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Managing Dislocations of the Hip in the ED

Source: EM Practice Podcast – Dec 2017
** There are no existing ACEP guidelines on this topic.


Pre-Hospital Management
  • 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

Overview

Etiology:

  • 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

Definitions:

  • Simple vs. Complex
    • Simple Dislocation – does not involve fracture
    • Complex Dislocation – involves fracture

Pathophysiology:

  • 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

Imaging
  • 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)

Consultation

  • Ortho Consultation are required for the following:
    • Complex hip dislocations
    • Irreducible dislocations
    • Non-concentric reductions
    • Neurovascular deficits despite reduction

Reductions

Who:
– Simple dislocations can & should be reduced by the ED physician!

When:
– 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

Transfers:
– 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%).

Analgesia:
– 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.

Reduction Techniques

Old School:
Allis’s Maneuver

Newer techniques:
Captain Morgan
Over-Under/Whistler
East Baltimore Lift

No evidence exists to recommend one technique over the other.


Immobilization

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


Other Recommendations
– 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

 

Case of the Week COW #12

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

PHYSICAL EXAM

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.

Labs:

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

Acetone: NEG

ESR: 65

CRP: 30

Lactic acid: 1.4

Images:

Repeat Vital Signs 139/81   89   16     99.7F   97% ON RA

MRI

 

 

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:

  1. 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.
  2. Make sure to undress the patient and examine the skin!
  3. If the patient is complaining of pain out of proportion to his/her exam, dig a little deeper for alternative differential!
  4. 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
  5. 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
  6. Pyomyositis is a purulent infection of skeletal muscle that arises from hematogenous spread, usually with abscess formation.
  7. Risk Factors: immunodeficiency (HIV).
  8. auerus is the most common cause of pyomyositis; it causes up to 75 – 90% of cases.
  9. 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.
  10. MRI is the most useful imaging modality for diagnosing the disease. It can distinguish the defining sites of infection and rule out other entities.
  11. Nonspecific lab findings include Leukocytosis and elevated inflammatory markers but CPK are often normal.
  12. 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.
  13. 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

Pain Pearls – Nitrous Oxide

Nitrous Oxide


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

Contraindications

  • Severe COPD or asthma
  • Active Otitis Media/Sinusitis
  • Active Bowel Obstruction
  • 1st -2nd trimester pregnancy
  • Altered level of consciousness
  • Severe Psychiatric disease
  • EtOH
  • 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
    • Dislocations
    • Splinting

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
Safety Features
  • 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

Getting started

  • 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

Positioning

  • 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

Your Done!!

  • Patient can be discharged with no driving or work restrictions
  • Throw away the breathing circuit
  • Return it to the trauma bay

REFERENCES:
  • 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!!!

Case of the week COW #11

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

PHYSICAL EXAM 

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.

LABS

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:

  • Retinoblastoma
  • Intraocular Mass
  • Cataract
  • Syphilis
  • 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

 

Euglycemic DKA

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

Posted by:

Ruth Lamm, MD FACEP
Assistant Professor
Emergency Medicine
Critical Care Medicine
Saint Joseph’s Hospital Medical Center
lammr@sjhmc.org

Case of the week COW #10

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

PMH: Diabetes

PSH: C-Section

Meds: None

Allergies: NKDA

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

 

Pertinent Labs:

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

Lipase: 60

UCG: negative

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.

EKG:

 

Working Diagnosis:

Thrombotic Thrombocytopenia Purpura (TTP)

Idiopathic Thrombocytopenic Purpura (ITP)

Hemolytic Uremic Syndrome (HUS)

Anemia due to blood loss

Infection/Sepsis

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.

Hospital Course:

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”

  1. Fever (50%)
    • Uncommon if they present early in the disease
    • High fever and chills suggest sepsis, so look for a source of infection.
  2. Thrombocytopenia
    • MAJOR diagnostic criterion
    • Mean platelet of 25, 000 but they reach 5000.
  3. 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.
  4. Renal Failure
    • Due to renal thrombotic microangiopathy
    • Urinalysis will show mild proteinuria +/- hematuria
    • Acute Rena insufficiency may be present and may require dialysis.
  5. 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.

Risk Factors

  • Obesity
  • African American race
  • Female
  • Ages 30-50 years
  • HIV/AIDS
  • Rheumatologic/autoimmune disease history

 Clinical Presentation

  • Fatigue, tachycardia, pallor, SOB or chest pain
  • Abdominal pain, back pain, Nausea, vomiting or diarrhea
  • New Onset jaundice and dark colored urine

Physical Exam

  • Diffuse, non-palpable petechial/purpuric rash.

Etiology

  • 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)
    • Thrombocytopenia
    • 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.
    • ITP
    • Sepsis
    • SLE
    • Viral infections (HIV, mumps, varicella, EBVS)
  • Management
    • 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)
    • Glucocorticoids
      • Adjunct Treatment and do not replace plasmapheresis
      • 1mg/kg Prednisone PO or Solu-Medrol 125mg IV
    • IVIG
      • Not first line but may be used in those who fail plasmapheresis
    •  Splenectomy
      • 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

Case of the Week COW #9

CC: “Post Surgical Pain” ; Abdominal pain

HPI: 8 year old Male with PMH of Sickle Cell Disease (HbSC), Post-opt Day 10 for laparoscopic splenectomy for recurrent sequestration crises presents to the Emergency Department (ED) complaining of abdominal pain x 2 days. The pain is described as diffuse and worse in the RUQ. Denies exacerbating or relieving factors. Pain is associated with constipation; last Bowel movement was 7 days prior. Mother states he did have one small BM shortly after surgery. He is tolerating PO without difficulty and does report flatus. She has been giving him Oxycodone 2mg every 6 hours for pain with minimal relief. Upon review of systems, patient reports feeling hot for the past 2 days but without a recorded temperature at home. Additionally, patient complained of a non-productive cough for 2 days and has been “breathing fast” for the same duration of time.

Physical Exam:

BP 112/74    HR 129     RR 24   SpO2 93% on RA   Temp 99.9F      26.3 kg

Constitutional: Well developed, well-nourished child who is awake, alert and in moderate distress due to pain and feeling hot; making tears

HEENT: NCAT, pupils PERRLA, neck supple

Respiratory: CTA B/L, no wheezing, rales or rhonchi

Chest/Axilla: Normal symmetrical motion, no tenderness

Cardiac: +S1/S2, RRR, no MRG,

Abdomen: Scars noted over splenectomy site which are clean dry and intact, healing well without discharge; Diminished Bowel Sounds in all quadrants; soft, non-distended with mild tenderness in all 4 quadrants. No rebound or guarding.

Neuro exam: AAO x 3. No deficits

Extremities: no edema, no tenderness or swelling

Pertinent Labs:

CBC: 42.1

HBG: 12.5

HCT: 36.9

Platelets: 721

Seg: 79

Lymphs: 9

Mono: 12

Reticulocyte count: reported as normal

Pertinent Imaging and other tests:

Working Diagnosis:

Generalized abdominal pains

Elevated WBC

Abscess of spleen

ED/Hospital course:

Surgery was consulted in the ED and they believed the pain was not related to the surgery. Abdominal U/S performed at their request showed “s/p splenectomy with gallbladder sludge.” Patient had moderate improvement in his pain after Toradol 15mg IV and Morphine 2mg IV were given in the ED. Patient also received Rocephin 75mg/kg and NS 500mL IV Fluid bolus for presumed infection with the leukocytosis of 42.1.

The patient was admitted to Pediatric Step down for further evaluation and management. Overnight, he remained comfortable with stable vital signs, afebrile and saturating 94-96% on 2L NC. On Hospital day #1, patient became febrile to 103F and continued to deny chest pain, SOB or difficulty breathing. The cough remained unchanged since admission. A repeat Chest X-Ray was obtained and the patient was diagnosed with Acute Chest Syndrome and received exchange transfusion the same day (Refer to Image below) Additionally, he received Ceftriaxone, Azithromycin, Nitric oxide and IVF at ¾ maintenance ate throughout hospitalization. On Hospital Day #4 he was discharged home.

Pearls:

Acute Chest Syndrome

  • It is the leading cause of death in patients with SCD in the United States
  • Most often occurs as a single episode, but patients may have multiple attacks resulting in chronic lung disease
  • Multiple Etiologies
    • Pulmonary infections
    • Iatrogenic cause including aggressive hydration for sickle cell painful crisis ——à causing Pulmonary Edema
    • Opioid use —–à Decreased inspiratory effort——à Atelectasis
  • New infiltrate identified on Chest X-Ray with at least one of the following: Fever, cough, wheezing, tachypnea, chest pain, hypoxemia.
  • Radiographic changes often lag behind clinical features so initially the Chest X-Ray may actually be normal (as in our case)
  • Treatment
    • Supportive: Early Supplemental Oxygen, analgesics and IV Hydration up to 1.5x maintenance rate
    • Antibiotic irrespective of cultures
    • Transfusion is believed to be lifesaving; recommendations based on empirical observations and not on firm evidence
    • Exchange transfusion seems to be more advantageous, especially in patients with a hemoglobin of > 9.0
      • It decreases the concentration of sickled hemoglobin with little iron gain
    • Inhaled Nitrous Oxide is beneficial
      • Due to its vasodilatory effects –à improved ventilation/perfusion in damaged lung tissue
      • Reduced RBC and leukocyte adhesion to endothelial cells, therefore affecting disease progression
    • Hydroxyurea reduces occurrence of acute chest syndrome

Case Presented by Greg Cassidy, MD

 

References:

  1. Stapczynski, J. S., & Tintinalli, J. E. (2016). Tintinalli’s emergency medicine: A comprehensive study guide (8th ed.). New York, N.Y.: McGraw-Hill Education LLC..

 

EM Conference Pearls (9/20)

Pediatric congenital heart disease

  • Congenital HD: Two types: Neonates with ductal dependent lesions and infants (2-6months) presents with CHF
  • Cyanosis presentation: When ductal-dependent lesion is required for pulmonary blood flow (Will not respond to oxygen)
  • Shock presentation: When ductal-dependent lesion is required for systemic blood flow (appear septic and not response to fluids, may get worse with fluids)
  • Hypoxic/cyanotic or shocky/acidotic baby treatment = Prostaglandin E1 (PGE1) and transfer to facility with pediatric cardiovascular surgeon.
  • PGE1 treatment may cause apnea (monitor closely and consider intubation)
  • CHF in infants = wheezing, retractions, tachypnea, sweating/crying, difficulty feeding

EBM in the ED

  • EBM = What the evidence shows in the literature + What the physician wants for the patient + what the patient wants for themselves
  • Just like we need to practice intubation, central lines –> Learning to read and interpret literature is a skill that needs to be practiced.

Aortic Dissection

  • AD: Chest pain plus disease (ex: CP + Neurodeficit)
  • If you find your self giving large amounts of strong pain meds (narcotics) while treating what is seemingly ACS…STOP..think about AD or alternative diagnosis of chest pain
  • The 3 important questions, aortic dissection is the subarachnoid hemorrhage of the torso, migrating pain, colicky pain + opioids = badness and pain that comes and goes can still be a dissection.
  • Treatment: Treat pain, HR, BP
  • Pain: Fentanyl 25 – 50 mcg bolus
  • HR: Goal of 60 bbpm
  • Esmolol 0.5 mg/kg bolus then 50 – 300 mcg/kg/min or
  • Labetalol 10 – 20 mg bolus then 0.5-2 mg/minor
  • BP control: Goal SBP =110
  • Nitroprusside 0.25 – 0.5 mcg/kg/min then titrate (CN toxicity)
  • Nicardipine 5 mg/hr
  • Warning: Giving a vasodilator without concomitant reduction in ionotropy may cause progression of dissection. Start BB first before vasodilation meds.

Case of the Week COW #8

CC: Altered Mental Status

HPI: 50 -year-old Male with PMH of HIV, CVA and Meningitis presents to the Emergency Department (ED) for altered mental status. As per the patient’s girlfriend at bedside, the patient woke up confused and was not making any sense when he spoke. He even urinated on the floor but does not remember doing so. Patient had been complaining of back pain, testicular pain and leg pain for the past couple of weeks and had been evaluated for it in the ED. Patient also states he is currently taking “something for his HIV” but is unclear what his last CD4+ count was. Denies sick contacts. The rest of the review of systems was limited by confusion, but denied vomiting, diarrhea, abdominal pain, or any other complaints.

Physical Exam:

BP 128/78   HR 129     RR 14   SpO2 96% on RA   Temp 102.4F

Constitutional: Diaphoretic, confused and intermittently following commands.

HEENT: NCAT, pupils PERRLA, neck supple

Respiratory: CTA B/L, no wheezing, rales or rhonchi

Cardiac: +S1/S2, tachycardia, no MRG, regular rhythm

Abdomen: soft, mildly distended with mild tenderness in RUQ and LUQ.  Was not able to appreciate any focal masses . No rebound or guarding

Neuro exam: Not oriented to time or situation, No focal deficits, moving all four extremities. Unable to complete a more detailed exam as patient remained confused.

Extremities: no edema, no tenderness or swelling

Skin: pink and warm with diaphoresis, no rashes, lacerations, or abrasions

Pertinent Labs:

(Per Sorian Inpatient) CD4 = 120 on June 2017

Sepsis workup summary (normal if not reported):

  • Trop 0.045ng/ml
  • Sodium 126
  • WBC 5.8       Chloride 93
  • RBC 3.72      CO2 19
  • HBG 10.3      Glucose 116
  • HCT 30.3       BUN 89
  • Platelets 108
  • Cr 2.90 (↑ from baseline)
  • Bands 27        Total Bili 4.5
  • Lymphs 3       Total Protein 5.7
  • Monos 2         Albumin 2.6
  • Lymphocytes 0.2
  • Alk Phos 346   Monocytes 0.1
  • AST 143
  • ALT 58
  • Lactic acid 3.4
  • U/A negative
  • CSF negative

Pertinent Imaging and other tests:

EKG remarkable for sinus tachycardia, left axis deviation, and an old RBBB

CT head w/o contrast remarkable for only mild frontal volume loss

Chest XR – unremarkable

RUQ Bedside US and then official US completed and showed:

Working Diagnosis:

Hepatic hydatid cysts from Echinococcus tape worm

Hepatic abscesses

Metastatic cancer

Multiple biliary hamartomas

Polycystic liver disease

Caroli Disease

ED/Hospital course:

In the ED, the patient received IV Fluid boluses of NS 30mg/kg and one 1000mL of NS along with Tylenol, Vancomycin and Zosyn. The patient was admitted to Infectious Disease service. Throughout the hospital stay, CT Scan of abdomen and pelvis w/o contrast (due to AKI) was remarkable for infiltrated liver, splenic lesions, and destructive lesions of the bilateral iliac wings and L5 with pathologic fracture of the posterior right rib, which may be due to metastatic disease. The underlying etiology is uncertain. Without contrast, it was not certain if there was underlying macronodular cirrhosis. There was also associated ascites. Initial blood cultures from the ED grew Salmonella species. The patient was initially admitted the medical floor but was transferred to the Medical ICU on day 7 of hospitalization for increased lethargy and worsening lactic acidosis, transaminitis, and AKI. He later went into multisystem organ failure and was intubated thereafter. His code status was also changed to DNR/DNI. The patient unfortunately expired before endoscopy, colonoscopy, and biopsy could be performed.

Official Ultrasound read – Findings consistent with metastatic disease to the liver.

Pearls:

Hepatic Hydatid infection

  • Caused by Echinococcus granulosus or Echinococcus multilocularis
  • granulosus – Endemic in North America & Australia with dogs & wolves main as main host
  • multilocularis – Found in Northern Hemisphere with red fox, dogs, & cats as main host
  • Ultrasound would show a multiseptate cyst with daughter cysts
  • X-ray would show calcified rings
  • CT Abd/Pelvis may show the water-lily sign, which occurs when the endocystic membrane becomes detached, resulting in floating membranes within the pericyst, which mimics the appearance of a water lily ( Refer to Figure 1).

Figure 1. A detached membrane within the contents of the cyst, known as the water-lily sign

Pearls

Hepatic Hydatid infection

  • Infection may be asymptomatic for many years, with a long latent period (up to 50 years of age!)
  • Albendazole for confirmed infection
  • Reserve antibiotics for those in which diagnosis is uncertain due to risk of anaphylaxis
  • Most cases in U.S. occur in immigrants from endemic countries (South America, Middle East, eastern Mediterranean, sub Saharan, African, West China, former Soviet Union)
  • Confirmed cases in U.S. are rare

Patients with HIV

  • Always ask for CD4+ count and if they are on medications for their HIV/AIDs
  • Have a low threshold for doing an aggressive workup for these individuals, especially if poor follow up
  • HIV is a risk factor for Salmonella bacteremia
    • Other risk factors include any immunosuppressed state, liver disease, hemoglobinopathies (decreased splenic function)
    • Most salmonella bacteremia can have a preceding diarrheal illness
    • Major complication is endovascular infection
    • Treatment is IV fluoroquinolones or 3rd generation cephalosporin

Case presented by Jessica Williams, MD, PGY1

Case of the Week COW #7

CC: Numbness and palpitations

HPI: 21-year-old Female presents to the Emergency Department (ED) complaining of palpitations and left arm weakness with perioral numbness, which began just prior to arrival. The patient states the episode lasted 30 minutes before completely resolving on its own. In the ED, she denies any other complaints except for a mild headache. Patient notes she experienced a similar episode of palpitations yesterday afternoon, while resting, which she described as “skipping beats”. On further questioning, the patient admitted to being hospitalized to a NYC hospital 2 weeks ago where she had a Cardiac Echocardiogram done which showed “hypertrophy.” Patient never followed up with cardiologist as instructed. In the past, a doctor in her country prescribed her an unknown antihypertensive medication, which she took for one year but stopped taking it once she moved to NJ. Denies fever, dizziness, chest pain, and shortness of breath, recent travels, calf pain or swelling.

Physical Exam:

BP 109/72   HR 82     RR 18     SpO2 100% on RA    Temp 97.0F

General: Well appearing female, in non-acute distress

HEENT: NCAT, pupils PERRLA, neck supple

Respiratory: CTA B/L, no wheezing, rales or rhonchi

Cardiac: +S1/S2, no MRG, regular rhythm

Abdomen: soft NT ND

Neuro exam: AAO X 3, No focal deficits

Extremities: no edema, no tenderness or swelling, 5/5 strength in all extremities. Sensory intact

Skin: pink and warm, No diaphoresis, no rashes, lacerations, or abrasions

Pertinent Labs: Troponin 0.308

Pertinent Imaging and other tests:

  • Chest X-Ray: Cardiomegaly with a boot shaped heart, which may indicated right heart failure.
  • CT Head: Normal 
  •  ECG: Normal Sinus Rhythm, Bi-atrial enlargement, RBBB, LVH

Working Diagnosis: Hypertrophic Cardiomyopathy (HCOM)

ED/Hospital course:  Patient was given 324 mg of ASA and admitted to Telemetry with a diagnosis of Hypertrophic Cardiomyopathy. While still in the ED waiting for a bed on Telemetry the patient had multiple runs of non-sustained V-Tach and Cardiology was consulted. The patient was started on ASA and Metoprolol PO. A 2D ECHO was done which was consistent with HCOM. Patient remained stable on Telemetry for 3 days prior to discharge. The patient’s Troponin was trended daily, 0.308 in the ED, 0.288 on day 1 of admission, and 0.314 on day 2 of admission. Patient was told to follow up with Cardiology Clinic for possible AICD placement planning.

Pearls:

Hypertrophic cardiomyopathy (HCM) is one of the most common inherited cardiac disorders (affecting ~ 1 in 500 people) and is the number one cause of sudden cardiac death in young athletes. Annual mortality is estimated at 1-2 %.

  • Pathology and Pathophysiology:
    • Dynamic Obstruction of the Left Ventricular Outflow Obstruction (LVOT)
    • Primarily Autosomal Dominant Inheritance
    • Left Ventricular diastolic dysfunction resulting from impaired relaxation and filling of the stiff and hypertrophied left ventricle (often associated with increased filling pressure)
    • Abnormal intramural coronary arteries with thickened walls and narrow lumens
    • Chaotic, disorganized left ventricular architecture (“ cellular disarray’) predisposing to abnormal transmission of electrical impulses and thus serving as a substrate for the formation of arrhythmia.
  • Clinical Manifestation
    • Exertional syncope or pre-syncope – this is the most worrisome symptom, suggesting dynamic LVOT obstruction with or without dysrhythmia, with the potential for sudden cardiac death.
    • Symptoms of pulmonary congestions due to left ventricular dysfunction (e.g. exertional dyspnea, fatigue, orthopnea, paroxysmal nocturnal dyspnea)
    • Chest pain – may be typical angina pain due to increased demand (thicker myocardial walls) and reduced supply (aberrant coronary arteries).
    • Palpitations due to supraventricular or ventricular arrhythmias.
  • ECG Features:
    • Left atrial enlargement
    • Left ventricular hypertrophy with associated ST segment / T-wave abnormalities
    • Deep, narrow (“dagger-like”) Q waves in the Lateral (V5-6, I, aVL) and inferior (II, III, aVF) leads. Most common in Lateral vs. Inferior
    • Giant precordial T-wave inversions in apical HCM
    • Signs of WPW (Short PR, delta wave)
    • Dysrhythmias: Atrial Fibrillation, supraventricular tachycardia, PACs, PVCs, VT

*** Infarction Q Waves are wider with a different morphology compared to HCM.

Pathologic Q Waves:

  • Usually > 40 ms (1mm) wide
  • > 2mm Deep
  • > 25% of depth of QRS Complex
  • Best seen in V1-V3

 

Post by Tyler Manis, MD, PGY4