EMS Protocol of the Week - Carbon Monoxide (Adult and Pediatric)

Anyone else start getting that dusty, musty smell from the heater in your apartment running for the first time since spring? Anyone get headaches with that must? Nausea, confusion? Syncope?

The prehospital protocol for carbon monoxide poisoning is primarily about recognition. Some services may carry CO monitors that can measure a patient’s SpCO, much like a pulse oximeter, but the more important thing is to have a healthy clinical suspicion for it the same way you would in the ED. Often, these crews will be responding to the scene of a fire, or where a CO detector has gone off, so ensuring scene safety is obviously the other crucial part of this approach.

Speaking of fires, what other considerations do we have for EMS when flames are involved? Stay tuned to find out! www.nycremsco.org or the protocol binder until then.

Dave

POTD: Cannabinoid Hyperemesis Syndrome

POTD: Cannabinoid Hyperemesis Syndrome

Happy Sunday everyone. Hope you had your fill of Thanksgiving, turkey, football, relatives, and political disagreements over the dinner table. Today I want to delve into a topic that I feel like we encounter relatively regularly in the ED. Let me set the scene: You’re walking into the South Side 7 PM shift, through the ambulance bay doors, hot coffee in one hand and a large and refreshing bottle of San Pellegrino Mineral Water in the other. Stepping through the triage area you first hear- then see- our patient. A young person, actively retching to a volume audible from the waiting room, clutching a kidney basin for dear life. They usually are with a concerned loved one who is rubbing their shoulder for comfort. One quick look and you can size them up- this person looks ill and uncomfortable, but not sick. We’ve all been there. With a new feeling of empathy for this person’s exceptionally vocal nausea, you mosey on to the doctor’s station to await sign-out from your eager and exhausted colleagues. Another beautiful night on South Side- better have 3 In 1 on speed dial for some munchies.

The patient encountered is suffering from cannabinoid hyperemesis syndrome. Cannabis has been used as a medicine for centuries. As legislation in many states in the USA eases restrictions on its use (as of March 31, 2021, it is legal for adults 21 and older to possess up to three ounces of cannabis for personal use in New York), we are seeing more and more patients appearing in the ED presenting with the relatively rare side-effects from marijuana, including hyperemesis. Ironically, cannabinoids are used very commonly to treat nausea and vomiting, particularly in patients with chemotherapy-related symptoms, or patients with cyclic vomiting syndrome. Theoretically, this paradoxical illness is caused by highly potent THC that effects genetically predisposed individuals by differentially downregulating CBD receptors and causing autonomic dysfunction. There is speculation that there is a dose-dependency, and that a biphasic mechanism of action of THC may have anti-emetic effects at low doses, but pro-emetic at higher doses. Cannabinoid CB1 and CB2 are the main receptors for THC, one of the main active substances in marijuana. The theory is that the CB receptors in the medulla are responsible for anti-emetic properties, but the CB receptors in the GI tract are the source of dysregulation. There is another theory that the TRPV1 receptor (transient receptor potential vanilloid subtype 1), which is activated by marijuana, capsaicin, and heat, is altered by chronic marijuana use. It is speculated that the reason patients with CHS take repetitive hot showers is to upregulated the TRPV1 receptor.

Diagnosis

While no diagnostic criteria currently exist for definitive CHS diagnosis major characteristics patients typically display are:

• History of regular cannabis use (100% Sensitivity)

• Cyclic nausea and vomiting (100%)

• Generalized, diffuse abdominal pain (85.1%)

• Compulsive hot showers with symptom improvement (92.3%)

• Symptoms resolve with marijuana use cessation (92.3%)

• A higher prevalence in males (72.9%)

Often patients will experience three phases of Cannabinoid Hyperemesis Syndrome (3,8):

1. The Pre-emetic or Prodromal Phase:

• Can last for months or years

• Characterized by diffuse abdominal discomfort, feelings of agitation or stress, morning nausea, and fear of vomiting

• May also include autonomic symptoms like flushing, sweating, and increased thirst

• Often have increased use of marijuana to treat these symptoms

1. Hyper-emetic Phase:

• 24-48 hours

• Multiple episodes of vomiting

• Diffuse, severe abdominal pain

1. Recovery Phase:

• Begins with total cessation of cannabis

• Often patients require a bowel regimen, IV fluids, and electrolyte replacement

• Resolution of symptoms may take up to one month

Common complications of CHS include electrolyte disturbances, dehydration or AKI, and muscle cramps or spasms. Life threatening complications that have been documented include pneumomediastinum from ruptured esophagus, and electrolyte derangement causing seizure or arrythmia. Patients with suspected CHS should be offered counseling, resources, and follow-up for marijuana cessation. Treatment in the symptomatic phase involves symptomatic treatment and pharmaceuticals. It is often necessary to take a multi-faceted approach by giving dopamine antagonists, antihistamines, serotonin antagonists, antipsychotics, and topical capsaicin. Capsaicin is thought to work by transiently activating TRPV1 (which remember, is speculated to be downregulated by chronic marijuana use, and is thought to be the reason for the relief from incessant hot showering). It is a cream that can be applied to the fatty areas of the backs of the arms and abdomen up to 3 times daily, and is available in concentrations from 0.025% to 0.15%.

Pearls

• Cannabinoid Hyperemesis Syndrome is increasing in frequency in the United States.

• CHS is characterized by nausea, vomiting, abdominal pain and chronic cannabis use.

• Consider CHS diagnosis in patients with recurrent presentations and negative abdominal pain work-ups.

• Avoid opiates for CHS treatment.

• Consider capsaicin cream, benzodiazepines, antiemetics and antipsychotics for treatment of CHS

Hope this was informative, and that everyone had a great weekend. See you in the ED this week.

Mak Sarich MD

References: http://www.emdocs.net/more-than-a-hot-shower-treatment-for-cannabinoid-hyperemesis-syndrome-chs/

POTD: Decompensated CHF - a deep dive

This is probably bread and butter for us at Maimo and we are roughly familiar with how to manage it.  Today, we take a deep dive into the classification and etiology of decompensated CHF to better understand the disease process. And then a short review on the basics of management just go through it systematically.

What is decompensated heart failure? 

• When something structural or functional happens to the heart, leading to inability to eject and/or accommodate blood within physiological levels.

• Leads to a functional limitation

• Requires immediate intervention

2 different scenarios:

1) New-onset acute CHF

• No prior history or symptoms of CHF

• Triggered by:

  • Acute MI

  • Hypertensive crisis

  • Rupture of chordae tendineae 

• Usually more prominent pulmonary congestion > systemic congestion

  • Usually normal blood volume

• Treatment focused on treating underlying cause

  • High dose diuretics less helpful

2) Decompensated (chronic) CHF

• Worsening of symptoms in existing CHF

• Most commonly caused by:

  • Low treatment adherence - med noncompliance or poor diet (high salt)

  • Infection

  • PE

  • Tachy/bradyarrhythmias 

    • Often new-onset afib 

Factors indicating poor prognosis in DHF:

• Pts with BUN > 90 and Cr > 2.75 on admission have a 21.9% risk of in-hospital mortality

• Age (above 65 years)

• Hyponatremia (sodium <130meq/L)

• Impaired renal function

• Anemia (hemoglobin <11g/dL)

• Signs of peripheral hypoperfusion

• Cachexia

• Complete left bundle branch block

• Atrial fibrillation

• Restrictive pattern on Doppler

• Persistent elevation of natriuretic peptides levels despite treatment

• Persistent congestion

• Persistent third heart sound

• Sustained ventricular tachycardia or ventricular fibrillation

Classification system - Stevenson Classification (below)

Here’s another similar classification chart that’s more visually stimulating:

Forrester Classification (below)

Use to guide management

• A (dry, warm) = compensated

• B (wet, warm) = most common

  • Vasodilators and diuretics

  • Consider inotropes especially when SBP b/w 90-120

• C (wet, cold) = worst prognosis

  • Ionotropes and diuretics

  • IV vasodilators if BP is being intensively monitored

• L (dry, cold) = rare

  • Volume resuscitation +/- inotropes

Causes of CHF exacerbation

Tsuyuki et al, 180 pts 

• Most common primary cause: excessive salt intake (15%)

• Noncardiac disorders (15%)

• Inappropriate reductions in CHF therapy (9%)

Ghali et al, 101 pts at Cook County Hospital in Chicago

• Lack of compliance with diet, drugs, or both (64.4%)

• Uncontrolled HTN (43.6%)

• Cardiac arrhythmias (28.7%)

Opasich et al, 161 pts referred to CHF service at Italian hospital

• Arrhythmias (24%)

• Infection (23%)

• Poor compliance (15%)

• Angina (14%)

My takeaway: there is wide variability in the causes of DHF and limited studies out there about the various causes. Given that poor medication / diet compliance is often at the top of the list, it seems like good patient education may go a long way in preventing CHF exacerbation. Consider taking the time to really get at why your patient is in CHF exacerbation. Do they not understand how often they’re supposed to take their diuretic? Are they in denial about junk food intake? 

You MUST understand the classification of your patient’s CHF in order to manage them appropriately. It’s not always cookie cutter diuretics. 

I also decided to touch on basics of CHF management because I thought this was a nice review by emcrit.

1. Treat the lungs

• BIPAP - reduce preload and afterload (like ACEI)

• Intubation - cardiogenic shock

• Drain large pleural effusions if causing respiratory distress

• Inhaled pulmonary bronchodilator - epoprostanol or NO

2. Optimize MAP - reduce afterload if pt can tolerate

•  High dose nitroglycerin - up to 200-250 mcg/min

• Transition to oral once stabilized - ACEI, ARB, hydralazine + isosorbide dinitrate 

• Manage hypotension with pressor - NOREPINEPHRINE IS KING

  • EPI is reasonable if reduced EF, hypotensive, with poor cardiac output

  • AVOID dopamine - evidence of harm compared to NE in SOAP-II trial

3. Optimize volume status

• Fluids?

  • End organ perfusion (AKI)

  • NO evidence of pulmonary congestion (no B lines on US)

  • Appears truly hypovolemic (no systemic congestion)

  • Give small boluses at a time and reassess

• Diuresis?

  • SIgnificant pulmonary or systemic congestion

  • Overall appears hypervolemic

4. Inotrope for HFrEF

• Very temporary improvement in hemodynamics and actually associated with worse outcomes in some studies

• Inotropes should ONLY be used if:

  •  Hypoperfusion with low-normal BP (like AKI with poor UO despite above interventions)

  • Refractory cardiogenic pulmonary edema (like if the interventions above don’t work and you still need to reduce pulmonary congestion)

• Dobutamine?

  • Shorter half life, more titratable than milrinone

  • Preferred for immediate stabilization of very ill patient, someone with marked pulmonary edema on the verge of intubation

• Milrionone?

  • More effective vasodilation than dobutamine

  • Renally excreted so tricky to titrate dose in renal failure - half life 2.3 hours in normal kidneys

• DIgoxin? 

  • The only positive inotrope that doesn’t correlate with increased mortality

  • Consider for patients with long standing afib and systolic HF

  • Not front line

5. Treat underlying cause

• New onset tachyarrhythmia - convert to sinus. Beware slowing HR if it isn’t high already

• Cardiogenic shock 2/2 MI - ASA, antiplatelet, anticoagulation

  • Revascularization is essential!!! Valuable even if delayed.

  • Thrombolysis works poorly

THINGS TO AVOID:

• Anything nephrotoxic - NSAIDs, ACE/ARB

• DO NOT suppress sinus tach since this is usually compensatory and keeping the patient alive

• Avoid diltiazem in afib with DHF

• Do NOT treat mild stable hypoNa with hypertonic or salt tablets

• Fluid and sodium restriction actually haven’t shown benefit in RCTs once they are in decompensated HF

• BEWARE BETA BLOCKERS - don’t start them in decompensated heart failure

  • Great for chronic compensated HF

  • Negative inotrope could impair cardiac function

  • Controversial if BB should be continued in patients who are already taking them -- in general should be held in cardiogenic shock 

References

https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/649270

Acute Precipitants of Congestive Heart Failure Exacerbations | Cardiology | JAMA Internal Medicine | JAMA Network

jamanetwork.com

Background&nbsp; Few studies have prospectively and systematically explored the factors that acutely precipitate exacerbation of congestive heart failure (CHF) in patients with left ventricular dysfunction. Knowledge of such factors is important in designing measures to prevent deterioration of...

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4878602/

Decompensated heart failure

www.ncbi.nlm.nih.gov

Heart failure is a disease with high incidence and prevalence in the population. The costs with hospitalization for decompensated heart failure reach approximately 60% of the total cost with heart failure treatment, and mortality during hospitalization ...

https://emcrit.org/ibcc/chf/#hemodynamic_evaluation_&_risk_stratification

Forrester classification

Forrester classification - management

Stevenson classification