Pediatric Urinary Tract Infection
By: Hima Khamar, PGY3
In a previous pediatric pearl, we discussed how to treat febrile infants below 60 days. This pearl discussed management of pediatric urinary tract infection (UTI), but also discusses patients above the age of 60 days with a fever with no obvious source in whom UTI as a source.
History and Physical
Duration of fever
Symptoms that suggest an alternative source
Hydration status History of recurring fever without source
History of UTI
History of constipation
Dysfunctional voiding by history
FH of vesicoureteral reflux (VUR) or renal diseases
Suprapubic, flank tenderness
Abdominal mass, palpable bladder
Evidence of spinal lesion
Other GU abnormalities
|Signs and Symptoms of UTI: Most common to least common*|
|Infants < 3 months||Fever
Failure to thrive
|Infants > 3 months – preverbal||Fever||Abdominal pain
Failure to thrive
|Verbal – 18 years||Frequency
Changes to continence
Risk factors for UTI
Infants >56 days who are not toilet trained
|Female risk factors
– T ≥ 39°C
– Fever ≥ 2 days
– No source
– < 12 months
>3 risk factors consider screening>4 risk factors recommend screening
|Male risk factors
– T ≥ 39°C
– Fever ≥ 2 days
– No source
– < 6 monthsCircumcised:
≥ 3 consider screening
≥ 4 recommend screening
≥ 2 consider screening
≥ 3 recommend screening
|Fully toilet trained – 18 yrs
– Symptoms referable to urinary tract
– Prior history of UTI, fever ≥ 2 days
– Prolonged fever (≥ 5 days)Recommend screening for any of the above factors
TO CATH OR NOT TO CATH?
The AAP recommends obtaining a catheterized specimen for diagnosis of UTI, but this is a level C recommendation. Upon further reading, they basically state a bagged specimen is acceptable as well. SO BASICALLY, GET THE URINE IN WHATEVER WAY YOU CAN.
Catheterization with >50,000 cfu/ml
Clean catch with >100,000 cfu/ml
Leukocyte esterase and nitrite positive
Nitrite positive, leukocyte esterase negative
Pyuria and bacteriuria positive
Bacteriuria positive and pyuria negative
Catheterization with >10,000 cfu/ml
Clean catch with >50,000 cfu/ml
Leukocyte esterase positive, nitrite negative = only treat if good evidence for UTI
Leukocyte esterase and nitrite negative = no UTI
Pyuria positive and bacteriuria negative = only treat for UTI if have good evidence
Bacteriuria and pyuria negative = no UTI
Whom to culture?
– Infants and children who are suspected to have acute pyelonephritis/upper urinary tract infection
– Infants under 3 months
– Infants and children with a positive result for leukocyte esterase or nitrite – EVERY POSITIVE URINALYSIS SHOULD BE CULTURED
– Infants and children with recurrent UTI
– Infants and children with an infection that does not respond to treatment within 24–48 hours, if no sample has already been sent
Oral vs. Parenteral Antibiotics
– Most patients will tolerate oral antibiotics. Patients should receive parenteral antibiotics if patient is ill appearing, not able to tolerate PO, or has any other contraindication to oral antibiotics.
-Antibiotics are recommended for 7-14 days. Shorter courses result in spread of infection and renal scarring.
|PARENTERAL ANTIBIOTICS||ORAL ANTIBIOTICS|
|Ceftriaxone 75 mg/kg Q24h
Cefotaxime 150 mg/kg divided into Q6-8h
Ceftazidime 100-150 mg/kg divided into Q8h
Gentamicin 7.5 mg/kg divided into Q8h
Tobramycin 5 mg/kg divided into Q8h
Piperacillin 300 mg/kg divided into Q6-8h
|Amox-clav 20-40 mg/kg divided into Q8h
TMP 6-12 mg/kg SMX 30-60 mg/kg divided into Q12h
Cefixime 8 mg/kg Q daily
Cefpodoxime 10 mg/kg divided into Q12h
Cefuroxime 20-30 mg/kg divided into Q12h
Cephalexin 50-100 mg/kg divided into Q6h
– Toxic appearance
– Dehydration requiring IVF
– Failed outpatient therapy
– Febrile infants < 60 days
– Non-febrile infants 31-60 days can be considered for outpatient therapy if they have good follow up within 24 hours
–ALL patients should have a renal bladder US (RBUS) after their first febrile UTI. RBUS should be obtained after the patient has recovered from the acute infection (4-6 weeks). Studies have shown that in the acute phase can have false positives due to structural changes that are transient caused by the infection, such as hydronephrosis. (THIS IS FOR THE OUTPATIENT PHYSICIAN)
-Obtain the RBUS during acute illness if: Hospitalized; Ill, concern for sepsis; Abdominal, pelvic mass; Inadequate response to 48 hours of therapy.
-Voiding cystourethrogram (VCUG) should not be obtained routinely after first febrile UTI.
-Obtain VCUG if RBUS is abnormal.
1. CHOP Clinical Pathways
2. Seattle Children’s Hospital Clinical Pathways
3. AAP Guidelines on UTI
4. NICE Guidelines on UTI
Presenting Resident: Katrina D’Amore, PGY4
Chief Complaint: Palpitations
Brief HPI: 36 y/o F G4P2012 at 18 weeks gestation presents complaining of palpitations that began this morning. Patient reports a history of “SVT” multiple times in the past and she even underwent ablation in 2012. Patient states that “Adenosine never ever works for me.” Patient denies any other symptoms and was in her usual state of health until the symptoms began this morning. Patient does report she was recently
started on Synthroid by her OB for subclinical hypothyroidism.
Pertinent PE and Vitals
VS: Afebrile, HR 203 bpm, BP 125/86, 98% on RA
Patient appears uncomfortable but not in distress. PE unremarkable except for tachycardia.
Working Diagnosis at time of Disposition:
Wide Complex Tachycardia: Ventricular Tachycardia vs SVT with aberrant conduction
ED & Hospital Course
Patient noted to be on 240 mg PO verapamil daily at home. Decision made to give Verapamil 5 mg IVP x 1. Patient immediately converted to Sinus rhythm at a rate of 100 bpm. Patient seen by both OB and EP at bedside. Electrolytes and troponin WNL. Normal Echo from 01/2019. Patient ultimately d/c with close f/u. Advised by EP to take extra ½ dose of Verapamil PO if palpitations recurred at home. Synthroid
Pearls & Takeaways
Diagnosis: Idiopathic Ventricular Tachycardia AKA Fascicular VT AKA Verapamil-sensitive VT AKA Belhassen-type VT
• Behaves like a reentrant tachycardia – usually seen in young adults (aged 15-40) w/o any structural heart disease (thus the term idiopathic)
• Mainly affects males (60-80% of cases)
• Fascicular VT is the most common idiopathic VT arising from the LEFT ventricle (thus the term fascicular)
• Most have QRS only modestly prolonged (~120-140ms) and fast initial forces (RS interval 60-80 ms)
• QRS relatively “narrow” due to the origin of the tachycardia being very early in the His-Purkinje system.
• Classified based on the site of origin/EKG morphology
o Posterior fascicular VT (95% of cases) – RBBB + LAD
o Anterior FT (5%) – RBBB + RAD
o Upper septal FT (very rare) – narrow QRS with RBBB
• OFTEN misdiagnosed as SVT with a RBBB – presence of capture or fusion beats indicates it is a ventricular tachycardia
• Usually stable despite high ventricular rates (>200/min)
• Will not respond to vagal maneuvers, adenosine, etc
• Belhassen et al first described its sensitivity to Verapamil
• Treatment: VERAPAMIL 2.5-10mg IVP (thus the term verapamil-sensitive VT)
• If you are uncertain of the diagnosis, first line treatment is synchronized cardioversion.
Reviriego S. Idiopathic fascicular left ventricular tachycardia. European Society of Cardiology 2010; 9 (13)
Belhassen B, Rotmensch HH, Laniado S. Response of recurrent sustained ventricular tachycardia
to verapamil. Br Heart J 1981; 46: 679-82.
TRANEXAMIC ACID (TXA)
By: Hima Khamar M.D., PGY3
Tranexamic acid (TXA) has become a huge asset in the world of emergency medicine when it comes to controlling hemorrhage. The main use in the ED is in traumatic hemorrhage, but there are many other uses for TXA. In this article, I will discuss some of the other uses of TXA in the hopes that the next time you come across a patient whose hemorrhage you are unable to control with conventional methods, TXA maybe an addition to your toolbox.
TXA is an antifibrinolytic agent. It reversibly binds plasminogen which prevents plasmin activation. Decreased plasmin activation results in inhibition of fibrin clot degradation, thereby stabilizing the clot. This increase in clot formation and stabilization is how TXA works to control hemorrhage.
TXA comes in both oral and intravenous formulations. The oral form comes in 500mg or 650mg tablets and is cheaper. The intravenous form comes in a vial that is usually 1000mg/10ml. Both of these formulations are used in different disease processes, which will be further discussed below.
Despite the many uses of TXA, there are only two indications for which it is approved: tooth extractions for hemophiliac patients (to be given prior to the procedure) and control of heavy menstrual bleeding (this is given orally on an outpatient basis). All the other uses are off label, despite many of them having great evidence.
USES OF TXA
- Traumatic hemorrhage
1g IV bolus over 10 minutes loading dose, followed by 1g IV infusion over 8 hours – MUST BE GIVEN WITHIN THE FIRST 3 HOURS.
Evidence for this came out of the CRASH 2 trial in 2010. The study concluded that TXA reduced all-cause mortality and reduced risk of death due to bleeding when compared to the placebo group. Also, the subgroup analysis showed only effective when given within 3 hours.
Topical. Soak cotton pledget or any other epistaxis control device, such as RhinoRocket in TXA prior to placing in the nostril.
Evidence for this came out of an RCT by Zahed et al. in 2017. The study showed topical TXA resulted in quicker resolution of epistaxis, decreased ED length of stay, decreased re-bleeding rate, and increased patient satisfaction when compared to placebo.
- Dental bleeding in relation to dental procedures (FDA use approved only for hemophilia patients)
Mouthwash. Create by either using 5mg of intravenous solution (1000mg/10ml) in 5ml to make 5% solution OR 650mg tablet crushed and placed in 20ml. A paste can also be created with the tablets and saline to placed directly onto the bleeding region.
Evidence for this came from multiple studies in the dental literature starting around the mid-2000s which showed TXA reduced bleeding when used in a mouth wash formulation both during the procedure and for 2-3 days after the dental procedure when compared to placebo. This was also proven in hemophilia patients and in patients on anticoagulants, such as Warfarin.
- Cyclic heavy menstrual bleeding (FDA approved use)
1300 mg PO 3x daily for up to 5 days.
Evidence for this came from multiple RCTs and is also in the ACOG guidelines for management of heavy menstrual bleeding.
- Traumatic hyphema
25 mg/kg PO 3x daily for 5-7 days.
There is not a lot of evidence for this use, but it has been looked at in small studies and it is a use recommended by the American Academy of Ophthalmology on a case by case basis. There was a study looking at topical (via drops), but the study was very small so not generalizable.
- Orthopedic and cardiac surgery
This is not in our realm, but orthopedic studies are by far the most numerous looking at various doses and various formulations to decrease intra-operative bleeding.
- Postpartum hemorrhage
1g IV bolus over 10 mins, if continues to have bleeding after 30 mins or has another re-bleed within 24 hours then give another 1g IV bolus over 10 mins. (Dosing based on study)
Evidence for this comes from the WOMAN trial published in 2017. The study concluded that “Tranexamic acid reduces death due to bleeding in women with post-partum haemorrhage with no adverse effects. When used as a treatment for postpartum haemorrhage, tranexamic acid should be given as soon as possible after bleeding onset.”
1g of TXA in 20ml of saline nebulized over 30 mins. (Dosing is controversial)
Evidence for this is based on various case reports. No large RCT exists at this time. This is very experimental, but definitely worth a try in those post-tonsillectomy patients (including pediatrics), cancer patients (oral or lung), or any other causes of hemoptysis.
These are just some of the uses documented in the literature. I think over time we will see more uses of TXA. I have personally used it in penile bleeding secondary to a false track created by a misplaced Foley catheter. I have also used it to stop bleeding topically for varicose veins. There are also current ongoing studies looking at its use in GI bleeding as well. SO, CONSIDER TXA THE NEXT TIME YOU ARE IN A BIND.
- Bryant-Smith et al. Antifibrinolytics for heavy menstrual bleeding. Cochrane Database Syst Rev. 2018 Apr 15.
- Carter et al. Current concepts of the management of dental extractions for patients taking warfarin. Aust Dent J. 2003 Jun;48(2):89-96.
- Carter et al. Tranexamic acid mouthwash: a prospective randomized study of a 2-day regimen vs 5-day regimen to prevent postoperative bleeding in anticoagulated patients requiring dental extractions. Int J Oral Maxillofac Surg. 2003 Oct;32(5):504-7.
- Coetzee, M J. 2007. The use of topical crushed tranexamic acid tablets to control bleeding after dental surgery and from skin ulcers in haemophilia. Haemophilia. 2007 Jul;13(4):443-4.
- Hankerson et al. Nebulized Tranexamic Acid as a Noninvasive Therapy for Cancer-Related Hemoptysis. Journal of Palliative Medicine. 2015. Volume 18, Number 12, 1060-62.
- Jahadi et al. Comparison between Topical and Oral Tranexamic Acid in Management of Traumatic Hyphema. Iran J Med Sci. 2014 Mar;39(2 Suppl):178-83.
- Komura et al. Hemoptysis? Tryi inhaled tranexamic acid. The Journal of Emergency Medicine. 2018. Vol. 54, No. 5, pp. e97–e99.
- Management of acute abnormal uterine bleeding in nonpregnant reproductive-aged women. Committee Opinion No. 557. American College of Obstetricians and Gynecologists. Obstetric Gynecology 2013;121:891–6.
- Nuvvula et al. Efficacy of tranexamic acid mouthwash as an alternative for factor replacement in gingival bleeding during dental scaling in cases of hemophilia: A randomized clinical trial. Contemp Clin Dent. 2014 Jan;5(1):49-53.
- Shakur et al. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomised, placebo-controlled trial. Lancet 2010; 376: 23–32.
- Shakur et al. Effect of early tranexamic acid administration on mortality, hysterectomy, and other morbidities in women with post-partum haemorrhage (WOMAN): an international, randomised, double-blind, placebo-controlled trial. Lancet 2017; 389: 2105–16.
- Zahed et al. Topical Tranexamic Acid Compared With Anterior Nasal Packing for Treatment of Epistaxis in Patients Taking Antiplatelet Drugs: Randomized Controlled Trial. Academic Emergency Medicine. 2018 Mar;25(3):261-266.
Pediatric Pearl – January
PAIN MANAGEMENT & VASO-OCCLUSIVE CRISIS IN SICKLE CELL DISEASE
By: Hima Khamar, PGY3 & Dr. Patel, PGY16
Sickle cell disease (SCD) is a common disease process we encounter in the ED. There are multiple complaints related to SCD that patients present with such as: pain, fever, stroke like symptoms, anemia. In this pediatric pearl article, we will discuss pain management during vaso-occlusive crisis (VOC) in the pediatric sickle cell patient.
We as emergency medicine physicians often tend to undertreat pain in SCD patients, we tend to be even more cautious with pediatric patients. The goal of this pediatric pearl article is to emphasize trusting patient reported pain, treating pain adequately, realizing opioids are the main stay for VOC, discussing dosing of various pain medications along with routes, and hopefully making you more comfortable treating VOC in pediatric patients.
Primary Goal on Arrival (provided patient’s ABCs are stable and the patient is neurologically intact): PAIN ASSESSMENT
- Assess, document pain – TRUST the PATIENT’S self-reported score
- Recent pain medication, dose, time of last dose
- Allergies to any medication (if they need Benadryl, ONLY PO, avoid use of IV or IM. DO NOT re-dose with every administration of pain medication. Dose every 4-6 hours as you normally do when using Benadryl.)
- Order pain medication immediately (ideally should be administered within 30 mins of arrival)
|History and Physical
Past Medical History
– Penicillin prophylaxis
– Folic acid
– Chronic pain medications
– VS, pulse oximetry reading
– General appearance, jaundice
– Pain assessment
– Respiratory, Circulatory, Neurologic status
– Evidence of focal infection
– Spleen size
– Presence of rash or petechiae
- CBC w/ differential – determine if there is any hemolytic or inflammatory process
- Reticulocyte count – determine if there is any hemolytic or inflammatory process
- Type and Screen
- Pale, persistent tachycardia, ill appearing
- Suspected splenic sequestration
- Acute chest syndrome
- Focal neurologic findings
- Hgb < 5 g/dL or Hgb drop > 2 g/dL from baseline Hgb
- Reticulocyte count < 1% (unless hemoglobin > 10 g/dL)
- Chest Radiograph – new hypoxia, chest pain, clinical suspicion for pneumonia/acute chest syndrome
- HCG – any females ≥ 12 years or < 12 with menarche
- Blood cultures – if infection is suspected
- Recommended onlyif O2 saturation is less than 92%
- Recommended: D5 ½ NS.
- As clinically indicated for: clinical dehydration/intravascular volume depletion
- If need to place patient on maintenance fluids because they are not tolerating adequate PO, then place on hypotonic solution, not hypertonic or isotonic solution. Note: IVF offers no therapeutic benefit for patients with VOE who have no signs of volume depletion.
|Ketorolac||IVP or IM||0.5 mg/kg
|Ensure patient has no history of renal insufficiency|
|Great for those patients who are in a lot of pain, while you are trying to get IV access.|
(Max 8 mg/dose)
(Max 2 mg/dose)
|No indication to give IM or IV, unless patient truly can’t tolerate PO, but may try giving PO after giving anti-emetic.|
|Oxycodone||PO||< 6 yrs: 0.15 mg/kg/dose up to 2.5 mg
6-12 yrs: 0.2 mg/kg/dose up to 5 mg
> 12 yrs: 0.2 mg/kg/dose up to 10 mg
|For outpatient management. Give up to 3 days, until they can see their heme-onc doctor.|
|Use as an adjunct to decrease opioid use provided there is no contraindication.|
|Use as an adjunct to decrease opioid use provided there is no contraindication.|
Incentive Spirometry – RECOMMENDED FOR ADMITTED PATIENTS
- Provide to all patients who are admitted for VOC.
- This will help decrease development of acute chest syndrome. Acute chest syndrome normally develops during inpatient stay. (We will discuss this in depth in another pearl.)
- Based on studies, high dose methylprednisolone may help in the acute event, but has been associated with high rate of rebound pain after stopping steroids.
- Currently, it is not routinely recommended for VOC.
Ketamine – need more studies
- In ED recommend 0.25-1 mg/kg; inpatient can place on continuous infusion of 3-5 mcg/kg/min
- Has been shown to be effective in some case series, but need more data and large, randomized control trials
Nitrous oxide – needs more studies
- May try as another modality to control pain
Patient controlled analgesia (PCAs) – RECOMMENDED FOR ADMITTED PATIENTS
- Pain management, which is under anesthesia can help with setting this up. You can get pager number from the operator. Recommended for patients who are admitted, and pain is not controlled with opioid pushes. Discuss with heme-onc team and may consider starting in ED, especially if patient is not going to get a bed for some time.
- Laxatives should be provided around the clock to prevent side effects of opioids.
- Antiemetics as needed.
- Antipyretics as needed.
CALCULATING PARENTERAL DOSE BASED ON HOME MEDICATIONS
The website listed below can help you convert a patient’s home medication into the parenteral dose you should be starting at in the ED. You can also do it manually using the conversion table provided below. On the right side is an example case on how to use the table. Whenever you are converting opioids, always convert to morphine and then convert to another opioid agent.
ADMISSION vs. DISCHARGE CRITERIA
- < 3 months of age
- Focal neurologic findings
- Acute chest syndrome
- Splenic sequestration
- Reticulocyte count < 1 % (unless Hgb > 10 g/dL)
- Severe anemia (Hgb < 5 g/dL)
- Patients with pain relief: After 1 – 3 doses of IV analgesia
- Patient continues to be pain free at least 60 minutes after PO analgesia
- Discharge with 3 days of PO analgesia until they can follow up with heme-onc doctor
- Absence of other complications of sickle cell disease
- TRUST the patient’s self-reported pain score
- Vital signs can be normal even if patient is in pain, so do not rely on vital signs as an indicator of pain.
- There is no lab test to definitively say a patient is having VOC or not.
- Acute VOC is considered acute, not chronic pain, and opioids are indicated and should be used to treat pain.
- Rapidly initiate analgesic therapy within 30 minutes of triage or within 60 minutes of registration.
- In adults and children with SCD and a VOC associated with mild to moderate pain who report relief with NSAIDS in the absence of contraindications to the use of NSAIDS, continue treatment with NSAIDS.
- In adults and children with SCD and a VOC associated with severe pain, rapidly initiate treatment with parenteral opioids.
- Calculate the parenteral (IV or subcutaneous) opioid dose based on total daily short-acting opioid dose currently being taken at home to manage the VOC.
- Administer parenteral opioids using the subcutaneous route when intravenous access is difficult.
- Reassess pain and re-administer opioids if necessary for continued severe pain every 15–30 minutes until pain is under control per patient report.
- Maintain or consider escalation of the dose by 25 percent until pain is controlled.
- Reassess after each dose for pain relief and side effects.
- In adults and children with SCD and a VOC, do not use meperidine unless it is the only effective opioid for an individual patient.
- In adults and children with a VOC, administer oral NSAIDS as an adjuvant analgesic in the absence of contraindications.
- In adults and children with a VOC who require antihistamines for itching secondary to opioid administration, prescribe agents orally, and do not re-administer with each dose of opioid in the acute VOC management phase. Re-administer every 4 to 6 hours if needed.
- To reduce the risk of acute chest syndrome in adults and children hospitalized for a VOC. Encourage use of incentive spirometry while awake. Encourage ambulation and activity as soon as possible.
- In adults and children with VOC, use adjunctive nonpharmacologic approaches to treat pain such as local heat application and distraction.
- In euvolemic adults and children with SCD and a VOC who are unable to drink fluids, provide intravenous hydration at no more than maintenance rate to avoid over-hydration.
- Assess all patients with sickle cell disease who present with acute pain to determine whether their pain is being caused by an acute painful sickle cell episode or whether an alternative diagnosis is possible, particularly if pain is reported as atypical by the patient.
- Patients who experience three or more acute painful episodes per year that require treatment with parenteral opioids in a medical facility are considered to have severe disease.
As physicians, we all decided to help others. Those of us in Emergency Medicine decided to help others at their most ill, at the most traumatic moment in their lives, or at their wits end as far as where to seek answers. Sometimes we can help, and sometimes we cannot. Regardless of what their reason or our ability to meet their expectations, patients come to offload some of their burdens of life. Maybe they can no longer care for themselves because their sepsis has drained them of all their energy. Or their addiction to substances (despite the number of times you’ve counseled them on breaking their habit) has brought them back to us either for either intoxicant effects or the pangs of being without for too long.
Regardless, we can feel the burden and it manifests as burnout. Burnout is a syndrome exemplified by emotional exhaustion, depersonalization and a sense of lack of accomplishment. It manifests in those whose careers aim at working with others. While stress is a normal part of life and work, when we cannot defuse the stress between shifts thereby allow it to build up will we be in danger of experiencing burnout. The syndrome can lead to us making clouded medical decisions which can have disastrous consequences.
Some studies suggest 1 of 3 physicians are experiencing burnout at any given time. The Medscape Physician Lifestyle Survey shows an increase of self-reported burnout from 39.8% in 2013 to 46% in 2015. Whether we don’t have enough time off between shifts, work too many shifts to pay off loans, or simply keep our feelings inside, it exists and knowledge of it is essential. Many of these habits perhaps are inculcated from medical pedagogy since day one of our education.
But there is a cure. Recognize it. In ourselves. In others. Talk about it. Talk to each other. Be there for one another. Recommend healthy coping strategies. Provide an ear. The National Academy of Medicine has validated tools for you to determine if you are burnt out.
As physicians, we have an obligation to patients. But as humans, we have an obligation to ourselves.
CC: “My heart is racing.”
HPI: 26 year old male with no past medical history presents to the Emergency Room with complaints of palpitations. Patient states that while exercising at the gym just prior to arrival, he suddenly developed palpitations along with associated lightheadedness. He reported one similar episode in the past that self-remitted. He denies chest pain, shortness of breath, nausea or vomiting but was experiencing intermittent lightheadedness. He denies taking any medication prior to arrival. Patient states he drinks ETOH infrequently with his last drink several days ago. He denies tobacco or illicit drug use. Patient also denies any family history of heart disease or arrhythmias.
Vitals: HR: 221 BP: 117/74 RR: 20 T: 98.8 Pulse Ox 100% on Room Air
General: Patient is awake, appears uncomfortable
Respiratory: No respiratory distress. Lungs are clear to auscultation.
Cardiovascular: +S1/+S2, tachycardic, irregular. No murmurs, rubs or gallops.
Abdomen: Soft, non-tender, non-distended
Extremities: Palpable, rapid pulses. No cyanosis, clubbing, or edema.
Neurological: Alert and oriented to person, place, time, and situation, following all commands, strength and sensation intact and equal bilaterally.
Lab work and radiography including troponins, complete blood count, complete metabolic panel, thyroid stimulating hormone, chest x-ray, and urine drug screen were all within normal limits. Image 1 is the EKG on presentation. The patient quickly became hypotensive 90/52 and complained of lightheadedness. The patient was quickly sedated and cardioverted with 150 joules. He returned to sinus rhythm at which time the underlying conduction was more apparent.
- What EKG abnormalities do you notice?
- EMS requests permission to administer 6mg of Adenosine to treat the arrhythmia.
What is your recommended treatment plan?
- This EKG demonstrates Wolff-Parkinson-White Syndrome with Atrial Fibrillation.
- Advise EMS not to treat with Adenosine or other A-V nodal blocking agents as this may precipitate ventricular tachycardia or ventricular fibrillation.
Wolff-Parkinson-White Syndrome is a pre-excitation syndrome where myogenic bundles known as the Bundles of Kent directly link the atria to the ventricles, bypassing the atrioventricular (AV) node and the organized infranodal system [source: Tintinalli]. Atrial Fibrillation (AFib) in Wolff-Parkinson-White Syndrome (WPW) is a presentation of this syndrome in up to 20% of cases.
Features include an irregularly irregular rhythm, very rapid ventricular rates often in the range of 250 to 300, and widened QRS complexes that differ in duration and morphology from one to the next.The accessory pathway present in patients with WPW allow for the multitude of additional ectopic atrial impulses present in AFib to bypass the AV node and conduct to the ventricles, accounting for the unusually rapid ventricular rates. The variation in QRS duration and morphology can also be attributed to simultaneous conduction through the traditional AV node-His-Purkinje pathway as well as the Bundle of Kent-Ventricle route.
WPW with AFib is often misdiagnosed as a supraventricular tachycardia (SVT), ventricular tachycardia (VT) or atrial fibrillation with a bundle branch block, all of which can be safely treated with AV nodal blockers such as Adenosine, Diltiazem, and Amiodarone. WPW in the presence of atrial fibrillation makes degeneration into ventricular fibrillation more likely and thus synchronized cardioversion, delivering 0.5 – 2 Joules/kilogram, is the first-line treatment. Second-line treatments include Procainamide or Ibutilide whose mechanism prolongs the refractory period of the accessory pathway and whose dosing is weight-based. Stable WPW in the presence of narrow-complex SVT can be treated with the traditional vagal maneuvers, adenosine, and calcium channel- or betablockers [source: Tintinalli]. Patients with WPW should undergo ablation as this syndrome can lead to sudden cardiac death by means of ventricular fibrillation.
Take Home Pearls:
- Wolff-Parkinson-White with Atrial Fibrillation presents as an irregularly irregular tachycardia with widened QRS complexes that vary in morphology and result in ventricular rates often greater than 250.
- If the QRS complex is widened, avoid use of any AV nodal blockers as they can precipitated ventricular arrhythmias.
- Procainamide and synchronized Cardioversion are the treatment of choice for WPW with AFib.
FOREIGN BODY INGESTION
By: Hima Khamar M.D., PGY3
WITNESSED or UNWITNESSED
Time of ingestion
Description of object: Size, Shape, Length, Width Sharp end, similar object for comparison
Last meal time
History of GI anomaly, surgery or disease
Refusing oral intake
Drooling, dysphagia, gagging
Choking or coughing with PO intake
Respiratory symptoms: Stridor, Hoarseness
Abdominal pain, vomiting (signs of perforation, obstruction)
Drooling, oral lesions
Neck crepitus, stridor
Wheezing, unequal breath sounds
Check ears and nose, especially if FB not confirmed on X-ray
Signs suggesting acute abdomen
AP and lateral view of chest, neck, and abdomen
Flat object location on AP:
-Esophagus: Coin appears circular
-Trachea: Coin appears as a slit
-Double ring on AP view
-Step-off between the anode and cathode on lateral view
-Difficult to reliably distinguish single from multiple magnets
-Avoid GI contrast studies for suspected esophageal FBs: May obscure visualization on endoscopy and also increases the risk of aspiration if there is an esophageal FB
-CT scan may be considered in special circumstances
WHO NEEDS ENDOSCOPY & WHEN
-Button battery – NO DELAY
-Sharp pointed objects
-Multiple magnetsStomach location
-Sharp longer objects in stomach with no symptoms
– FB > 2cm wide
– FB > 5cm long
BUTTON BATTERY INGESTION
Button Battery Facts
-Serious burns can occur within 2 hrs of ingestion
-Symptoms may be delayed
-If mucosal injury is present after removal, observe for delayed complications (esophageal perforation, TEF, vocal cord paralysis, tracheal stenosis, mediastinitis, aspiration pneumonia, perforation into a large vessel)
-Complications may be delayed weeks, months
-Lithium cell batteries are most frequently involved in esophageal injuries
-Determination of battery diameter prior to removal or passage is unlikely in at least 40% of cases
-Assume hearing aid batteries are < 12 mm
-X-ray overestimates the diameter
Coins/Blunt Objects Facts
-Items within the stomach:
—Width > 2 cm, length > 5 cm (less likely to pass pylorus/duodenum)
Within 2-3 weeks if Age < 2 yrs or Quarter
Within 1 week if Cylindrical battery
Sooner if symptomatic
Items beyond the stomach:
-Return if symptoms
Coins usually appear larger on the X-ray due to magnification
-Quarter à 24 mm
-Nickel à 21 mm
-Penny à 19 mm
-Dime à 18 mm
COINS/BLUNT OBJECTS INGESTION
RADIOPAQUE/SHARP RADIOTRANSLUSCENT OBJECT INGESTION
|Presenting Resident||Nicholas Mota, DO PGY3|
|Chief Complaint||Double vision|
|Brief HPI||30-year-old male with no past medical history presented with acute onset left ocular pain and double vision x1d. Patient states that last night he turned off the light and had immediate symptoms. Patient denies using glasses or contact lenses. Patient has never felt this before. Patient has not taken anything for the symptoms. No primary care physician. Denies any associated fever, chills, blurry vision, redness of the eye, discharge from the eye, nausea or vomiting, focal weakness, dysphagia, dysarthria, parasthesias, sob, chest pain, cough, abd pain, trauma.|
|Pertinent PE and Vitals||T: 36.4 °C HR: 86 RR: 20 BP: 146/79 SpO2: 98%
Constitutional: Alert, awake, comfortable
Neck: ROM is full and without pain, no spinous process tenderness, trachea midline
|Pertinent Labs, Pertinent Imaging/EKG (if any)||n/a|
|Working Diagnosis||Acute Angle Closure Glaucoma|
|ED & Hospital Course||Ophthalmology was consulted and requested acetazolamide 500 mg IV, mannitol 50 g IV, Combigan gtt (brimonidine/timolol), and pilocarpine gtt. Pt to f/u in office for YAG iridotomy. Patient was given drops with resultant resolution of anisocoria and APD. Patient had brother pick him up and drive him to ophthalmology office.|
|Pearls & Takeaways||Ø Glaucoma is characterized by increased intraocular pressure which will compress the optic nerve and can cause vision disturbances and, if left untreated, blindness.
Ø Aqueous humor normally drains from the posterior chamber, through the iris/lens interface into the anterior chamber, through the trabecular meshwork and out through the canal of Schlemm and into the episcleral vein.
Ø Acute angle closure attacks are mostly precipitated by pupillary dilation, increased iris/lens contact, blocked aqueous flow into the anterior chamber and increased posterior chamber pressure that causes worsening bowing or the iris against the canal.
o Tonopen: Be kind and anesthetize the eye. Instruct patient to look straight ahead. Contact cornea for 10 applanations; you do not need to indent the cornea and it may lead to incorrect readings and corneal injury. Error codes are displayed. Two numbers will appear: the first is the IOP measurement and the second (smaller) number is the statistical confidence indicator (95 is acceptable, repeat if 80 or 80-). Tonopen tip should be cleaned with canned air for 3 seconds and should occur monthly if 10 pts/week.
o Shiotz: Measures via indentation tonometry and is dependent upon scleral rigidity.
o Goldmann applanation: gold standard
Ø TREATMENT: should be in co-ordination with specialist but based on following principle:
CC: Shortness of Breath
HPI: ALS box call to St. Joseph Wayne ED # 1: 92 year old female from nursing home with PMH of Alzheimer Disease and failure to thrive, RUE DVT on Eliquis with complaints of SOB. BiPAP was initiated in the nursing home with minimal improvement. On arrival, Patient was in severe respiratory distress, tripoding and with an O2 saturation of 75% on BiPAP. Patient was tachycardic with initial HR of 130bpm, BP 100/80 with a RR of 30.
Med control: Intubation was advised with 50 mcg of Fentanyl, 18 mg of Etomidate, 75 mg of Succinylcholine, and 1 mg of Ativan for post-intubation sedation. NS IV Fluids were started and patient was to be transported to PCI Center St. Joseph Regional Center Paterson for Cardiac catheterization.
ALS box call to St. Joseph Wayne (SJW) ED #2: Patient los pulses after intubation. CPR was in progress.
Med control: Transfer to SJW, continue ACLS
Patient arrives in SJW with return of spontaneous circulation (ROSC) status-post Epinephrine x 2 and total CPR time 3-4 minutes.
Palpable Carotid Pulses. Endotracheal Tube (ETT) was confirmed
BP 81 / 68 HR140 RR20 T: 96.5 F SaO2 94%.
Intubated, GCS 3T, Pupils 4mm equal and reactive bilaterally
Respiratory exam: Equal but diminished breath sounds throughout.
GI: Abdomen soft
Extremities: 2+ femoral pulses B/L, no peripheral edema.
Pertinent Labs (if any):
Na: 138 K: 3.7 CL: 116 CO2: 10 BUN: 37 Cr: 1.14 Platelet: 195
WBC: 10 Hg: 6.6 Platelet: 265
UA: nitrite +, large LE, WBC 6-10, Moderate bacteria, Large blood, RBC TNTC
Lactic Acid: 6.3
Pertinent Imaging/EKG: Bedside Cardiac Echocardiogram: Severe pericardial effusion with diastolic RV collapse.
Initial EKG post intervention: Sinus tachycardia, low voltage
Working Diagnosis at time of Disposition: Urinary Tract Infection and Pneumonia with Sepsis
Acute Respiratory Failure
Cardiac Arrest with ROSC
Cardiac Tamponade, possibly iatrogenic
A blind subxiphoid pericardiocentesis was performed. 50cc of frank blood was aspirated and no coagulation of aspirate was noted. Repeat vitals signs were BP 94 /74; Pulse 103; RR 20; Pulse Ox 98%.
Ultrasound was used to confirm the presence of the guide wire in the pericardial space. A triple lumen was passed over the guide wire and secured into placed. A total of 350cc was aspirated with repeat vitals: BP 111/73; Pulse 74; RR 20; Temp 97.6; Pulse Ox 99%.
A subclavian triple lumen catheter was placed and patient was given 2 PRBCs, 2 FFPs, 10mg IV Vitamin K, and 1L NS. Cardiologist from St. Joseph in Paterson was called and he accepted the transferred to their CCU. Patient was started on Fentanyl and Ativan Drip. Levophed gtt was also started for transport.
While in the CCU, patient was continued on antibiotics and vasopressors for septic shock.
Cardiac ECHO showed LV EF 65 to 70%, impaired relaxation pattern of LV diastolic filling, moderate concentric LVH, moderate pericardial effusion is present, no hemodynamic compromise, echogenic material adherent to the visceral pericardium, especially anteriorly measuring approximately 0.5 cm in thickness.
On Hospital day 2 (HOD), Cardiothoracic was consulted. They determined “patient currently very ill and unable to tolerate OR. Not stable for OR at this time.” Pericardial fluid was sent for evaluation.
Pericardial fluid results: Exudative as LDH 1613 with RBC count 1 million; ANA positive, RF negative.
Patient was additionally seen by palliative care. It was also determined there was no surgical interventions needed for the effusion. Sputum culture grew MRSA.
On Hospital day #4, Patient was following commands and was taken off the vasopressors. She self extubated and failed a trial on BiPAP and was re-intubated.
Patient was extubated on HOD #9 and discharged back to Nursing Home on HOD#15.
EKG post ER interventions: NSR, improved amplitude, prolonged QT
CXR post procedure: Enlarged heart, LLL infiltrate with obscured L hemi-diaphragm, ETT above carina, R subclavian central line, Pericardardial drain
|Pearls & Takeaways||· Tamponade:
o Obstructive shock from impaired cardiac filling due to pericardial accumulation
o As fluid accumulates, pericardial pressure become greater than the cardiac relaxing pressures
o Incidence 2/10,000 in USA.
o TB #1 cause in developing countries. Viral and postsurgical complications #1 cause in developed countries. Differential includes malignancy, infectious including HIV, idiopathic, atrogenic, trauma, uremia, hypothyroid, rheumatologic, and post radiation.
o Symptom development depends on rate of fluid accumulation and amount. Pericardial compliance accommodates a slower rate of volume expansion.
o Signs include persistent tachycardia, JVD, muffled heart sounds, pericardial friction rub, hepatomegaly, peripheral edema, pulsus paradoxus. Hypotension and bradycardia precede cardiac arrest.
o Pulsus paradoxus reportedly present in 98% of tamponade cases even prior to onset of hypotension.
o Pulsus paradoxus (decrease in SBP >10% during inspiration) occurs because the negative intrathoracic pressure during inspiration increases venous return and pulmonary vasculature compliance with subsequent pulmonary vascular pooling. RV engorges with septal shift causing decreased LV filling, SV, and SBP.
o Pulsus paradoxus can be seen on plethysmogram. 1998 study by Frey of 57 PICU patients shows sensitivity of 89% and specificity of 90% to detect pulsus paradoxus 10% change with a pleth variation of 8mm.
o EKG findings include low voltage, tachycardia, electrical alternans, PR depression, nonspecific ST/T changes
o CXR may show enlarged silhouette
o Bedside ECHO
· Trivial is seen only in systole
· Mild < 10mm
· Moderate 10-20mm
· Severe >20mm
§ Collapse of chambers during relaxation
· Atrial collapse precedes ventricular collapse
· Atrial collapse longer than 1/3 of cardiac cycle has 100% sensitivity and specificity of tamponade
· M Mode with EKG tracing through collapsing wall
· RV indentation is more sensitive and specific than pulsus paradoxus
§ IVC size > 20mm is 92% sensitive
· Pericardiocentesis: Indicated when hemodynamic compromise is present
§ US may guide you if necessary: if only RA collapse and RV unaffected, may wait to CTS consult
o Needle aspiration with drain placement for repeat aspiration if re-accumulation occurs
§ Triple lumen catheter is most readily available in the ER though CTS prefers pigtail catheters due to decreased clotting
o Subxiphoid approach (blind or US guided)
§ Insert needle at xiphoid process at 45 degree angle and aim towards tip of left scapula/left areola. Advance slowly until fluid aspirated.
§ US guided may be limited by habitus. Needle will enter pericardium inferior to the RV.
o Parasternal (US)
§ Probe on left parasternal position at 4th intercostal space (Long axis view). Needle should be inserted in-plane with probe at a 45 degree angle. Will enter pericardial space anterior to RV.
§ Preferred over subxiphoid due to closer proximity to effusion and better ability to avoid liver and lung
§ Aspirated blood should not clot due to anticoagulative factors in space
§ Agitated saline flush showing “snow-storm appearance”
§ Repeat vitals after aspiration
§ Myocardial, coronary artery injury
§ Cardiac arrest
§ Liver injury
Case presented by Nick