Case of the week COW #6

CC: Vomiting for 2 days

HPI: 32 yo female with PMH of Romano Ward Syndrome s/p AICD, previous cardiac arrest, Atrial Fibrillation s/p Ablation, renal artery thrombosis on Coumadin and deafness presents to the Emegency Department (ED) via ALS after being found unresponsive at home and with ventricular tachycardia. Paramedics state they were called to the patient’s home for an “unconscious” person. They arrived to find the patient lethargic but arousable, cool, pale, and diaphoretic with BP 90/50. The patient soon became unresponsive and was in Ventricular tachycardia on the monitor. Patient underwent synchronized cardioversion with 150 Joules and converted to sinus tachycardia. Patient also received 150 mg Amiodarone bolus and 250 mL of Normal Saline IVF. Patient’s sister arrived to ED approximately 10 minutes after patient’s arrival and states that patient had multiple episodes of becoming unconscious at home earlier today. Denied recent illness, fever/chills, vomiting, diarrhea

Physical Exam:

BP 133/105,   HR 115 Sinus tachycardia,   RR 20,   SpO2 100% on 3 lpm NC,    Temp 97.0F

General: Lethargic but arousable to painful stimuli

HEENT: NCAT, pupils PERRLA, neck supple

Respiratory: Moderate respiratory distress with bibasilar rales, otherwise clear, no wheezing

Chest: AICD in left anterior chest

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

Abdomen: soft NT ND

Neuro exam: arousable to painful stimuli, pt reading lips, answering appropriately

Extremities: weak thready pulses throughout, no edema

Skin: cool, pale, diaphoretic, no rashes, lacerations, or abrasions

 Labs:

CBC: Unremarkable     CMP: K 3.2   Glucose 595     BUN/Cr 17/1.62

AST/ALT 359/401       INR: 1.7             Troponin 0.122

ED Course: Approximately 5 minutes after arrival to the ED during the initial exam, patient became unresponsive and was noted to be in Ventricular Fibrillation on the monitor. CPR/ACLS was started and patient was intubated immediately. Her defibrillator appeared to be delivering shocks however there was no conversion of the rhythm. ACLS was performed for 30 minutes and pulses were regained multiple times. Patient was in V-fib, then PEA, then V-tach arrest. 100mg Lidocaine and 2 grams Magnesium were also given. Defibrillation with external pads ultimately led to Return of Spontaneous circulation. Bloody, frothy sputum was also noted from the ETT post-arrest. A right IJ central line was placed

EKG:

Pre-arrest: Atrial-paced with PACs. QTc 503      Post-arrest: Atrial tachycardia. QTc 609

DX: VFib & VTach arrest s/p ROSC in the setting of Congenital Long QT syndrome and AICD non-capture.

ED/Hospital course:  Post-ROSC EKG did not show STEMI. Post-ROSC Chest XR demonstrated diffused pulmonary edema. Patient was hypoxic with SpO2 in the 80s on 100% FiO2. Decreased tidal volume and increased PEEP improved oxygenation. Bedside cardiac Ultrasound showed global hypokinesis and no pericardial effusion. CT Head w/o contrast was normal. Amiodarone drip was started. Hypothermia protocol was initiated. The patient was admitted to the CCU. She did not code again while in the ED. Her AICD was interrogated and it showed she had been in sustained Vtach to which her AICD gave multiple shocks without capture. She was in the hospital for 11 days where she initially was improving and was therefore extubated after 7 days. Unfortunately she again went into Vtach arrest multiple times and then PEA arrest and was pronounced dead.

Pearls:

Congenital Long QT Syndrome (LQTS)

  • The major variant of congenital prolonged QT syndrome (there are 6 total). Affects estimated 1/2500 to 1/7000 people worldwide
  • Can have varying degrees of penetrance
  • Thought to account for ~3000/year of sudden deaths in children
  • May play a roll in prevalence of SIDS
  • Autosomal dominant inheritance, results in mutation of genes responsible for creating ion-channel proteins. The impaired transport of ions in cardiac tissue causes prolonged QT à impaired repolarization à ventricular arrhythmias (symptomatically syncope, seizure, cardiac arrest). May also present with AV blocks and bradydysrhythmias.
  • Romano-Ward is the more common, autosomal dominant (AD) form with purely cardiac phenotype.
  • The Jervell and Lange-Nielsen syndrome refers to the autosomal recessive (AR) phenotype of congenital LQTS that is associated with profound sensorineural hearing loss and a high risk for sudden death. MORE MALIGNANT CLINICAL COURSE. Our patient likely had this variation since she also had deafness.

Management and treatment

  • Beta- blockers = 1st line treatment in symptomatic patients. Blunts catecholaminergic response
  • Whenever syncopal episodes recur despite full-dose beta-blocking therapy, left cardiac sympathetic denervation (LCSD) should be considered. Cardiac pacing is only rarely indicated (e.g. in infants or young children with 2:1 atrioventricular block).
  • Implantable cardioverter defibrillators (ICDs) are always indicated after cardiac arrest, or when requested by the patient, and whenever syncope recurs despite beta-blockade and LCSD.
  • Potassium supplementation or spironolactone
  • Other antiarrhythmic therapy based on genotype

Risk Factors  for syncope or SCD

  • Congenital deafness
  • Hx/o syncope
  • Hx/o Ventricular arrhythmia
  • Family hx/o SCD
  • Female gender
  • QTc > 600ms
  • Medical non-compliance

Event triggers (vary depending on which genetic mutation)

  • Exercise-related
  • Auditory stimuli (alarm clock, telephone ringing!)
  • Acute emotional events
  • Catecholamine-induced
  • Pregnancy and up to 9 months post-partum
  • Onset of menopause

Post by Katrina D’Amore, DO.

 

EM Conference Pearls (7/26/17)

Pediatrics Trauma Radiology Review (Dr. Flannery) – When in doubt splint

  • Salter Harris: Take home memorize classification and management
    • SH1: Clinical Dx – Splint and f/u
    • SH2: Splint and f/u, most common
    • SH3: Ortho consult
    • SH4: OR
    • SH5: OR
  • Supracondylar Fx : Take home: Type II/III requires OR
    • SC Fx type I: Look for posterior/anterior fat pads
      • Tx: Posterior splint, f/u ortho
    • SC Fx type II: Splint and Ortho consult
    • SC Fx type III: OR
  • Misc Fx
    • Greenstick fracture
    • Toddle Fx: Tx with posterior splint and out pt f/u (For non displaced)
      • When in doubt splint and f/u ortho
    • Buckle Fx: Volar splint
  • SCFE
    • Klein’s line should intersect the femoral head
    • Can be bilateral
  • SCIWORA
    • Always recheck spinal (ROM/focal findings) after a negative CT cervical

Trauma Board Review (Dr. Patel)

  • Hip/Femur fracture
    • Most are operative, recognize they are sick patients.
    • Fermoral head fx, neck fx, trochanteric (Inter/sub)
    • Pain control, Ortho consult, Most cases OR
  • Tibial plateau fracture
    • Maybe radiographically occult
    • Patella alta
  • Maisonneuve fracture
    • Proximal fibular fx + medial malleolar fracture ( or disruption of deltoid ligatment, IO membrane syndesmosis)
  • Lisfranc fracture
    • Tarso-metatarsal fracture-dislocation
    • Mal-alignment Metatarsals with cuneiforms.
  • Calcaneal fractures
    • 10% associated lumbar fractures
    • Boehler’s angle <20
  • Jones fracture: High rate on non-union
  • Pseudojones fractures: Bulky dressing and pain control
  • Hip dislocations
    • MC: Posterior dislocation (90%)
    • High rate of AVN femoral head, peroneal nerve dysfx, sciatic nerve injuries)
  • Knee dislocation
    • 50% will spontaneous reduce!!!
    • Need a good Neurovascular evaluation
    • ABI < 0.9
    • Vascular surgery/ortho eval à Arteriography or CT Angio
  • Ankle Sprain:
    • Ottawa ankle rule
  • Scapular fracture
    • Associated with concomitant injuries such as internal thoracic injuries
  • Clavicle fracture
    • Op: Open fx, unstable floating shoulder, NV compromise.
  • Radial head fx
  • Monteggia fracture
  • Galeazzi fracture
  • Scaphoid fx – Thumb spica, risk of non-union and AVN
  • Bannette’s fx – Thumb spica,
  • Rolando fx
  • Posterior shoulder dislocation: Light bulb / Drum stick appearance
  • Compartment syndrome
    • 6P’s. Money is on pain and paresthesia.
  • High pressure injury injection injury
    • Limb threatening
    • Surgical emergency

Trauma in pregnancy (Dr. Kashani)

  • Prepare for difficult airway
  • Be aware of Hemodynamic changes
  • Rh sensitization
  • >20 weeks with abdominal trauma monitor for 4 hrs
  • Peri mortem C-section best outcome if performed within 4 – 5 minutes of CPR 

Thanks to Chief Mike Hong, DO PGY-4 for writing up today’s CONFERENCE PEARLS

Case of the Week (COW) #5

CC: Vomiting for 2 days

HPI: 47 year old female with PMHX of HTN and ETOH abuse presents with abdominal pain. Patient states that beginning two days ago she was woken up from her sleep with sudden onset non-bloody vomiting as well as epigastric pain which radiates to the back and is sharp in nature. She admits to over 15 episodes of vomiting. She is also having cramping of her feet bilaterally. She admits to daily ETOH use, and states her last intake was two days ago, denies illicit drug use. Denies taking any medication prior to arrival. Denies fever, chills, chest pain, SOB or dysuria. Denies recent travel or sick contacts. PMHX/PSHX: none Meds: none Allergies: none

Physical Exam: Vitals: BP 150/96 P 98 RR 16 O2 sat 98% RA General: Awake, alert, anxious Cardiac: Regular rate, no murmurs Lungs: CTAB, no rales, no rhonchi, no wheezing Abd: soft, non-distended, Mild tenderness to palpation epigastric area

Labs: Magnesium- 1.3 Potassium- 3.5 Troponin- 0.017

EKG:

DX: Prolonged QT interval with non-sustained polymorphic Ventricular tachycardia secondary to Hypomagnesemia

ED/Hospital course:  Upon arrival to ED patient had Epigastric pain with vomiting, Patient started on IVF and received Pepcid and Zofran. EKG at this time showed QT prolongation and patient found to have magnesium of 1.3. While waiting for magnesium, she started to have short runs of polymorphic ventricular tachycardia and during these times she complained of chest tightness. After 2 grams of magnesium patients repeat EKG showed normal QT and runs of ventricular tachycardia stopped. She received another 2mg of Magnesium and 40 mEq of Potassium Chloride. Patient was then admitted to Telemetry floor. Patient observed for 24hours and discharged to home with follow up with a cardiologist and Norvasc 5 mg 1tab PO daily, Losartan 100 mg 1tab PO daily, Ranitidine 150mg 1tab PO BI.

Pearls:

  • An abnormally prolonged QTc, especially >500 is associated with an increased risk of ventricular arrhythmias, Torsade’s de Pointes
  • Prolonged QT with prolonged T wave is due to: HypoK, HypoMg, Medications, Elevated ICP, Cardiac ischemia, Congenital.
  • Prolonged QT with prolonged ST-segment is due to: HypoCa, Hypothermia.
  • If EKG reveals long QT start by reviewing drug history and checking electrolytes. Stop any offending agents. Suppress early after depolarization with IV magnesium sulfate and keep potassium >4.5meq/L.
  • If non responsive to magnesium, may consider cardiac pacing and rarely isoproterenol infusion. Acceleration of the heart rate may produce suppression of arrhythmias, with a reduction in the QT interval.
  • Unstable patients should undergo non-synchronized electrical defibrillation.

Post by: Dr. Kerri Clayton, DO

 

Case of the Week (COW) #4

 

 

CC: Generalized Weakness

HPI: 55 y/o male presents complaining of 4 days of gradually worsening weakness in bilateral arms and legs. The patient also reports lower extremity pain one week ago, which resolved. Patient also complains of intermittent left sided back pain for the past couple of months that is exacerbated by walking. ROS: Positive for non-bloody diarrhea 2 weeks prior to presentation. Denies fever and vomiting at any time. No recent travels or sick contacts. Denies HA, dizziness, CP, SOB, or abdominal pain

Pertinent PE and Vitals: BP 172 / 82; Pulse 89; Resp 16; Temp 97.1; Pulse Ox 100% on R/A

GEN: Awake NAD.

EYES: PERRL, EOMI

NECK: supple, FROM, no meningismus

PULM: CTA in all fields, no tachypnea CARD: S1/S2 Normal. Normal rate.

NEURO: AAOX3. Lucid. Follows commands. CN 2-12 intact. No dysmetria bilaterally. No focal neurological deficits appreciated. Sensory intact. No drifts present in upper extremities. No dysarthria. Back: Mild painful ROM of lumbar region. No midline vertebral tenderness. No deformities. Deep tendon reflexes intact. 5/5 strength in all extremities.

Pertinent Labs (if any):

WBC 15.8 without any shift.

ED & Hospital Course: Patient was walked to evaluate gait in the setting of generalized weakness. She was able to ambulate with no ataxia. However, she was moving very slow and appeared globally weak. Patient stated this was not how she usually walks. A CT Head w/o Contrast followed by a lumbar puncture was then performed.

Lumbar Puncture (CSF Labs): RBC : 17,515   WBC: 21    Glucose: 103    Total Protein : 109

*LP was a traumatic 2nd attempt PLUS the samples were accidentally sent in a tube to the lab and dropped by the receiving lab tech. This contributed to the high RBC. Bonus Pearl – CSF tubes should always be hand delivered.

Working Diagnosis at time of Disposition : Guillain Barre Syndrome (GBS)

Neurology was consulted. Negative Inspiratory Force was performed with normal results. Patient was admitted to Neurology Floor with diagnosis of GBS. The patient improved after multiple doses of IVIG and was discharged from the hospital 1 week later with outpatient Neurology follow up

Pearls & Takeaways

Get a thorough history. Diarrhea is usually never important but in this case it was helpful in making the diagnosis. Ø Always walk your patients prior to discharge. Ø GBS is typically followed by a viral illness. Signs and symptoms include symmetric motor weakness that is usually ascending with little to no sensory involvement. Ø Progression of disease is over days to weeks. Ø Paralysis can ascend to the diaphragm. A Negative Inspiratory Force (NIF) test should be performed to evaluate the respiratory muscles. Intubate if FVC <15 mL/kg or negative inspiratory pressure < -25 cm H2O. Ø Albumin-cytological dissociation of CSF (high protein (>45) and low WBC count