R4 Case Follow Up WITH DR. POLSINELLI
This case comes from the SICU. The patient is a middle-aged female with a remote history of a Nissen fundoplication that was complicated by esophageal perforation who initially presented from a long term care facility after falling down and pulling out her g-tube. She has been stable since admission until she suddenly develops hemoptysis and codes. After a short code and resuscitation with blood products, she gets ROSC and is awake and alert. After imaging and an EGD, the source of the bleeding is unclear. After another 24 hours, she sustains a vifb arrest event with massive hemoptysis and hemorrhage from the g-tube, and unfortunately does not survive. The patient ultimately is found to have an aortoenteric fistula (AEF) on autopsy.
- There are primary and secondary fistulas, both of which are more common in men.
- The most common kind of primary AEF is due to AAAs and pressure necrosis. Radiation therapy, trauma, diverticulitis and malignancy can also lead to AEFs.
- Secondary fistulas are due to surgery and are the more common kind of AEFs.
- It is a challenging and rare diagnosis, with 50% being diagnosed on autopsy.
- 36% present without any GI bleeding at all, and may present instead as sepsis; other common presenting symptoms include melena and upper GI bleeding.
- Many patients will present with a herald bleed, marking the best opportunity for intervention if the AEF is recognized at this time.
- The sensitivity of EGD for diagnosing AEFs is 50%; CTA has a sensitivity of 79%.
- Suspect AEF in patients who present with GI bleeding and have a history of AAA, aortic grafting, foreign body ingestion or cancer.
- Also suspect AEF in patients with a history of aortic grafts who present with sepsis without a clear source.
- Management involves resuscitation, early vascular surgery consult, CTA and potentially Blakemore tubes depending on the suspected location of the fistula.
- Many of these patients are or become septic; empiric antibiotics should cover MRSA, salmonella, strep pneumo and potentially fungal sources if the patient is immunosuppressed.
Wellness Curriculum: Burnout WITH DRS. MURPHY & LAFOLLETTE
- Based on several studies, emergency physicians are at the highest risk of burnout than any other medical specialty.
- Burnout is linked to many negative things such as higher rates of physician turnover, alcohol and drug use, and depression.
- Symptoms of burnout include exhaustion, depersonalization and lack of efficacy.
- Resilience is a concept that is frequently discussed as a tool to mitigating burnout.
In small groups, we sat down and shared examples of personal and professional failures. We discussed how these situations made us feel, how we processed these events, and coping strategies we have used to deal with these situations. Specifically, we discussed strategies such as reaching out to peers, journaling, meditation and mindfulness, and exercise. We also brainstormed ideas to prepare for future difficult situations.
Pharmacy Updates WITH AMANDA SHIGLE, PharmD AND LEEANN GERAGHTY, PharmD
Calcium Channel Blocker and Beta Blocker Overdose
- Calcium channel blocker (CCB) and beta blocker (BB) overdoses are increasing in the United States
- High dose insulin remains a first-line option for patients with myocardial dysfunction for a variety of reasons, including increasing myocardial glucose uptake
- The dosing involves giving a bolus of regular insulin 1 U/kg followed by an infusion of 1-10 U/kg/hr, along with a dextrose infusion
- Glucagon also remains an option, but is very expensive and considered a second-line treatment for BB overdose, and should likely not be used in CCB overdoses
- In our institution, we had 19 CCB/BB overdoses in the past year; the majority of these overdoses (42%) were coingestions of both CCBs and BBs
- We have created a protocol for symptomatic CCB/BB overdoses that involves high-dose insulin drips, dextrose administration, calcium administration and other electrolyte repletion, and vasopressors
Amiodarone for Atrial Fibrillation
- Cardioversion remains one of the mainstays of treatment for symptomatic a fib, but runs the risk of thromboembolism if the patient is not appropriately anticoagulated
- Amiodarone as a rate control agent can also cause spontaneous cardioversion
- In general, patients who have been in afib for less than 48 hours do not need anticoagulation prior to cardioversion, although some people may feel that 24 hours is safer given more recent data
- In a chart review, 24% of patients who received amiodarone and converted in the ED had not been anticoagulated and had been in afib for greater than 48 hours
- You may consider heparinization in these patients at the same time as ordering the amiodarone, although the optimal timing of this remains controversial
Mastering Minor Care Series: Arthrocentesis WITH DR. CONAL ROCHE
- Beware polyarthritis in immunocompromised patients
- Septic joints should be tapped dry if possible -- better for you and for the patient's comfort
- Stay objective -- don't avoid tapping the joint for fear of failure or need for specialist rescue
- Proper positioning and a wide prep are keys to a successful procedure; if at first you don't succeed, reposition the patient or try another approach
- Leave the syringe off when tapping small joints or difficult taps
- 55 y/o M with hx of HTN, obesity, ETOH and "occasional" IVDU who has been told in the past he has gout
- Presents with ankle pain and swelling for several days that hasn't responded to NSAIDs with temp of 99.9F
- Multiple ways to tap the ankle; the lateral approach is probably easier
- 38 y/o with acute-on-chronic right shoulder pain with abduction; has received steroid injections in the past
- Impingement tests are positive
- May not be unreasonable to offer the patient a steroid injection in the ED; see our TtS post on shoulder arthrocentesis for more info
- 30 y/o male who presents after being stabbed near the elbow with concern for open joint
- Elbow arthrocentesis involves putting the elbow somewhere from neutral to 70 degrees of extension; aim towards the medial epicondyle
- 22 y/o male with wrist pain as well as a history of recent migratory polyarthritis and STI symptoms
- GC is a common cause of polyarthritis in certain populations
- To tap the wrist, have the patient extend their fingers so you can identify Lister's tubercle and the lunate, and go between these two structures
Combined Peds-EM Sim
Simulation: Non-Accidental Trauma
The patient is a 5 month old child who presents to a community ED for fussiness. The patient is brought by his mother due to concern this afternoon for fussiness. She reports he was in his usual state of health this morning, but this evening he wouldn't take his bottle and won't stop crying. He also seems more lethargic than usual. He is otherwise healthy and fully immunized.
Vitals: HR 80 RR 30 BP 110/78 98% RA Temp 37.6 rectal
On exam, he appears slightly lethargic but will intermittently respond with crying when examined. There are no signs of head trauma, and the patient has soft fontanelles. His pupils are equal and reactive, and his cap refill is brisk. Cardiac examination is normal. Breath sounds are clear bilaterally and the abdomen is soft. When the patient's skin is examined, there is a hand-shaped bruise on the child's back.
Additional history reveals that the patient had been watched by an uncle for the day, and when the mother got home from work, the patient was altered. This raises concern for non-accidental trauma (NAT).
A head CT shows a subdural hematoma with shift. The patient becomes progressively hypoxic, bradycardic and hypertensive to the 130s systolic. The decision is made to intubate the patient with succinylcholine and etomidate after premedication with lidocaine. Hypertonic saline was also given. The patient was transferred to a higher level of care via air transport.
Afterwards, we discussed the recognition, diagnosis and management of non-accidental trauma and increased intracranial pressure in infants and children. Upon presentation, this patient was profoundly bradycardic for his age -- this should prompt the provider to pause and think through the differential for bradycardia in this patient. In the setting of hypertension and altered mental status, non-accidental trauma and increased ICP should be at the top of your list. In the setting of hypoxic with a TBI, this may prompt you to take his airway earlier to prevent any secondary injury from hypoxemia.
There is a paucity of evidence about premedication for intubation in pediatric patients with TBI. In general, follow the same principles as in adults and attempt to avoid hypotension, hypoxia and hypertension. Hypertonic saline at a dose of 3-10% mL/kg over 10-60 minutes is recommended in children with symptomatic increased ICP, although the dosing may differ between institutions.
The patient is a 3 week old female infant who presents to your community ED with vomiting. The patient's mother reports that her "typical baby spit-up" has changed over the past three days and she is now vomiting with every feed. The vomit is described as looking like formula and is non-bloody and non-bilious. She remains hungry. The vomit is increasingly forceful. She has been acting normally. No fevers. Remains with good urine output and normal stool patterns.
The patient was born at 35 weeks via spontaneous vaginal delivery and was in the NICU for 12 days for "feeding issues." She was born at 3.4 kg; you do not have any other weights recorded in the system for the patient. She is on zantac but is otherwise healthy. Mom denies coughing/choking with feeds.
Vitals are notable for: Temp 36.7 rectal HR 140 BP 86/40 RR 30 SpO2 98% RA 3.5 kg
On exam, the child is well appearing. Her abdomen is soft, NT/ND. Her oral exam is normal. Her mucous membranes are moist with good skin turgor. However, her capillary refill is slightly delayed at 4 seconds. The remainder of her exam is unremarkable. A fingerstick is 67.
Differential for this child includes pyloric stenosis, NEC, food/formula intolerance, GERD, genetic issues/inborn errors of metabolism, malrotation and NAT. A urinalysis is normal without ketonuria or proteinuria. A BMP was normal as well with the exception of a slightly elevated Cr of 0.6 (for age). You start a fluid bolus. An abdominal ultrasound reveals a thickened pylorus, consistent with pyloric stenosis. The patient is transferred to the local Children's hospital for further evaluation.
A helpful way to remember the normal measurements for pyloric stenosis in neonates is to remember pi (3.14): the thickness should be under 3mm and the length should be under 14 mm.
The patient is a 3 month old male infant who presents with fussiness and poor feeding. Mom reports that he has been more fussy lately, and not been feeding well over the past several days, taking less PO than usual. He has had slightly less wet diapers than usual. He has otherwise been healthy, afebrile and without any illnesses lately. He had an uneventful prenatal course and is otherwise healthy.
Temp 37.5 rectal HR 230 BP 90/62 RR 50 SpO2 99% RA 7 kg
On exam, the patient is crying loudly and is neurologically intact. Oral exam is normal, and the head is atraumatic. Cardiac exam is notable for tachycardia without murmurs, and the patient has a clear lung exam. The abdomen is soft, NT/ND and the skin is normal. Capillary refill is 3 seconds. The remainder of the exam is normal. When the mother tries to feed the child, the child refuses the bottle and continues crying.
Differential for this child involves NAT, primary cardiac issues such as SVT, sepsis, endocrine abnormalities, other causes of crying (e.g. hair tourniquet, corneal abrasion). Labs -- including a BMP, CBC, procal and urine -- are all normal. A CXR was also normal. An EKG reveals a narrow complex SVT. A bag of ice is placed on the patient's face, without improvement. You move to adenosine at a dose of 0.1 mg/kg rapid bolus. This is unsuccessful, so you try again at 0.2 mg/kg. This is also unsuccessful at improving the patient's rate. After a small amount of sedation the patient is then cardioverted at 0.5 J/kg successfully, and is then transferred to a Children's hospital for definitive care.
For a recap on the diagnosis and management of pediatric SVT, please see our Annals of B Pod article here!