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8/16/2018 0 Comments

Pain Management in Our ED

Sergey Motov, MD
@painfreeED

General Principles:

Management of acute pain in the ED should be patient-centered and pan syndrome specific by using multimodal approach that include non-pharmacological modalities and pharmacological ones that include non-opioid and opioid analgesics.
Assessment of acute pain should be based on a need for analgesics to improve functionality, rather than patients-reported pain scores.
ED clinicians should engage patients in shared decision-making about overall treatment goals and expectations, the natural trajectory of the specific painful condition, and analgesic options including short-term and long-term benefits and risks of adverse effects.
When opioids are used for acute pain, ED clinicians should combine them with non-pharmacologic and non-opioid pharmacologic therapy: Yoga, exercise, cognitive behavioral therapy, complementary/alternative medical therapies (acupuncture); NSAID’s, Acetaminophen, Topical Analgesics, Nerve blocks, etc.
When considering opioids for acute pain, ED clinicians should involve patients in shared decision-making about analgesic options and opioid alternatives, risks and benefits of opioid therapies, and rational expectations about the pain trajectory and management approach.
When consider opioids for acute pain, EM providers should counsel patients regarding serious adverse effects such as sedation and respiratory depression; pruritus and constipation, and rapid development of tolerance and hyperalgesia
If acute pain lasting beyond the expected duration, complications of acute pain should be ruled out and transition to non-opioid therapy and non-pharmacological therapy should be attempted
When considering administration of opioids for acute pain, ED providers should make every effort to accesses respective state’s Prescription Drug Monitoring Program (PDMP). The data obtained from PDMP’s to be used to identify excessive dosages and dangerous combinations, identify and counsel patients with opioid use disorder, offer referral for addiction treatment.

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8/9/2018 0 Comments

What's in your Code Cart? Know your Meds

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8/5/2018 0 Comments

Hyperemesis Gravidarum

Hyperemesis Gravidarum:

Hyperemesis Gravidarum is severe nausea and vomiting during early pregnancy, typically starting prior to 9 weeks gestation.
- NOT associated with significant pain
- Do not turn off your brain, rule out serious causes before diagnosing the patient with hyperemesis gravidarum
Workup includes basic chemistry and urinalysis to evaluate electrolytes and signs of starvation ketosis
Confirm IUP
- Molar pregnancies or multiple gestation pregnancies can cause a higher amount of HCG and these patients are more likely to have hyperemesis.

First line treatment for this condition is Vitamin B6 and doxylamine. Some women will respond to P6 acupressure or ginger pills.
Treatment includes fluids with a source of glucose and antiemetics.
- Promethazine, metoclopromide, and ondansetron are all recommended options by the American College of Obstetrics and Gynecology (ACOG)[1].
- Ondansetron
  - There are insufficient data on fetal safety with ondansetron use and further studies are warranted
  - There have been studies that fetal exposure to ondansetron increases the risk of pediatric cardiac abnormalities and cleft palate; however, the data is inconsistent.
  - Individual studies of the association between ondansetron and congenital malformations are inconsistent, with some showing an increase in birth defects and others showing no difference [2,3,4]. A recent systematic review of ondansetron use in early pregnancy found eight studies that were adequate for inclusion [5]. Although there was a small increase in the risk of cardiac defects in two of the studies (odds ratio [OR], 2.0; 95% CI; 1.3-3.1 and OR, 1.62; 95% CI; 1.04-2.14), there was no increase in the overall rate of malformations in the ondansetron-exposed patients.
  - ACOG says, “Although some studies have shown an increased risk of birth defects with early ondansetron use, other studies have not. The absolute risk to any fetus is low.”
  - The American College of Obstetrics and Gynecology recommend Ondansetron as an option for patients not controlled on the first line medications Vitamin B6 and doxylamine.
  - Consult with your local Obstetricians

Erick, Miriam, et al. “ACOG Practice Bulletin 189.” Obstetrics & Gynecology, vol. 131, no. 5, 2018, p. 935., doi:10.1097/aog.0000000000002604.
Pasternak B, Svanstrom H, Hviid A. Ondansetron in pregnancy and risk of adverse fetal outcomes [published erratum appears in N Engl J Med 2013;368:2146]. N Engl J Med 2013;368:814–23.
Danielsson B, Wikner BN, Kallen B. Use of ondansetron during pregnancy and congenital malformations in the infant. Reprod Toxicol 2014;50:134–7.
Einarson A, Maltepe C, Navioz Y, Kennedy D, Tan MP, Koren G. The safety of ondansetron for nausea and vomiting of pregnancy: a prospective comparative study. BJOG 2004;111:940–3.
Carstairs SD. Ondansetron use in pregnancy and birth defects: a systematic review. Obstet Gynecol 2016;127:878–83.

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8/2/2018 0 Comments

Pediatric Nasal Foreign Bodies

Background:

Most common site of foreign body insertion in children
Can be missed and remain for weeks or months
Population at risk:
- Children between 2–6 years-old most common
- Mental retardation
- Psychiatric illness
Complications:
- Sinusitis is the most common complication
- Septal perforation
- Bronchial aspiration
High risk of complications with button batteries:
- Mucosa ischemia
- Turbinate or septal damage -> Saddle-nose deformity

Etiology:

Organic vs. Inorganic
Button batteries: High risk of complications compared with other foreign bodies (tissue necrosis, septal perforation, saddle-nose deformity); require rapid removal!
- Septal perforation can occur in as little as 4 hours
Magnets (Used to mimic nasal piercing)
- May cause intestinal perforation if swallowed, especially newer high-powered neodymium magnets

Signs & Symptoms:

Most nasal foreign bodies are asymptomatic
Unilateral nasal obstruction with nasal pain
Purulent/foul-smelling nasal discharge
Persistent epistaxis

History:

Child witnessed putting object into nose or FB noticed by parent/caretaker
Many children are reluctant to admit to placing a foreign body for fear of adult disapproval
Child may present weeks after with nasal discharge and bleeding
*Often misdiagnosed at this stage as sinusitis

Diagnosis:

Laboratory studies usually unnecessary
Fiberoptic visualization if foreign body cannot be visualized on rhinoscopy
Sinus films if present for extended period or suspicion of battery or magnet
May need chest or abdomen films for aspiration/ingestion

Treatment:

Keep in sitting position to avoid posterior displacement and possible aspiration of foreign body
Avoid interventions that upset the child
Topical vasoconstrictors:
- Nebulized epinephrine
- Cocaine: 4%
- Oxymetazoline: 0.05%
- Phenylephrine: 0.125–0.5%

*NOT recommended for button batteries as may increase leakage of caustic materials

Hooked probe, alligator forceps
- Used for anterior foreign bodies that are easily grasped
Headlamp, nasal speculum will facilitate use!
Suction catheter can be used for round, smooth objects
Balloon catheters (or Katz extractor) can be used primarily when instrumentation fails
- Can use a 5F or 6F Foley or Fogarty balloon catheter lubricated with 2% lidocaine jelly
Positive pressure for children or the “parent’s kiss”
- Positive pressure applied to mouth only
- Parent may tell the child he or she will be given a “big kiss.”
- Deliver brisk puff as child begins to inhale
- Alternatively, deliver puff with a bag-valve mask over the mouth and O2 at 10–15 L/min.
Procedural sedation may be necessary
- Need availability of advanced airway as foreign body has potential for dislodgment posteriorly and aspiration!
Snare technique (for you MacGyver’s out there):
- 24-gauge wire made into a loop with a hemostat
- Slip through swollen tissue, behind object, pulling it free

Disposition:

Admission Criteria:
- Foreign body cannot be recovered in ED or posteriorly displaced
- Removal under general anesthesia is required
- Mucosal ischemia or turbinate/septal damage
Discharge Criteria
- Ensure that there is no airway compromise
- If a button battery was removed, monitor for delayed sequelae as outpatient
- May require follow-up with ENT if removal unsuccessful in ED or concern for nasal mucosa injury

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7/14/2018 0 Comments

Upper GI Bleeds

Stable UGIB

DDx:

PUD: most common cause. Associated with NSAID use and H.Pylori, smoking.
Erosive gastritis/esophagitis: Associated with alcohol, salicylates/NSAIDs, infectious, stress from severe illness (cushings)
Varices: Portal HTN
Mallory- Weiss Syndrome: Repetitive vomiting
Dieulafoy Lesion:
1. Arteries that protrude through the GI submucosa and can cause intermittent bleeding with negative endoscopic findings.
2. NSAIDs and liver disease can predispose to this
AVMs
Malignancy
Aortoenteric fisula
Ischemia/perforation
Epistaxis/Upper airway bleed
Ingestions

Hx:

Is this really a GI bleed?
1. Nosebleed
2. Ingestions (guiac card)

Timing/amount
H/o GIB

If so h/o scope

EtoH, NSAID, Smoking hx
Anti-platlet /anti-coagulation history
Good ROS

PE:

Vital signs
Abdominal Exam
Rectal Exam (guiaic)
S/s Liver failure
1. Jaundice
2. Ascites
3. Palmar erythema
4. Spider nevi
5. Caput medusa
6. Hepatomegaly/splenomegaly

Labs:

Hb/hct
CBC
Basic Chemistry
1. BUN: Cr ?30 suggestive of bleed

Coags
Type and screen

Treatment:

PPIs
1. oral (omeprazole, pantoprazole, lansoprazole) vs IV therapy. No difference
2. Continuous vs intermittent IV PPI boluses
  1. JAMA systematic review that showed 13 different RCTs revealing no difference between gtt vs bolus in mortality, rebleeding, LOS, PRBC transfusion
3. PPI vs placebo
  1. No difference in mortality
  2. Reduced surgical intervention
  3. Reduced Rebleeding (NNT = 15)

Somatostatin (Octreotide-long acting somatostatin):
1. Decrease gastric acid, decrease blood flow to stomach/duodenum, splanchnic vasoconstriction
2. 50 mcg bolus
Antibiotics
1. Cirrhotic patients are innately immunocompromised -> increased risk of gut bacterial translocation
2. 1 g Rocephin
3. ONLY Tx that has mortality benefit with NNT = 4 to prevent an infection NNT = 22 to save a life!
Pro-motility agents
1. Ertyhromycin/Azithromycin (500mg)
2. Decreases need for second EGD
Transfusion
1. Threshold use to be Hbg < 9, yet theres mortality benefit with transfusion of Hbg < 7
2. If thrombocytopenia <50k with active GIB, transfuse platelets

Disposition:

Risk scoring systems to help risk stratify

Glasgow Blatchford Scale:
1. NPV of a GBS score of <1 for the outcome of transfusion, death or need for intervention was 99%
2. Approximately 20% of patients’ presenting with upper GI hemorrhage have a Blatchford score of zero

Rockall Score
AIM65 Score

Unstable UGIB

Airway/breathing
1. Preoxygenate
  1. Limit BVM
  2. Hbg dissociation curve shift right in anemia
2. Upright
3. RSI vs DSI
Circulation
1. MTP 1:1:1 Resuscitation
2. Reverse Coagulopathy
  1. Cirrhotics —> Vit K IV, FFP, ? 4 factor FFP
  2. NOAC reversal: praxibind, kcentra
  3. Thrombocytopenia —> Plts
  4. ESRD/ASA —> DDAVP 0.3mcg/kg
3. Permissive Hypotension —> MAP goal 60-65
4. TXA —> HALT-IT data to come in May 2019.
Medications
1. PPI
2. Octreotide
3. Antibiotics
4. Pressor of choice? Vasopressin
Treatment/Consultants
1. Ballon Tamponade
  1. Call for xray
  2. 3 ports: Esophagus balloon, Gastric ballon, Suction
  3. Measure out your E and G with NGT at 50 cm mark on Blakemore
  4. Insert it with lube
  5. Insufflate 50 ccs of air into gastric lavage port
  6. Insufflate 50 ccs of air into gastric port
  7. Xray, make sure ballon bubble below diaphragm
  8. Put another 200 ccs of air in gastric port for total 250 ccs
  9. Place on traction
  10. Insert your NGT to esophageal port
  11. Blakemore holds approximately 50-100ccs of air
  12. Get manometer
  13. Goal manomatry for esophagus 30-45 mmHg
2. Endoscopy
3. IR for embodied vs emergent TIPs (Transjugular Intrahepatic Portosystemic Shunts)
4. Surgery

Core Concepts:

Keep your DDx broad for UGIB and perform a focused H&P and PE
Use risk stratification tools like GBS, Rockall, and AIMS 65 to help with your disposition
Remember that the most important intervention that affects mortality is antibiotics in your cirrhotic UGIBs as well as restrictive transfusion with only those with Hbg < 7
Other treatment remedies include PPIs (no difference between IV vs oral or gtt vs bolus), somatostatin (or somatostatin analogs like octreotide), and promotility agents
In a hemodynamically unstable UGIB, remember your ABCs. Secure your airway early, resuscitate with blood products, consider reversal of coagulopathies.
Know how to place your hail mary Blakemore while making early consultations to your ICU, GI, IR and surgical colleagues.

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7/3/2018 0 Comments

Hepatorenal Syndrome

Hepatorenal Syndrome: Core Concepts

Hepatorenal Syndrome (HRS) = Liver Disease + Acute Kidney Injury (AKI)

Liver disease with portal hypertension with an AKI without other etiology
Diagnosis of exclusion

Type 1 HRS: Doubling of serum creatinine to Cr > 2.5mg/dL in less than 2 weeks
- Median survival = 2 weeks

Type 2 HRS: Renal impairment less severe than HRS Type 1
- Median survival = 6 months

Treatment

Liver transplant is the only treatment that will reverse the disease pathology
Dialysis is used only a bridge while awaiting transplant
- If patient is not a liver transplant candidate, dialysis is not offered as it does not treat the underlying pathology
TIPS procedure is only indicated if there is another acute process going on, like a GI bleed. Not indicated for HRS alone

Management in the ED

Identify patients with screening labs and urinalysis
Resuscitate with albumin (Goal 1g/kg over the first 24 hours)
Resuscitate further with vasoactive agents with goal of raising MAPS 10-15mmHg
- Norepinephrine, vasopressin, and somatostatin can all be used for vasoconstriction, specifically at the splanchnic circulation
- Look for inciting conditions such as infection

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5/6/2018 0 Comments

Acute Urinary Retention Slides by Dr. Covell below:

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4/12/2018 0 Comments

The Dying Asthma Patient

Outline The Dying Asthmatic Patient:

Critical asthma syndrome:
- Inability to speak
- PEFR< 25% predicted
- Failed frequent bronchodilator/IV steroids
Start with the basics:
- Inhaled bronchodilators: Beta agonists, anticholinergics
  - MDI versus Nebulizer: equally effective in mild/moderate asthma
  - Continuous nebs benefit in severe disease
- Systemic beta-agonists
  - IM Terbutaline: 0.25 mg subq q20min
  - IM Epinephrine: 0.3-0.5 mg subq q20min
- Steroids
  - Give within 1 hour to significantly decrease admission rates
  - Use oral prednisone/dexamethasone or in more severe cases IV methylprednisolone
- IV Magnesium
  - 2 grams over 15 minutes to avoid hypotension
  - Significant improvement in pulmonary function in severe asthma exacerbations
Consider other therapies:
- Heliox
  - Helium oxygen mixture 80:20
- Ketamine:
  - Bronchodilation and vagolytic
Non-invasive pressure ventilation
- IPAP=ventilation (high CO2=need IPAP)
- EPAP=oxygenation (opens up alveoli)
- Consider starting settings at IPAP 10 to EPAP 2 with FiO2 of 100%
Endotracheal intubation
- Don’t do it too early, don’t do it too late
- Consider DSI vs RSI
- Permissive hypercapnia
Post intubation hypotension
- SH!T: stacking, hypovolemia, induction drugs, tension pneumothorax
Last ditch efforts
- Inhaled paralytics
- VV ECMO

Core Concepts:
- Start with the basics: nebs, steroids, mag
- Remember the your back pocket tricks: heliox, ketamine, NIPPV
- Intubation, don’t do it too early, don’t do it too late. Consider DSI vs RSI
- Post intubation remember to manage your vents carefully including your i to e ration, avoiding barotrauma
- With your post intubation hypotension mnemonic oh sh!t!: stacking, hypovolemia, induction drugs, tension pneumothorax
- Know what hail marys are available at your hospital including inhaled anesthetics or ECMO

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3/25/2018 0 Comments

INcreased ICP

Increased Intracranial Pressure
Russell Trigonis PGY-2, Katie Lupez PGY-2, and Chris Gardner PGY-1

Increased intracranial pressures (ICP) can have many different causes with traumatic brain injuries (TBI) being one of the most common ones we see in the ED
Intracranial pressure, mean arterial pressure (MAP), and cerebral perfusion pressure (CPP) are linked according to following formula

CPP = MAP - ICP

In situations where intracranial pressure is elevated by a factor like a traumatic bleed, cerebral perfusion pressure will if the MAP remains constant. If the MAP drops too, the CPP can decrease to a critical level at which point the brain becomes ischemic
Increased intracranial pressure can be suspected with changes in GCS, localizing symptoms, or hemodynamic changes like bradycardia and hypertension (Cushings reflex)
If you suspect increased ICP, evaluate them quickly focusing on the ABCDs with a good neuro exam
If GCS < 8 or appears to be declining quickly, intubate to protect the airway

Consider ketamine and rocuronium for intubation
- Ketamine has been proven safe in patients with increased ICP and shows no additional increase in ICP when used for RSI followed by mechanical ventilation
- Rocuronium has been associated with improved mortality compared to succinylcholine in TBI patients
Make first attempt best attempt for intubation. Use video laryngoscopy if available as your first line agent to allow proper immobilization of C-spine as well as better first pass success.

Passive techniques to allow maximal venous and CSF drainage to minimize ICP
- Elevated head-of-bed or reverse Trendelenburg positioning (30 degrees)
- Properly fitted and positioned c-collar
- Low mean airway pressures

Active techniques to decrease ICP
- Consider sedation and paralytics only if patient requires it (cough, agitation). Otherwise these agents can cause hypotension or minimize your ability to perform serial neurological exams]
- Hypertonic saline (3% NaCl) with a bolus of 150 – 250cc in adults may be more beneficial than mannitol (1-3 g/kg) to avoid AKI and hypovolemia
- Can also consider 2 Amps of Sodium Bicarbonate (100cc of ~6% hypertonic solution)

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3/11/2018 0 Comments

MEthylene Blue use in the ED

Methylene Blue Summary

Uses include methemeglobinemia and vasoplegia. There is also some evidence supporting its use in angioedema.

Dose for methemeglobinemia is 1.5mg/kg over 1-2min
Dose for vasoplegia is 1-2mg/kg over 1-2min, then option infusion of 1-2mg/kg/hr over a maximum of 1-2hrs.

Mechanism of action: lots of biochemistry involved, but it breaks down to methylene blue inhibiting soluble cGMP to prevent NO endothelium-dependent relaxation in vascular smooth muscle to halt NO induced vasodilation.

Adverse effects of methylene blue administration include pain/burning at the injection site, nausea, HA
Avoid use in patients with G6PD deficiency, and use with caution in patients on multiple serotonergic agents (SSRIs, SNRIs, TCAs) as methylene blue can induce serotonin syndrome. This last point is especially important when using the drug as an infusion as there is high risk for serotonin syndrome with prolonged use.
Don’t forget to warn you nursing/support staff that the pulse ox reading may be artificially low while the methylene blue is being infused, however this reaction is transient.

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From the J. Lee Garvey Innovation Studio in the
Department of Emergency Medicine
Carolinas Medical Center
Charlotte, NC

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YOUR CART

Pain Management in Our ED

What's in your Code Cart? Know your Meds

Hyperemesis Gravidarum

Pediatric Nasal Foreign Bodies

Upper GI Bleeds

Hepatorenal Syndrome

Acute Urinary Retention

Acute Urinary Retention Slides by Dr. Covell below:

The Dying Asthma Patient

INcreased ICP

MEthylene Blue use in the ED

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