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..

 

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

Recent Pubs

We’ve had a bunch of publications in both peer-reviewed and non peer-reviewed sources over the past few weeks! Check them out when you get a chance:

Traficante and Kashani in the Journal of Clinical Toxicology talking about a Massive Calcium Channel Blocker OD

McGovern and D’Amore in Annals of Emergency Medicine talking about Peds EM Education 

D’Amore, McGovern and McNamee in ACEP Now talking about End-tidal for DKA and COPD

Pena, Mota and McGovern in AAEM/RSA Blog going over the elusive Porphyria diagnosis and management 

DeFranco and McGovern in ACOEP’s Fast Track talking about Isolated Bandemia 

 

Lisfranc injuries

Quick Review of Lisfranc Injuries

Lisfranc injures are a spectrum which result in a sprain or complete disruption of the tarsometatarsal joints of the midfoot.  They most commonly occur at the base of the 2nd metatarsal with oftentimes subtle or even absent findings on standards x-ray views, especially when they result from low velocity injury.

What is mechanism of Injury?

Usually a result of plantar flexion with external rotation of the ankle (ie. fall from a horse with the foot caught in the foot stirrup, MVC, foot planted in a hole or step off a curb)

Physical Exam on Suspected Lisfranc Fracture

  • Unable to bear weight
  • Hematoma/ecchymosis on medial plantar aspect of foot
  • Dorsal midfoot swelling

Lisfranc foot

For suspected Lisfranc injuries you’ll need three views (AP, lateral and oblique).  On normal foot x-rays you should notice alignment of the 2nd metatarsal on AP view and the medial edge of the base of the 2nd metatarsal should line up with the medial edge of the medial cuneiform.   On the oblique view the 3rd and 4th metatarsal should have the medial edge of the 3rd and 4th metatarsal lining up with the medial edges of the middle and lateral cuneiform.

Lisfranc xray1Lisfranc xry2

Common X-ray findings for Lisfranc Fracture.

  • Widening of > 2mm between the base of the 1st and 2nd or 3rd and 4th metatarsal bases needs surgical intervention
  • “ Fleck Sign” is pathognomonic for a Lisfranc Injury. This is a small bony fragment avulsed from the 2nd metatarsal base or medial cuneiform

lisfranc xray3

What if the X-ray is normal but a Lisfranc injury is still clinically suspected?

  • Add a 30 degree oblique X-ray view
  • Consider ankle nerve block with standing views (Weight bearing stress views).  Similar to the example below with a normal appearing non weight bearing x-ray (left) and then weight-bearing (right) revealing the injury.
  • In patients with clinically suspected Lisfranc injuries and normal or indeterminate radiographic findings, CT or MRI imaging is recommended.
  • Given the superior depiction of soft tissue supporting structures and the ability of soft tissue supporting structures and the ability to detect soft tissue injuries in patients with unstable injuries on MR images, the American College of Radiology Appropriateness Criteria guidelines favors the use of MR imagining
  • Orthopedics surgeons may request high resolution 3D CT images for preoperative planning and for depicting and further characterizing fractures.

 

lisfranc 6       lisfranc6b

 

ED management for patients with Lisfranc Injury

For nondisplaced or suspected injury without radiographic findings, you may place the patient in a posterior back slab. Patient should be non-weight bearing and arrange for orthopedic outpatient follow up two weeks later.  For significantly displaced injury or dislocation (> 2mm widening at the Lisfranc Joint) , Immediate orthopedic referral is needed for urgent outpatient surgical intervention

Post by: Yenis Paez-Perez, DO

Lunate and perilunate dislocations

A weekend warrior trying to finish up painting that last side of the house takes a tumble off his ladder and lands on his left hand.  He has a palpable deformity on the volar aspect of the distal radius and painful active and passive ROM but is otherwise neurovascularly intact with no median nerve neuropathy.  The following x-ray is obtained:

Lunate dislocationSp splint

You realize something is not where it’s supposed to be!  The patient has a lunate dislocation to the point where it has migrated proximally to the forearm.  After attempts at closed reduction by the Orthopedist, a CT is obtained which shows associated triquetral fracture and improved position of the lunate.  The patient is admitted and scheduled for open reduction and repair of intercarpal ligaments in the OR.

Lunate and perilunate dislocations come in a variety of shapes and sizes but the orthopedists organize them into 4 different stages of instability that we’ll go over here.


Stage 1 instability: Scapholunate dissociation 


Typically these patients FOOSH’d onto their wrist sustaining the injury with minimal swelling and pain on physical exam.  On xray we are looking for widening of the scapholunate space of > 2-4mm which is our indication that there has been disruption of the ligament.  You’ll hear the term, the “Terry Thomas” sign to describe the gaping of the metacarpals similar to his teeth.  Depending on the orthopedist these can be managed conservatively with a sugar tong splint or operatively.

terry thomas


Stage 2 instability: Perilunate dislocation 

These injuries will typically be a higher mechanism of injury with more significant physical exam findings than the stage 1’s we just discussed.  On x-ray you’ll notice that the lunate remains aligned with the distal radius while the remaining carpal bones are displaced, usually dorsally.  Most of the time these are going to need a CT to look for any radiooccult fractures of the scaphoid and radial styloid.  These will need operative management to prevent any of the nasty sequelae of median nerve palsy, compartment syndrome, long term wrist dysfunction, etc.

stage2


Stage 3 instability: Midcarpal dislocation


These are going to have a similar mechanism of injury but result in disruption of the triquetrolunate ligament or a triquetral fracture. The radiographs will show neither the capitate or lunate aligned with the distal radius.  You’re going to need ortho for this one.

midcarpal


Stage 4 instability: Lunate dislocation

These aren’t known to be the most common, but they are more severe.  The differentiating factor between this and a perilunate dislocation is that the lunate and distal radius articulation is preserved in perilunate dislocation, but not so in lunate dislocations.  On the AP film you’ll see the “piece of pie” sign (below, left) and on the lateral you’ll see the “spilled teacup” (below, right).  This is yet another one that you’re going to get ortho involved with pretty early on for an urgent reduction and operative management.

spilled pie

ct lunate

We talk a lot about those pesky radiooccult scaphoid fractures and have seen enough distal radius fractures to make us physically ill, but there’s a lot more that can go wrong in the wrist.  These are, for the most part, relatively apparent injuries that have devastating consequences if missed.  So get ortho involved early in these cases so the patient can receive the treatment they need.

Post by: Katrina D’Amore DO, MPH

Endophthal….what?

It’s difficult to miss a raging STEMI or a CVA with unilateral flaccid paralysis, but there are other, less-sexy diagnoses that we have the opportunity to make in the Emergency Department that can be as important and impactful to the patient’s health.  Endophthalmitis is a difficult word to spell and equally as difficult to diagnose if you’re not looking for it.  Check out Dave Traficante’s recent post on EM Resident on Endophthalmitis.

BOGO on TOAs

Lower abdominal pain in women can be challenging diagnostic dilemma in the Emergency Department. We had a case of a 50-year-old woman that had been previously seen by her PMD 3 days prior and diagnosed with a “small kidney stone” without any imaging, but did get the ever-reliable percocet prescription. Needless to say, she came to the ED because her pain wasn’t getting any better and now she was having increasing lower abdominal pain with high fevers. In the ED she was febrile (T: 104.5) and tachycardic (HR: 120s), but her BP was normal. She ended up having a WBC: 17k/mm3, bands: 20% and a pretty nasty UTI. Her pain persisted and we ended up doing a CT abd/pelvis with contrast to see if she had anything brewing. From the images below you can see that she had bilateral tubo-ovarian abscesses causing bilateral hydronephrosis seen on CT and confirmed with ultrasound. She was started on ampicillin, clindamycin and gentamicin and her abscesses were drained with CT guidance, yielding 400cc of thick, brown, purulent fluid. Yum

Figure 1 Figure 2

Up to one half of all cases of tubo-ovarian abscesses occur in patients with a history of pelvic inflammatory disease (PID). The theoretical etiology of tubo-ovarian abscesses is thought to revolve around an ascending infection arising in the lower reproductive tract, into the uterus and subsequently the fallopian tubes and ovaries. While Neisseria gonorrhea and Chlamydia trachomatis are commonly associated with PID, TOAs are typically polymicrobial and rarely grow either chlamydia or gonorrhea when cultured. As with most pelvic pathology, ultrasound remains the initial diagnostic modality of choice for tubo-ovarian abscesses to best visualize the upper reproductive tract. Ultrasound remains very specific (86-98%), whereas the sensitivity ranges between 56-93%. There is evidence however that computed tomography of the pelvis with contrast may provide better sensitivity than ultrasound in evaluation of TOAs. In the Emergency Department, a triple coverage antibiotic regimen (i.e. ampicillin/clindamycin/gentamicin) should be initiated despite whether the patient is going to need surgical exploration, percutaneous abscess drainage or conservative management. If the patient’s clinical status has either worsened or not improved after 48-72 hours the gynecologist will likely proceed with minimally invasive drainage procedures that have become more readily available, similar to our case.

Post by: Terrance McGovern DO, MPH (@drtmcg13)

Abdominal CPR?

There was a case report published in the Western Journal of Emergency Medicine last year about interposed abdominal compression CPR (IAC-CPR).  Personally, I’ve never heard anything of the sort and had to take a deeper look into it.  Essentially, you need two people to do compressions, one for the chest and one for the abdomen.  The abdominal compressor performs CPR with their hands about 5cm above the umbilicus and compressing about as deep as you would need to palpate the abdominal aorta pulse.  Both compress at the same rate and alternate their compressions; chest-abdomen-chest-abdomen and so on.  Theoretically, the abdominal compressor is acting as an external intra-aortic balloon pump.  By compressing the aorta during diastole, there is retrograde blood flow back into the coronaries.  Additionally, this abdominal compression increases venous return and promotes forward flow of the intrathoracic blood pool.  There have been no intra-abdominal injuries noted in survivors besides one pediatric traumatic pancreatitis reported in 1984.  The most recent review of IAC-CPR in Resuscitation showed significant improvements in the probability of achieving ROSC in the pre-hospital and in-hospital cardiac arrests when compared to standard CPR.  The question for me is why are we not doing this more? Is there harm in trying it if the person is already in cardiac arrest?

Post by: Terrance McGovern DO, MPH (@drtmcg13)

Octreotide for sulfonylurea poisoning

Newer second generation sulfonylureas are used extensively for treating type-2 diabetes mellitus (i.e. glyburide, glipizide, glimepiride and gliclazide). They are rapidly absorbed and reach peak plasma concentration typically within 2-4 hours; and have a duration of action up to 24 hours long. In 2010, the American Association of Poison Control centers reported nearly 4,000 cases of sulfonylurea exposures that led to no reported fatalities. Previous treatment has revolved around IV dextrose and glucagon for treatment of sulfonylurea associated hypoglycemia, but octreotide is another option for treating these exposures.

Mechanism of Octreotide and Sulonylureas

Sulfonylureas help to increase the amount of endogenous insulin release from the pancreatic beta cells. They bind to sulfonylurea receptors that are associated with ATP dependent potassium channels on the pancreatic beta cell membrane. By inhibiting potassium efflux, the membrane depolarizes causing influx of calcium and subsequent exocytosis of insulin. Octreotide counters this mechanism by closing the calcium channels after binding to somatostatin receptors, which prevents the secretion of the insulin.

Dosing

For adults we can use 50-100ug SC every 6-12h and for children 1-2 ug/kg SC up to 50ug q6-12h. Typically the patient will received 3 doses of octreotide as well as supplemental IV dextrose which can be gradually tapered off as tolerated. An extended length of observation may be needed for patients with renal impairment as sulfonylureas and insulin clearance will be impaired.

Check out The Poison Review for a couple posts on using octreotide for sulfonylurea poisoning here and here.

Post by: Terrance McGovern DO, MPH (@drtmcg13)