those unresponsive to empiric therapies above, may require endoscopy to assess for structural complications, with biopsy  to assess for H Pylori infection, and dysplasia suggesting Barrett’s.

**Based on a recent CMAJ publication, the Canadian Task Force recommends NOT screening folks with chronic GERD for Barrett’s or Adenocarcinoma**

Objective Five:
Given a suspected diagnosis of pulmonary embolism:
a)   Do not rule out the diagnosis solely on the basis of a test with low sensitivity and specificity.

If your gestalt suggests a PE, and they are haemodynamically stable, skip everything and send them for a CT-PA.

If they’re stable, Thrombosis Canada suggests running the major variables for a DVT/PE through the Wells Score. If they score above 4.5, then you cannot say it is low-likelihood and further steps are needed. If it is below 4.5 on Wells, then you can use the PERC score

So, say your patient scores 2.5 because they had cancer and a previous VTE. This is considered ‘PE unlikely’ and so we can run it through the PERC score.

Now this is a rule-out score, so it is veeeery sensitive. If your patient scores zero here, we can comfortably exclude a Pulmonary Embolism.

However, if your patient with low-pretest probability based on gestalt/Wells Score gets even one point, then you need to get a D-Dimer. This is quite sensitive and can also rule-out a PE if it is negative.

  • Age x 10ug/L for patients over 50yo, or
  • 500ug/L for everyone under 50 years of age.

Now, if your D-Dimer is positive, you need to get a CT-PA

If your Wells Score was ‘high probability’ or 4.5 points or higher, then you’re going straight to CT-PA as this is the best test.

b) Begin Appropriate Treatment Immediately

Unless bleed risk is high such as the patient is actively bleeding or they are immediately post-operative, quick acting anticoagulation should be initiated for anyone with high probability of a Pulmonary Embolism. Meaning, before the confirmatory testing with CT-PA is done.

If they have low or intermediated pre-test probability, then this can be held as long as testing can be done shortly: within 24 hours for low risk, or 4 hours for intermediate risk.

Anticoagulation includes:

  • DOAC monotherapy is generally preferred: Apixaban or Rivaroxaban
  • If thrombolysis for haemodynamic instability is being considered, then IV unfractionated heparin is preferred
  • Low molecular weight heparin bridge to Dabigatrain and Edoxaban
  • Low molecular weight heparin bridge to Warfarin
  • Low molecular weight heparin monotherapy is still recommended for patients with active cancer

All VTEs should be treated with anticoagulation for at least 3 months, unless there is no apparent trigger or it is recurrent, in which case may need longer treatment. Talk to your Haematology colleagues.

Thrombosis Canada

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