CC: Chest Pain
HPI: 49-year-old female brought in via ALS presents complaining of Chest pain. As per the Paramedics, the patient was found to be in no acute distress, stating she had exertional chest pain, which had subsided. The pre-hospital ECG was suspicious for ischemia and she was given ASA. Patient states she was walking home from the store when she began to have a pressure like pain on the left side of her chest, which was non-radiating and persisted when she laid down. She admits to feeling similar symptoms over the past few months, but today was the most severe. Upon arrival to Emergency Department, she denied chest pain, SOB, palpitations, abdominal pain, nausea or vomiting. Denied ETOH or illicit drugs use
BP:128/91, Hr:88, RR: 14, Temp: 98.0, Pulse O2: 100% RA
General: Patient lying comfortably in bed, in no distress
HEENT: NCAT, pupils PERRLA, neck supple
Respiratory: non-labored, CTA B/L, no wheezing, rales or rhonchi
Cardiac: +S1/S2, no MRG, regular rate and rhythm
Abdomen: soft NT ND, + BS
Neuro exam: AAO X 3, lucid, strength is 5/5 in all extremities, muscle tone is intact,
Skin: No rash or peripheral edema.
Troponin: Negative (< 0.010)
CXR: no acute infiltrate, No Pneumothorax or cardiomegaly. Normal Chest X-ray
ECG in the ED
Working Diagnosis: Left Main Insufficiency
ED Course: Repeat ECG in ED showed NSR and had completely normalized. Case was discussed with Interventional cardiologist on call. A Code STEMI was activated and patient was taken emergently to the Cath lab. She was given a Heparin bolus as well as Plavix.
ED/Hospital course: The catheterization report revealed 80-90% Distal left main, 30 % mid LAD, and LM stenosis improved partially during catheterization with nitroglycerin. Patient admitted to recently using cocaine. CT surgery was called due to the fact that patient had recent cocaine use and it was believed she might have had Left Main Coronary spasm. On hospital day 2, patient went back for repeat catheterization, which revealed Left main distal 30% and LAD mid 30% stenosis. Patient was transferred to telemetry, and discharged on hospital day 4.
aVR in ACS
Typical ECG findings with left main coronary artery (LMCA) occlusion:
- Widespread horizontal ST depression, most prominent in Leads I, II and V4-6
- ST elevation in aVR ≥ 1mm
- ST elevation in aVR ≥ V1
(Don’t worry so much about STE 0.5mm or less in lead aVR, because it lacks specificity. Using 1.0mm or greater in lead aVR, has better specificity)
ST-Segment Elevation in lead aVR foreshadows a worse prognosis in ACS and often predicts the need for CABG. Patients with NSTEMI and ST elevation ≥ 1mm in aVR are likely to have multi-vessel or LMCA disease and are likely to require CABG, therefore withholding Clopidogrel may be prudent. ST-segment elevation in aVR can be caused by any of the following 4 mechanisms
- Critical narrowing of the LMCA causing sub-endocardial ischemia due to insufficient blood flow. (LMCA insufficiency)
- Transmural infarction of the basal septum due to a very proximal LAD occlusion or complete LMCA occlusion (patient will be VERY sick)
- Severe multi-vessel coronary artery disease.
- Diffuse sub-endocardial ischemia from oxygen supply/demand mismatch.
Patients with complete occlusion of the LMCA (mechanism 2), often present in cardiogenic shock and require immediate revascularization. Patients with acute coronary occlusions typically will have active symptoms and look sick!
There is an estimated 70% mortality without immediate PCI. Medical therapy (including thrombolytic) does not improve mortality. Emergency PCI may decrease mortality to 40%.
What Else can Cause STE in aVR that Won’t Benefit from Going to the Cath Lab?
Other causes of global cardiac ischemia
o Thoracic aortic dissection
o Large pulmonary embolism
o Severe anemia
o Post-arrest (within 15 min. of epinephrine or defibrillation)
o Supraventricular Tachycardia (esp. AVRT)
o Left bundle branch block (LBBB) & paced rhythms
o LVH with strain (from severe hypertension)
o Severe hypokalemia
o Na+ channel blockade (TCA toxicity, hyperkalemia, Brugada, etc.)
REMEMBER: ST-Segment Elevation in Lead aVR is NOT SPECIFIC for an acute LMCA Lesion, Acute Proximal LAD Lesion, or Acute Triple Vessel DiseasE
- Correlate Your ECG with the Patient’s Clinical Status
- Patients with ACS due to LMCA Blockage, Triple Vessel Disease, or Proximal LAD blockage will look “sick” due to global cardiac ischemia
Case presented by Dr. Kerri Clayton.
- Disorder that is commonly caused by a viral lower respiratory tract infection in infants
- Characterized by acute inflammation, edema and necrosis of epithelial cells lining small airways and increased mucus production
- Rhino virus
- Parainfluenza virus
- RSV (respiratory syncytial virus) – MOST COMMON!
- Incidence – December-March
- Most infections occur within first 2 years of life
- About 40% experience lower respiratory infection during initial infection
- RSV doesn’t grant permanent or long-term immunity – RE-INFECTION COMMON
- The risk of significant viral or bacterial lower respiratory tract infection or pneumonia in an infant is low
- Direct contact with secretions
- Young children shed virus for >2 weeks
- 30-70% of household contacts become ill
- Natural history
- Begins with URI – Rhinorrhea, congestion, cough
- Progresses to LRI in 2-6 days – Airway obstruction (tachypnea, wheezing, respiratory distress)
- Variable and dynamic course
- Lasts 2-4 weeks
7-month-old male presents to the emergency room with his parents due to cough, runny nose, congestion and SOB that started 3 days ago.
VS: RR – 65, HR – 140, Temp – 99.1°F, O2 sat – 93% on RA
- Typical Presentation of Bronchiolitis
- Viral URI and cough with signs of lower respiratory tract infection
- Work of breathing – grunting, nasal flaring, intercostal/subcostal retractions
- Coarse rales
- Viral URI and cough with signs of lower respiratory tract infection
- TIPS for a better exam
- Upper airway obstruction can contribute to work of breathing
- Suctioning and positioning may decrease the work of breathing and improve the quality of your examination
- Counting respiratory rate over the course of 1 min is more accurate than shorter observations
- Assess mental status, respiratory rate, work of breathing, oxygen status, listen to breath sounds, and assess hydration status
- DIAGNOSIS IS CLINICAL – NO LABS OR RADIOLOGICIAL STUDIES ARE NEEDED
- When to consider CXR – if child has had >2 days of fever, an asymmetric chest exam, does not demonstrate improvement or has an unusually high O2 need
- Diagnostic testing may be considered if:
- Need cohorting – this is why we get testing for those we admit
- Uncertain clinical diagnosis
- Age <2 months
- To assess for influenza – also needed this for those we admit
Classify patient as mild, moderate, or severe based on the above physical exam
|1. Consider suction bulb
|1. Suction bulb
2. No bronchodilators
3. Discharge or admit
|1. Suction bulb or wall
2. No bronchodilators
3. If no improvement consider starting high flow NC
- IVF – moderately or severely dehydrated, secretions are thick and difficult to mobilize or severe respiratory distress
- PO feeds – mildly to moderately dehydrated and can tolerate PO
- Considerations for severely ill patients
- Consider ONE TIME albuterol MDI trial if:
- Severe respiratory distress OR
- Increased risk for asthma
- >12 months old, wheeze and once of the following
- personal history of atopy or recurrent wheezing
- strong family history of atopy or asthma
- if responds to albuterol then consider switching to asthma pathway
- >12 months old, wheeze and once of the following
- Consider HFNC for significant hypoxia OR severe respiratory distress not improving with rigorous supportive care
- Consider ONE TIME albuterol MDI trial if:
|Discharge criteria||Admission criteria|
|– Oxygen saturation >90%
– Adequate oral intake
– Mild/moderate work of breathing
– Reliable caretaker
– Able to obtain follow up care
– MDI/spacer teaching if response to albuterol
|– Admit if discharge criteria not met:
o Inpatient: Requires 02 or progression expected
o OBS: Mild disease with expected LOS < 24 hours
o ICU: Apnea, severe distress; Requires HFNC / CPAP / intubation
– Infants with these risk factors present early in the illness have higher risk of progression:
o Gestational age < 34 weeks
o Respiratory rate ≥ 70
o Age < 3 months
- Differentiate infants with probable viral bronchiolitis from those with other disorders
- The above management points to do take into consideration patients with significant medical history such as congenital heart disease, anatomic airway defects, neuromuscular disease, immunodeficiency, chronic lung disease – ADMIT, HIGH RISK!
- The physical exam will vary from minute to minute depending on child’s position, level of alertness, response to treatment – CONSTANTLY RE-EVALUATE!
- If patient presents within the first couple of days, they may worsen and need admission at a later point – PARENT EDUCATION IS KEY!
- Viral illness, treated by hydration and suction
- Signs of respiratory distress
- How to suction
- When to suction
- Frequent feeds and watch hydration status
- Cough may last 2-4 weeks, do not use OTC cough and cold medications
- Avoid tobacco smoke
- NOT RECOMMENDED!
- Albuterol – Wheezing is due to the airways being clogged with debris not bronchospasm
- Racemic epinephrine
- Chest physiotherapy
- Hypertonic Saline
- Routine testing
- Chest X-rays
Special thanks to Dr. Hima Khamar, MD PGY-2 for her contribution to this month’s Pediatric Pearls!
Varicella (chickenpox) is a highly contagious disease caused by primary infection with varicella-zoster virus (VZV)2 and may cause maternal mortality or serious morbidity
> Reactivation of latent infection, usually many years after the primary infection, may result in herpes zoster (shingles), a painful vesicular eruption in the distribution of sensory nerve roots2
> Both varicella (chickenpox) and zoster (shingles) are notifiable diseases. Notification must be made to the Communicable Disease Control Branch of SA Health as soon as possible and at least within three days of suspicion of diagnosis, by telephone or post.
Route of transmission
> Infection with chickenpox is transmitted through airborne / respiratory droplets and direct contact with vesicle fluid
> 10 to 21 days (may be up to 35 days in contacts given high titre zoster immunoglobulin, ZIG)
Period of infectivity
> 48 hours before the onset of rash until crusting of all lesions (usually day 6 of rash)
> Infectious period may be prolonged in people with impaired immunity
> Non-immune staff should not care for the woman / baby infected with chickenpox
> Varicella (and herpes zoster) vesicles contain large numbers of virus particles. Ensure appropriate transmission based (standard, contact and airborne) precautions including:
> A negative pressure room with door shut (chickenpox and disseminated shingles)
> Immune staff in attendance
> Gloves, gown
> All dressing materials should be treated as medical waste
> Chickenpox and disseminated shingles use standard, contact and airborne precautions
> Localized shingles use contact precautions (only immune staff in attendance, single room, gloves, gown)
> In herpes zoster (shingles), transmission of infection usually requires contact with vesicle fluid; however, there is also evidence of respiratory spread. Localized shingles requires standard and contact precautions (not airborne precautions)
Susceptibility to varicella
> Women and babies susceptible to infection with VZV (may be severe or life-threatening) include:
> No history of varicella (chickenpox or shingles)
> Seronegative for varicella antibodies (VZV-IgG negative)
> No documented evidence of varicella vaccination
> For the purpose of infection control and prophylaxis, significant exposure of a susceptible woman who is pregnant to varicella includes:
> Living in the same household as a person with active varicella or herpes zoster
> Direct face to face contact with a person with varicella or herpes zoster for at least 5 minutes
> Being in the same room for at least 1 hour
> Chickenpox cases are infectious from 2 days before rash until lesions crusted
Management of maternal exposure to varicella-zoster virus
History of previous chickenpox
> No action required
No or uncertain history of chickenpox
> Obtain serology for antibody status (VZV-IgG) (if practicable)
> ZIG if required should be given within 96 hours. Testing should only be done if ZIG would still be able to be given, if required, within this window
Within 96 hours from exposure
> Zoster immunoglobulin (ZIG) should be given to all seronegative women within 96 hours (see adult dose under ZIG dosage below)
> However there may be some limited effect out to as late as 10 days post exposure
> Advise to seek medical care immediately if chickenpox develops
More than 96 hours following exposure
> Oral aciclovir or valaciclovir (see dosage below) should be considered for women:
> In the second half of pregnancy
> With a history of an underlying lung disease
> Who are immuno-compromised
> Who are smokers
Note: Advise women to seek medical care immediately if chickenpox develops
Management of varicella-zoster in pregnancy
Less than 24 hours since appearance of rash
> Oral aciclovir 800 mg 5 times a day for 7 days OR oral valaciclovir 1 g three times a day for 7 days]
> Monitor at home
More than 24 hours since onset of rash
> No oral aciclovir / valaciclovir and monitor at home if:
> No underlying lung disease
> Not immunocompromised
> Monitor in hospital if any of the above risk factors
> Offer appropriate fetal medicine counselling
> Advise to seek medical attention for the following complications:
> Respiratory symptoms
> Haemorrhagic rash or bleeding
> New pocks developing after 6 days
> Persistent fever
> 6 days
> Neurological symptoms
> Give aciclovir 10 mg / kg every 8 hours for 7 to 10 days (IV followed by oral [see dosage below]) and administer supportive therapy
Consider caesarean section if:
> Signs of significant fetal compromise
> Evidence of maternal respiratory failure exacerbated by advanced
Risk of fetal varicella syndrome (FVS) after maternal VZV
Timing of maternal infection:
>Less than 12 weeks gestation- 0.55%
>12-28 weeks gestation- 1.4%
>More than 28 weeks gestation- No cases of FVS reported
Refer to maternal fetal specialist for prenatal diagnosis and counselling
> Detailed fetal ultrasound for anomalies is recommended at least five weeks after primary infection
> Repeat ultrasounds until delivery. If abnormal may consider fetal MRI
> VZV fetal serology is unhelpful
> Amniocentesis not routinely advised if ultrasound normal, because risks of FVS low but negative VZV PCR may be reassuring
Management of infants exposed to maternal varicella zoster
Maternal chickenpox > 7 days before delivery
> No zoster immunoglobulin (ZIG) required
> No isolation required
> Encourage breastfeeding
> No other interventions even if baby has chickenpox at or very soon after birth unless preterm < 28 weeks gestation or low birth weight < 1,000 g > Very preterm infants (≤ 28 weeks gestation) born with chickenpox should receive intravenous aciclovir 20 mg / kg / dose every 8 hours as a slow infusion (1-2 hours)
Thank you to Christine DeFranco PGY-4 EM Resident for this review of VZV in pregnancy!
Source: EM Practice Podcast – Dec 2017
** There are no existing ACEP guidelines on this topic.
- Stabilizing and pain control
- Neurovascular compromise
- If suspected then d/w med control for considerate of immediate reduction and splinting vs. rapid transport to ED
- If no suspicion the patient can be immobilized in current position
- Don’t forget C-spine precautions as these injuries are often distracting
- Typically traumatic in origin
- Over 2/3 Hip dislocations occur in patients who present after MVCs without seat belts with the knee hitting the dashboard and the body moving forward over a fixed femur.
- Often associated with posterior wall/lip fractures of the acetabulum
- Simple vs. Complex
- Simple Dislocation – does not involve fracture
- Complex Dislocation – involves fracture
- Posterior & Inferior dislocations are most common – about 90% of dislocations
- Fracture of >40% of the acetabular rim is considered an UNSTABLE FRACTURE (requires ORIF)
- If there is a posterior acetabular fracture you must get a CT to eval for unstable fractures
- Sciatic nerve injury
- Seen in about 14% of traumatic hip dislocations
- Check sensory along the posterior leg, ability to dorsiflex the ankle and ankle reflexes
- 95% of traumatic hip dislocations will have another associated injury
- Be sure to complete a full trauma survey on these patients per ATLS guidelines
- Initial image should be a bedside AP pelvic radiograph
- Look for Shenton’s Line
- Lateral film can seal the diagnosis if unsure based on initial bedside AP
- CT if neeeded
Treatment for Native Hips (non-prosthetic)
- Ortho Consultation are required for the following:
- Complex hip dislocations
- Irreducible dislocations
- Non-concentric reductions
- Neurovascular deficits despite reduction
– Simple dislocations can & should be reduced by the ED physician!
– Reduction should be performed within 6 hours of injury to decrease risk of avascular necrosis
– No more than 3 attempts at reduction should be made by the ED provider
– If patient requires transfer to a different hospital, an attempt at reduction should be made by the ED provider.
– Patients transferred without reduction had a 4-fold risk of severe sciatic nerve compared to those transferred after reduction (16% vs 4%).
– Be sure pain is controlled prior to attempting reduction
- Ultrasound guided fascia iliaca compartmental block work great
- Reduces need for systemic analgesics
- Improves patient comfort
- Increases likelihood of successful reduction
- Reduce need for procedural sedation
- Be sure to have completed a full neurological exam prior to blocking your patient
LINK TO VIDEO
- In many cases, procedural sedation and systemic analgesia may also be needed (in addition to nerve block) in order to adequate pain control and muscle relaxation.
No evidence exists to recommend one technique over the other.
After successful reduction the hip should be immobilized in extension and external rotation with slight abduction
– Use an abduction pillow to help hold this position
– Knee immobilizer can be used if no abduction pillow is available
Don’t forget to obtain a post reduction film to confirm alignment
– Early passive range of motion and rehab is usually recommended
– Patients should remain non-weight bearing until seen by an Orthopedist
Notes on Prosthetic Hip Dislocations
- Quite common
- Incidence of ~2% of patients who undergo THA
- 60% occur within first 3 mo, 77% occur within the first year
- Often the result of minimal force like bending over to pick something up off the floor
- Use the same techniques as a native hip reduction
- Do not need abduction bracing after the reduction
- If the patient can walk after the reduction, they can be safely discharged (after discussion with their orthopedist)
- Less urgency, no risk of avascular necrosis as the femoral head has already been replaced
- Remember, these injuries are painful and although less urgent, the reduction should occur as soon as possible
CC: Left leg pain
HPI: 52 year old male with PMH of IDDM presents to the Emergency Dept. (ED) with left leg pain for the past 9 days which has become progressively worse. He is a taxi driver and reports that a part of the seat, which supports his legs, has been rubbing against his left hip/buttock/thigh and he thinks this is what’s causing the pain. He reports pain to the back of his left buttock, which radiates down the leg “like a shooting pain.” The patient has been to the ED multiple times already for similar complaints, requesting for stronger pain medications. He is upset because he feels the medicine just isn’t working. At this point, the patient is uncooperative and refuses to answer any more questions. Further history was obtained from his previous visit history, which stated he was discharged yesterday with a diagnosis of sciatica and a prescription for Lidoderm patch, Motrin and Percocet.
PMH/Birth History: N/A
Social History: N/A, refused to answer any further questions
VS: BP 125/59 HR 108 RR18 T: 98F 98% RA
General: In moderate acute distress, appears stated age, in moderate pain, uncomfortable and diaphoretic.
HEENT: Atraumatic, normo-cephalic. No deformities. PEERLA
Respiratory: Lungs CTA bilaterally.
Cardiac: +S1/S2, no MRG, regular rate and rhythm
Abdomen: soft NT ND
Extremities: B/L DP 2+, Cap refill < 3 seconds, positive straight leg (LLE); pain isolated to (L) buttock and posterior lateral thigh.
Neuro exam: CN III –XII intact. 5/5 strength in all 4 extremities with limited ROM in the LLE secondary to pain.
Skin: Diffuse erythema over the Left buttock extending down to the posterior lateral left thigh, with pitting edema. No fluctuance or streaking noted.
WBC: 24.7 H/H: 13.1 / 39.4 Platelets 245 PMH: 22.1 Lymph: 0.7 Mono: 1.5
Na: 126 K: 5.5 Cl: 89 CO2: 22 Glucose: 438
Bun: 38 Cr: 1.17 Alk P: 140 LFT: WNL Albumin 3.2
Lactic acid: 1.4
Repeat Vital Signs 139/81 89 16 99.7F 97% ON RA
Working Differential Diagnosis: Pyomyositis
ED/Hospital course: Orthopedic Surgery was consulted. X-Ray did not show obvious bony involvement and ESR/CRP was not suggestive of osteomyelitis. MRI was performed on the LLE, which sowed a hyper-intense signal within multiple muscles of the pelvis and left thigh consistent with myositis. Collection within the Obturator Externus and Gluteus Maximus muscles likely represented an abscess consistent with pyomyositis. The patient was started on Vancomycin and Zosyn and sent to Interventional Radiology for drainage of the abscess. The cultures grew back MSSA. The left knee tap did not grow any organisms on Gram Stain. IR drainage was followed by orthopedic washout and debridement of the musculature with insertion of JP drain for continuous drainage. The patient’s antibiotics were switched to Levaquin and he was subsequently discharged home with Clindamycin and Bactrim for 2 more weeks. He tested negative for HIV.
Pearls & Takeaways:
- Don’t blow off patient’s complaints! Our patient presented with History and Physical exam consistent with sciatica with a positive straight leg test. He was on Percocet and kept asking for stronger medications for his previously diagnosed Sciatica.
- Make sure to undress the patient and examine the skin!
- If the patient is complaining of pain out of proportion to his/her exam, dig a little deeper for alternative differential!
- Since his Accucheck was High, further laboratory testing was done which revealed leukocytosis. The elevated white count prompted me to perform a further work up
- Always re-evaluate the patient! On re-evaluation, he appeared sicker and with cool, damp skin on his back and neck, solidifying my gestalt that maybe I am missing something
- Pyomyositis is a purulent infection of skeletal muscle that arises from hematogenous spread, usually with abscess formation.
- Risk Factors: immunodeficiency (HIV).
- auerus is the most common cause of pyomyositis; it causes up to 75 – 90% of cases.
- Pyomyositis presents with fever and pain and cramping localized to a single muscle group. It develops most often in the lower extremity (sites include the thigh, calf and gluteal muscles) but any group of muscles can be involved including iliopsoas, pelvic, trunk, Paraspinal and upper extremities.
- MRI is the most useful imaging modality for diagnosing the disease. It can distinguish the defining sites of infection and rule out other entities.
- Nonspecific lab findings include Leukocytosis and elevated inflammatory markers but CPK are often normal.
- Empiric antibiotics should be directed against Staph/Strep for immunocompetent. Immunocompromised should be covered for Gram negative, gram positive and anaerobic organisms should be considered.
- Pyomyositis is graded based on stages.
- Stage 1 (Invasive stage, 1-2 weeks, may only have pain) can be treated with Antibiotics alone.
- Most patients present with Stage 2 (Suppurative stage, weeks 3-4)
- Stage 3 (Late stage) due to delay in diagnosis and usually requires drainage for definitive management.
Case presented by Dr. Michael Hong
Introduction to Nitrous in the ED
- Tasteless colorless gas administered in combination with oxygen
- Maximum concentration 70% N20
- Absorbed via pulmonary vasculature and does not combine with hemoglobin or other body tissues
- Rapid onset and elimination
- <60 seconds
- Analgesic and anxiolytic agent
- Use along with local anesthetic or other non-opioid pain medications
- Administered via facemask
- Only monitoring needed is pulse oximetry
- No NPO requirements, patient can drive after administration, no IV line needed, no RN necessary at bedside
- Nitrous is NOT procedural sedation and should be thought of as a pain medication
- Studies show it is similar to morphine 10 mg IM
- It works only when the patient is breathing it in and stops working immediately when the gas is off
- Severe COPD or asthma
- Active Otitis Media/Sinusitis
- Active Bowel Obstruction
- 1st -2nd trimester pregnancy
- Altered level of consciousness
- Severe Psychiatric disease
- Head Injury
- Complex Advanced Active Cardiac Disease
Indications (really any procedural pain)
- Laceration repair
- Incision & Drainage
- Wound Care
- Foreign body removal
- Central Venous Access
- Peripheral venous access
- Fecal Disimpaction
- Adjunct for
Nitrous as an adjunct
- If using nitrous to try and reduce a joint
- Use IN ketamine
- Intra-articular lidocaine
- Concomitant admin of nitrous with opioids, benzos, or propofol is considered PSA
- If giving an IV opioid you should wait 30-45 minutes before using nitrous to avoid excessive sedation or airway issues
What do we have?
Porter Standard Flowmeter
- Stored in the trauma bay
- Extra tank rack across from peds resus bed
- Must use disposable breathing circuit
- Located next to desk in trauma bay
- There are adults small, youth medium, and peds small
- Nitrous oxide flow stops if oxygen is shut off or supply becomes limited
- Can never supply more than 70% nitrous oxide
- Exhaled gas is scavenged away to avoid unnecessary exposure to providers
- Wheel to bedside
- Plug green oxygen tube into oxygen port in the wall (may have to remove Christmas tree)
- The gray tube scavenging tube plug into to the suction port in the wall
- Breathing circuit only fits one way, push big lumen tube into top (by gray bag) and the clear little tube below breathing bag
- Position the patient comfortably
- Bring unit close to the patient so you can reach the dials
- Make sure pulse oximetry is connected and you can see the waveform
- Once the mask is on…
- Set oxygen flow rate then titrate nitrous oxide to desired percentage
- Watch gray breathing bag as a guide to adjust flow (titrate flow)
- If bag is fully collapsing, increase overall flow
- If bag is not moving, decrease overall flow
- Once nitrous oxide percentage is set, regardless of flow rate, percentage stays the same
During The Procedure
- Titrate nitrous oxide up and down as needed for “desired analgesia”, watch breathing bag to determine overall flow
- Once procedure is complete, turn off nitrous oxide, allow patient to breath oxygen only for 60 seconds
- Continue to watch breathing bag
- Then remove mask completely
- Patient can be discharged with no driving or work restrictions
- Throw away the breathing circuit
- Return it to the trauma bay
- Becker 2008
- Babl 2015
- Zhang 1999
- Champman 1979
- Jastek 1991
Special thanks to Dr. Alexis LaPietra for her contribution! Watch out for next times pain pearls…….. Haldol as an analgesic!!!
CC: Can’t see for 2 months
HPI: 10 year old male with no significant past medical history presents to the Emergency Dept. complaining of painless vision loss in the right eye for 2-3 months. Patient states he has been having difficulty seeing out of his right eye for 2 months despite changing positions in class, taking on and off his glasses and using eye drops. Vision loss has become progressively worse and now he can only distinguish whether lights are on or off. Mother states she did not do anything about this problem because she thought he was kidding and she didn’t’ have money or health insurance to seek medical attention. Patient has been wearing Bifocals for myopia since the age of 6, with corrective vision lenses at age 5. Denies associated trauma. Patient moved to the U.S from Nigeria 5 years ago. He lives with his mother and sister. Vaccines are up to date.
PMH/Birth History: NSVD at 39 weeks, 1 day. Birth took place in Nigeria and mother denies any infection during or after pregnancy. Following birth, patient did not have any complications such as pneumonia, eye infections or rashes.
Social History: Denies drug abuse. Denies exposure to chemicals. Denies contact with dirt, dogs or pigs. Patient did not live on a farm. As per mother, there was no domestic abuse in the family
Vitals within normal Limits
General: In no acute distress, appears stated age.
Head: Atraumatic, normocephalic. No deformities.
Eye: Right (OD): pupil non-reactive and remains white in color and approximately 2mm. Afferent reflex is present CN II; efferent reflex is absent. There is a complete visual field defect on the right side. Visual Acuity: Can only distinguish between light and dark. Unable to count fingers at any distance or visual objects even in motion. On Fundoscopic exam, the fundus is gray/dull, with no retina visualized. ALL CONSISTENT WITH LEUKOCORIA
Respiratory: Lungs CTA bilaterally.
Cardiac: +S1/S2, no MRG, regular rate and rhythm
Abdomen: soft NT ND
Neuro exam: CN III –XII intact. No motor, sensory, vibratory, temperature or pain deficits. Gait is steady and normal, without any difficulty. Cerebellar function intact, no dysmetria bilaterally.
Extremities: Full ROM in all extremities. 5/5 strength in all extremities
Skin: No edema, rashes, lacerations, or abrasions. Skin is warm, pink, moist and intact.
CBC: Unremarkable with WBC: 7.1 Hemoglobin: 13.5 Platelets 211.
CMP: WNL CRP and ESR = WNL
Tonometry: IOP approx. 17-18 x 3 times
Wood lamp: No corneal abrasion, dendritic ulcers, lesions or depositions OU
Bedside U/S: Completed within 10 minutes of arrival ( Only Right eye is shown)
Working Differential Diagnosis:
- Intraocular Mass
- Parasitic infiltrate
- Posterior Infarct
CT Max/Facial w/o Contrast to rule out intracranial pathologies: Negative for masses; positive for homologous material in the right lobe. MRI was recommended for further evaluation
ED/Hospital course: Ophthalmologist on call was consulted, and said there was nothing more to do. Unfortunately because his vision loss was > 2 months, no life saving surgery was imminent as the retina was already detached causing ischemia to the rods and cones within it. Patient was to follow up in ophthalmology clinic the following day. Patient’s Pediatrician was also contacted and he referred the patient to a Pediatric Ophthalmic specialist in University Hospital, with a scheduled appointment within the same week. Approximately one week ago, patient underwent surgery and the leading diagnosis was Toxocariasis as per MRI. Biopsy results to follow. As per mother, the patient is still without vision in his right eye.
|LEUKOCORIA, UNILATERAL, 10 YO MALE DIFFERENTIALS
Coats disease— is an exudative retinal vascular disorder characterized by retinal telangiectasias and subretinal exudation leading to serous retinal detachment. Presenting complaints include decreased visual acuity, strabismus, or leukocoria. The leukocoria in Coats disease is generally more yellow than white due to the presence of subretinal lipid. Coats disease is almost always unilateral and the vast majority of cases occur in boys. The majority of cases presenting with leukocoria are diagnosed between five and nine years of age, which is older than the majority of retinoblastoma patients.
Clinical examination: subretinal lipid and abnormal telangiectatic vessels US: demonstrates complete retinal detachment with massive subretinal lipid. Intraocular calcification is almost never present in Coats disease, another feature that helps to distinguish it from retinoblastoma.
The retinal photograph depicts bullous retinal detachment in the Left eye of a 1-year-old child with Coat’s disease simulating retinoblastoma. The magnetic resonance images confirm the diagnosis of retinal detachment and exclude retinoblastoma because of the absence of intraocular mass.
|Toxocariasis — Toxocariasis, or visceral larva migrans, is an infection caused by the dog ascarid Toxocara canis or, less commonly, the cat ascarid Toxocara catis. There may be a history of living in an underdeveloped country, and exposure to dirt or undomesticated dogs. It occurs most commonly in children one to five years of age. Common presenting signs of toxocariasis are strabismus and poor vision. The ocular lesion is caused by the inflammatory response to the second-stage larva, which may localize in the one eye or both eyes
Chorioretinitis characteristic of toxoplasmosis. A pigmented scar is seen with an adjacent area of active chorioretinitis. The diagnosis of toxoplasmosis is based primarily on the appearance of the chorioretinal lesion rather than serologic studies. Courtesy of James T Rosenbaum, MD.
Retinopathy of prematurity (ROP) — developmental vascular proliferative disorder that occurs in the incompletely vascularized retina of preterm infants and can lead to retinal detachment and permanent blindness. The most important risk factor for developing ROP is prematurity. There needs to be a history of prematurity, and/or mother mentions patient was on O2 for awhile.
Vitreous hemorrhage — Vitreous hemorrhage causes leukocoria when there is extensive organization of the blood into a clot before degradation. With time, the reddish hue of the blood is lost and the hemorrhage transforms into “whitish debris.” Etiology includes advanced ROP, trauma (MOST common), leukemia or hemorrhagic disease of newborn
Retinablastoma– Retinoblastoma is the most common primary intraocular malignancy of childhood and accounts for 10 to 15 percent of cancers that occur within the first year of life. Retinoblastoma typically presents as leukocoria in a child under the age of two years. Untreated retinoblastoma is a deadly disease; however, with advances in treatment, survival in the contemporary era is >95 percent. Most common age group is birth- 2 years. Very uncommon in children over the age of 5, although 1-2 case reports have occurred in 18 year old males
Pearls & Takeaways:
- Leukocoria Requires further investigation – On exam, History and Diagnostic
- The use of tonometry, fundoscopy and ocular ultrasound are an easy, noninvasive way to add to your ophthalmic exam. Slit-lamp exam could have been considered here
- Ocular ultrasound is really cool and fun!
- Advocate for your patients! Make sure they have proper follow up with a specialist
- If any abuse or neglect is suspected, be sure to turn on “Sherlock Holmes” senses and investigate.
Case presented by Dr. Sarah Bolan
Hi all. I wanted to bring to your attention a great case. The case was a young woman with relative euglycemic diabetic ketoacidosis. This diagnosis used to be quite rare and associated with pregnancy or very poor PO intake. However, with the use of SGLT2 inhibitors (which this young woman was taking) the incidence is increasing. The diagnosis highlights some very important factors about the treatment of DKA:
- Don’t just look at the blood sugar. Calculate your anion gap. Look at the bicarb. Calculate the strong ion difference. Check for ketones. A VBG is fine for a rough estimate of pH. If you really want to get fancy, an ABG will give you an accurate base deficit that can help you figure out (along with your lactic acid, strong ion gap, or delta-delta) exactly what else is going on with the patient in the setting of multiple competing metabolic processes. But that’s only if you want to get fancy. I think you can provide great initial resuscitation without it.
- Remember why we do what we do in DKA and all the complications you can get from treatment. The treatment is based on exactly the same principles that guide the treatment of “regular” DKA. However, they are not starting at the exact same metabolically disturbed place as most patients do. They can be just as sick, if not more, but the initial treatment has to take into consideration exactly where they are in their metabolic disarray. Things to think about as you are coming up with a treatment plan:
- These patients need fluid. Fluid will be your friend (more on that later)
- These patients need glucose. From the start. For a glucose less than 100-125, consider starting D10 instead of D5.
- They need glucose because they need insulin too. They still may have some relative insulin resistance so giving them glucose alone won’t help them if they cannot get the glucose into any cells. However, as you are already starting from a lower glucose, be very gentle. If you still bolus insulin in DKA (which I do- in selected cases- and would be glad to have conversation about whether we should or not at another time) do NOT bolus these patients. I don’t have great evidence as to where to start a drip so I pick a low number. Like 1 low. I can always move up. If anyone has a better scientific explanation on how to pick your infusion rate, I’d love to hear it.
- They need insulin so you better be sure you aren’t going to cause a malignant arrhythmia if you give it to them. Make sure your potassium isn’t going to plummet when you start insulin. Rough guideline is to make sure it is >3.3 . This is true for all DKA.
- They don’t have a sodium correction because the glucose is normal. If their sodium is already on the higher side (around >140), think of starting with ½ NS as your base.
The attending on the case did an excellent job with this patient. He focused on fluid and recognized her severe metabolic disturbance, despite the fact that her blood sugar was trying to hide it.
I’ve included two articles below. One is two case reports on euglycemic DKA and the other talks specifically about cases involving SGLT2 inhibitors. They aren’t the best articles I’ve ever read but they are more official than I am so felt I should include them. As a said, this is a relatively new class of medications and a relatively new phenomenon.
Euglycemic diabetic ketoacidosis: a diagnostic and therapeutic dilemma, EDM Case Reports, September 2017
Euglycemic Diabetic Ketoacidosis: A Potential Complication of Treatment With Sodium–Glucose Cotransporter 2 Inhibition, Diabetes Care, Volume 38, September 2015
Ruth Lamm, MD FACEP
Critical Care Medicine
Saint Joseph’s Hospital Medical Center
CC: Nausea and vomiting and “ I think my sugar is low”
HPI: 36-year-old Female with PMH of Diabetes presents to the Emergency Department complaining of multiple episodes of non-bloody, non-bilious vomiting for the past 5 days. Associated symptoms include chills and a mild sore throat. Denies fever, HA, neck pain, chest pain, SOB, abdominal pain, diarrhea or bloody stools. Denies dysuria, hematuria or urinary frequency or urgency. Denies recent travels or sick contacts. LMP: Currently menstruating
Social: Admits to smoking 2 cigarettes per day for the past 10 years. Smokes marijuana daily. Denies alcohol use
Physical Exam :
BP 171/82 HR 82 RR 20 SpO2 100% on RA Temp 97.8F 108.86 kg
Constitutional: Alert, wake, and in no acute distress. Obese
HEENT: NCAT, pupils PERRLA, neck is supple. Oral mucosa is pink, dry and intact. No lesions. Normal conjuctiva
Respiratory: CTA B/L, no rales, rhonchi, no stridor or wheezing
Cardiac: +S1/S2, regular rate and rhythm, no murmur, rubs or gallop
Abdomen: Soft, with mild tenderness in epigastric area. No rebound or guarding. Normal BS
Neuro: AAO x 3. No focal deficits, moving all four extremities. Steady gate without difficulty.
MSK/Extremities: no edema, tenderness or swelling.
Skin: Moderate ecchymosis overlying RUQ and RUE. Normal moisture. No rash or lesions noted
WBC: 8.4 HGB: 9.3 HCT: 26.8 Platelet: 9L
Na: 136 K: 3.4 Cl: 104 Co2: 26 BUN: 16 Cr: 0.95 Glucose: 109
PT: 14.4 PTT: 28.7 INR: 1.1
Calcium 8.8 Total Bilirubin: 2.8 Alk Phos: 56 AST: 21 ALT: 12
Urinalysis: Large Blood with negative Nitrites and Leukocyte Esterase without ketones. UA Protein: 100
Pertinent Images and other tests: Chest X ray: Borderline heart size. NO active disease
Upper Abdominal U/S: Normal Liver and spleen. The spleen measured 10.9 cm in greatest dimension and was homogeneous in echotexture. No focal splenic lesion identified. The liver measured 16.5 cm and appeared normal.
Thrombotic Thrombocytopenia Purpura (TTP)
Idiopathic Thrombocytopenic Purpura (ITP)
Hemolytic Uremic Syndrome (HUS)
Anemia due to blood loss
ED Course: On further questioning, patient states she has been menstruating for 3 weeks now and bleeding is heavier as compared to the previous cycle. In the ED, patient was given NS 0.9% 1000mL IV bolus once, Zofran 4 mg IV once, Reglan 10mg IV once. Type and screen and blood cultures were also sent and patient was admitted to the Medical ICU for thrombocytopenia and anemia.
In the Medical ICU, further lab results demonstrated elevated the following:
LDH: 699 Fibrinogen: 410 Haptoglobin: < 10 Troponin 0.44
Blood Cultures: No Growth
Urine Toxicology: Positive for cannabinoids
Hepatitis C antibody: < 0.1
HIV Ag/Ab: Non reactive
In the ICU, patient was given a 125mg bolus of IV Solu-Medrol and then started on 60mg IV every 8 hours. She was transfused 1 Unit of platelet with no response, as the following day, platelets actually dropped to 5.Hematology/Oncology was also consulted. They stated that the occasional schistocytes seen on blood smear with low Haptoglobin levels and elevated reticulocyte count and LDH was suggestive of microangiopathic hemolytic anemia, making TTP a more likely diagnosis. Heme/Onc recommended against any further platelet transfusion and ADAMS 13 levels were sent. On hospital day #3, patient’s LDH levels had increased to 1586 and Troponin was elevated to 1.2 with symptoms of dyspnea. Patient also had worsening anemia as hemoglobin dropped to 7.0, and platelets remained at 9. The same day, Surgery was consulted and patient was transfused 2 Units of PRBs and 2 Units of FFP in preparation for Shiley Catheter insertion for plasmapheresis. Cardiology was also consulted for the elevated troponin, which they attributed to ongoing demand ischemia without any evidence of ACS. Unfortunately, the following night at 1:25 AM and before a Shiley was ever placed, the patient became minimally responsive and Saturating at 90% on RA. Immediately, she became bradycardic and lost pulses. CPR was initiated as patient was simultaneously intubated. Total duration of CPR was 60 minutes. The patient received Epinephrine x 20, Amiodarone 300 mg x 1 and Insulin with 1 amp of D50W, Calcium chloride and Sodium Bicarbonate for Potassium of 6.1 on ABG. Sadly, the patient was pronounced at 2:25AM.
PEARLS : Thrombotic Thrombocytopenic Purpura (TTP)
PENTAD = ‘FAT RN”
- Fever (50%)
- Uncommon if they present early in the disease
- High fever and chills suggest sepsis, so look for a source of infection.
- MAJOR diagnostic criterion
- Mean platelet of 25, 000 but they reach 5000.
- Microangiopathic Hemolytic Anemia
- MAJOR diagnostic criterion
- Non-immune hemolysis with schistocytes
- Results in elevated LDH, Low haptoglobin and high indirect bilirubin
- Severely elevated LDH has been associated with MI, arrhythmias, shock and heart failure.
- Renal Failure
- Due to renal thrombotic microangiopathy
- Urinalysis will show mild proteinuria +/- hematuria
- Acute Rena insufficiency may be present and may require dialysis.
- Neurological Symptoms: (Seizure, AMS, HA, coma, hemiplegia, aphasia, etc.)
- Focal Deficits less prevalent
- Occurs in 25-60% of patients
- Symptoms are usually transient and subtle, so you must ask the patient about prior symptoms!
*** KEEP in mind; all features of the PENTAD do NOT to be present at the same time for diagnosis to be made.
- African American race
- Ages 30-50 years
- Rheumatologic/autoimmune disease history
- Fatigue, tachycardia, pallor, SOB or chest pain
- Abdominal pain, back pain, Nausea, vomiting or diarrhea
- New Onset jaundice and dark colored urine
- Diffuse, non-palpable petechial/purpuric rash.
- ADAMTS-13 protease enzyme deficiency
- 60% of cases
- Enzyme cleaves von Willebrand factor (vWF) multimers. Without it, excessive platelet aggregation, thrombocytopenia and thrombosis occurs
- Idiopathic or Secondary Causes
- 40% of cases
- (i.e. HIV, malignancy, Infection, Pregnancy, pancreatitis, autoimmune disease, pancreatitis and medications such s Acyclovir, Quinine, Oxymorphoine, Plavix and Tacrolimus)
- Diagnosis/Lab findings
- NORMAL PT, PTT and Fibrinogen levels (Unlike in DIC)
- Anemia and elevated indirect bilirubin
- A peripheral smear is important for diagnosis, as 100% of patients will have schistocytes present during the course of the disease
- ADAMTS-13 activity < 10% (normal activity is > 50%)
*** Remember that TTP is a clinical diagnosis. Do NOT delay treatment!
- Differential Diagnosis
- Other Causes of Microangiopathic Hemolytic Anemia (MAHA)
- DIC, HUS, HELLP Syndrome, Malignant Hypertension, Heparin induced thrombocytopenia, Paroxysmal Nocturnal Hemoglobinuria, etc.
- Viral infections (HIV, mumps, varicella, EBVS)
- Other Causes of Microangiopathic Hemolytic Anemia (MAHA)
- Consult Hematology!
- AVOID Platelet Transfusion if possible!
- It can lead to renal failure, higher rates of arterial thrombosis and death
- Should be AVOIDED EXCEPT in life-threatening bleeding or ICH
- Plasma Exchange (Plasmapheresis) is First Line treatment!
- Replaces defective or insufficient ADAMTS-13 and clears vWF multimers
- LDH can be used to evaluate for treatment response
- FFP Transfusion
- Contains ADAMTS-13
- Can be helpful if delay in plasmapheresis
- Transfusion of RBCs (indicated ONLY in severe bleeding with a delay in plasma exchange)
- Adjunct Treatment and do not replace plasmapheresis
- 1mg/kg Prednisone PO or Solu-Medrol 125mg IV
- Not first line but may be used in those who fail plasmapheresis
- Last line therapy after stabilization
- Inhibitor antibody is made in the spleen
Suspect TTP in any patient with MAHA and thrombocytopenia!
Case presented by Dr. Yenisleidy Paez Perez, DO