Enter your email address to follow this blog and receive notifications of new posts by email.

Morning Report – Fluid Responsiveness

Resident Presenter: Patrick Charles

Topic: Fluid Responsiveness Series (part 1 of 2)
Summary:
45 yo M with a PMHx of DM and HTN presents with SOB and fever. He
complains of progressively worsening fatigue and cough over the last few days
and developed acute onset fever, shaking chills, and difficulty breathing on the
day of presentation. His vitals are 101.5oF, 132, 22, 90/44, 94% RA. Physical
examination reveals right lower lung field crackles, and a chest x-ray
demonstrates a right lower lobe infiltrate.
What do you do next?
Fluids?
How many liters would you empirically give this patient?
When do you pull the trigger and start pressors?
Learning Points:
WHAT IS FLUID RESPONSIVENESS? Is this concept
synonymous with the fact that the patient needs more
fluid?
– Fluid responsiveness does not mean that a patient
should be given fluids!
– Fluid Responsiveness = An increase in their stroke
volume (SV) by 10–15% via rapid infusion of 500 ml of
crystalloid (fluid challenge) or straight leg raise thus
improving CO if the patient falls on the preload zone of
the Frank-Starling Curve.
– If there is compressibility (or distensibility in a ventilated
patient) of the IVC >20% and <50% then evaluate for
fluid responsiveness. Perform a passive leg raise while
reassessing the IVC if the IVC collapse <20% then the
patient may not be a fluid responder
– The data clearly established that there is a poor relationship between the CVP
and the intravascular volume status, and no relationship between the CVP and
fluid responsiveness.
– CVP and PCWP are static tests that are less sensitive, less specific and less
useful that dynamic tests (i.e.
passive leg raising)

Preau et al: A prospective study in
France that looked at 34 ICU
spontaneously breathing patients.
They performed passive leg raising
which equates to a 500cc rapid
volume expansion. They concluded
that stroke volume increased >/= 10%
after a volume expansion = passive
leg raise were responders which
predicted fluid responsiveness with
sensitivity of 86% and specificity of
90%. The pulse pressure increase of
>/= 9% which predicted fluid
responsiveness with sensitivity of 79%
and specificity of 85%. The velocity of
femoral artery flow increase of >/= 8%
which predicted fluid responsiveness
with a sensitivity of 86% and specificity
of 80%. This concluded that passive
leg raising are accurate and
interchangeable indices for predicting
fluid responsiveness in non-intubated
patients.
DO IVC MEASUREMENTS CORRELATE WITH CVP?
– Kircher et al: reported that Caval Index (CI) >50% was strongly associated with
a CVP <8 mm Hg and futhermore was indicative of right atrial (RA) pressures
<10 mm Hg. In comparison the CI <50% was associated with a CVP >12 and
indicated RA pressures >10 mm Hg
WHAT DO YOU DO IF THEY ARE RESPONDERS BUT REMAIN IN SHOCK?
– (Step 1) If the CI is <50% perform a TTE and Lung US (e.g. hyperdynamic heart
and no B-lines) to assess if the patient can handle more fluids. (Step 2) If so add
Levophed (or vasopressor of your choice). (Step 3) After a few minutes repeat
passive leg raise and assess if the patient is a responder.
LIMITATIONS OF IVC U/S
– respirophasic changes in intrathoracic pressure are difficult to quantify when the
inspiratory force itself cannot be measured or standardized in a spontaneous
breathing patient
– location at which measurements are obtained varies greatly in the literature –
caudal to the junction of the middle hepatic vein, approximately 2 to 4 cm from
the IVC/RA junction
– craniocaudial movement – Mechanical displacement of the diaphragm during
respiration frequently results in measurement of the IVC at 2 different locations
during inspiration and expiration, and the IVC exhibits different degrees of
collapsibility at different locations along its course
– subcostal window may not afford adequate visualization of the IVC, particularly
in patients with obesity, abdominal pain, gastric insufflation, large amounts of
bowel gas, or post-surgical wounds and/or pneumoperitoneum.
-IVC diameter and CI are significantly influenced by pulmonary hypertension,
tricuspid regurgitation, tachycardia and variations in tidal volumes and patterns of
respiration in spontaneously breathing patients. abdominal compartment
syndrome
EBM Article:
1) Stone et al. Inferior Vena Cava Assessment, Correlation with CVP and
Plethora in Tamponade. Global Heart, Vol. 8, no. 4, 2013
2) Préau et al. Passive leg raising is predictive of fluid responsiveness in
spontaneously breathing patients with severe sepsis or acute pancreatitis. Crit
Care Med, Vol. 38, No. 3, 2010
3) Muller et al. Respiratory variations of inferior vena cava diameter to predict
fluid responsiveness in spontaneously breathing patients with acute
circulatory failure: need for a cautious use. Critical Care, 16:R188, 2012
4) Marik et al. Fluid responsiveness: an evolution of our understanding, British
Journal of Anaesthesia, 2014
5) Kircher et al, Noninvasive estimation of right atrial pressure from the
inspiratory collapse of the inferior vena cava; Am J Cardiol. 1990 Aug
15;66(4):493-6.
6) http://lifeinthefastlane.com/ccc/fluid-responsiveness/
7) http://emcrit.org/blogpost/ivc-roundup/
8)http://www.ultrasoundpodcast.com/2013/10/integrated-ultrasound-approach-
fluid-responsiveness-canadian-style-foamedMorningReport-FluidResponsiveness- Patrick Charles Figure 1MorningReport-FluidResponsiveness- Patrick Charles Figure 2

Figures may be externally copyrighted and all rights belong with the holders.

Morning Report – Atypical Cause of Chest Pain

Resident Presenter: Molly Malone PGY1

Topic: Atypical Cause of Chest Pain

Summary:

Patient is a 70 year old female with a PMHx significant for HTN, HLD, COPD, diaphragmatic hernia and anxiety presenting to the ED for chest pain x5 days. Pt reports the pain is located in her b/l chest and radiates to her b/l back. She categorizes it as 8/10, persistent lower rib cage pain, sharp in nature, and exacerbated with deep breathing. Pt endorses mild relief with Advil and 2 episodes of emesis yesterday. Pt denies, SOB, cough, abdominal pain, nausea, or fever.

Initial vitals: T: 36.4°C | HR: 101 | BP: 100/68 | RR: 16 | O2 Sat: 97% RA

Pt was in NAD had an unkempt odor about her and physical exam was unremarkable except for tachycardia and b/l chest tenderness.

Initial plan was for ACS work up including EKG, CXR, labs, Trops. When these came back negative the work up was extended to include PE. The patient received a CT-PE and was found to have:

“Mural thickening and adjacent stranding of the mid to distal esophagus. Within the esophagus just proximal to the GE junction there is a questioned focus of intramural air possibly reflecting a Mallory-Weiss tear. No evidence of mediastinal emphysema”

http://ispub.com/IJTCVS/13/1/3124#

Learning Points:

  • Atypical causes of chest pain: Mallory-Weiss tear, Boerhaave Syndrome, Diaphragmatic Hernia
  • Upright CXR, Esophogram, CT-chest
  • Treatment for Boerhaave: Conservative and Operative
    • 1st call to CT surgery
    • Conservative Management – Disruption contained in the mediastinum or between the mediastinum and visceral lung pleura; drainage of the cavity back into the esophagus; minimal symptoms; and minimal signs of clinical sepsis
    • Volume resuscitation – IVF and broad spectrum antibiotics to include anaerobes
  • Toby Factor: effusion usually occur and are seen in the LEFT plural cavity

Articles:

See comment in PubMed Commons below Spontaneous esophageal rupture: a frequently missed diagnosis, Am Surg. 1999 May;65(5):449-52.

A case of rapid diagnosis of Boerhaave syndrome by thoracic drainage: J Emerg Med. 2012 Dec;43(6):e419-23. doi: 10.1016/j.jemermed.2011.05.079. Epub 2011 Dec 22.

Against all odds. Conservative management of Boerhaave’s syndrome: BMJ Case Rep. 2014 May 21;2014. pii: bcr2013200485. doi: 10.1136/bcr-2013-200485.

Morning Report – Psoas Abscess

Presenter: Emily Sze PGY-1

Topic: psoas abscess

Summary: In this case, a 47-year-old male presents to the ED complaining of 2 weeks of worsening of his chronic lower back and abdominal pain, along with nausea, vomiting, diarrhea, and dysuria. He is a current IVDU, most recently injected heroin 1 week ago, and was previously in a methadone program. He also smoked crack a few days ago. He had his appendix removed as a teenager. He was seen at Bon Secours hospital a few days ago for the same complaint and sent home with oxycodone and Valium.

On exam: 37.3C (99.1F), intoxicated, +ttp abdomen, –ttp spinal/paraspinal region, neuro exam normal.

Work-up: wbc count 19.9, mild anemia hgb 10.9, wet abd CT showed a psoas abscess of size 1.8x2cm.

Learning points:

  • Always consider psoas abscess in differential for lower back pain, particularly in a patient with risk factors
  • Psoas abscess has high mortality rate (2.4% for primary, 18.9% for secondary), usually due to sepsis from delayed diagnosis/treatment
    1. Look for +psoas sign, position of comfort (hip flexion/lumbar lordosis)
  • Primary psoas abscess – caused by hematogenous/lymphatic spread (20-60% of psoas abscesses in USA)
    1. Risk factors:
      1. IVDU
      2. Immunosuppression (diabetes, renal failure, HIV, etc)
  • Epi: males, childhood to young adulthood, tropical/developing countries
  1. Bugs: Staph aureus (#1), including MRSA; Mycobacterium tuberculosis in endemic areas -> vancomycin, clindamycin, linezolid
  • Secondary psoas abscess – caused by direct spread
    1. Risk factors:
      1. Trauma
      2. Vertebral osteomyelitis, especially from Pott’s disease
  • Crohn’s ileocolitis (0.4-4.3% incidence)
  1. Infected aortic aneurysm (20% incidence)
  2. Ruptured renal or pancreatic abscess
  3. Septic hip arthritis (hip bursa communicates with iliopsoas bursa in 15% of people
  • Iatrogenic: instrumentation, epidural catheter, total hip arthroplasty (12%), shock wave lithotripsy, nephrectomy
  1. Bugs: usually enteric, often polymicrobial ? Zosyn, fluoroquinolone, cephalosporin, Flagyl
  • Imaging: dry CT, wet CT, MRI are options
    1. Sensitivity for all 3 modalities is 100% after 6 days of symptoms
    2. Earlier than 6 days, sensitivity is 33%, 50%, and 50%

Light bedtime reading (EBM article):

  1. Eric B. Tomich, DO and David Della-Giustina, MD. Bilateral Psoas Abscess in the Emergency Department. West J Emerg Med. 2009 Nov; 10(4): 288–291.
  2. Takada T, Terada K, Kajiwara H, Ohira Y. Limitations of Using Imaging Diagnosis for Psoas Abscess in Its Early Stage. Intern Med. 2015;54(20):2589-93.

Article of the Week 10-21-15

Hi Colleagues,

EBM Article of the Week: It’s the hot-off-the-presses AHA guidelines for CPR.
It’s hard to get excited about guidelines but you will notice a few changes to cardiac arrest resuscitation.
Notable changes include…
– No longer using Vasopressin in place of Epi.
– Amiodarone>Lidocaine
– Mg should not be used routinely.
– ETCO2 to monitor for correct ETT placement and predictor of survival.

Morning Report – Sepsis

Resident Presenter: Jordan Treworgy PGY-2

Topic: Sepsis

Summary:

82 yo female with weakness and 3 falls in the last day. Previously well and ambulating without difficulty. Found to be uroseptic on u/a. Patient was placed on sepsis protocol and expired the next day as a DNR per husband and son.

Learning Points:

-Documentation must include 5 things: Timestamp, blood cultures x2 prior to antibiotics, Lactate x2, 30cc/kg bolus withing 3 hours from the time septic.

-Antibiotics must be listed as hung by nursing within 3 hours (you will be dinged!)

-Bolus must be listed as given within the three hours regardless of comorbidities and actual weight to be used with no upper limit.

EBM Article:

http://www.survivingsepsis.org/sitecollectiondocuments/protocols-sepsis-treatment-stony-brook.pdf

EBM Article of the Week 10-16-15

This weeks EBM Article is from JAMA and reviews oral steroids for acute radiculopathy. It’s a well done randomized trial that demonstrates mild to moderate improvement in functional scores at three weeks for select patients.  Enjoy the read!

  1. Oral steroids for acute radiculopathy due to a herniated lumbar disk: a randomized clinical trial. Goldberg H, Firtch W, Tyburski M, Pressman A, Ackerson L, Hamilton L, Smith W, Carver R, Maratukulam A, Won LA, Carragee E, Avins AL. JAMA. 2015 May 19;313(19):1915-23. doi: 10.1001/jama.2015.4468.

Article of the Week 10/8/15

You may have already seen it or heard the buzz around it. It’s the recently released NEJM study of central venous catheter complications. The authors essentially randomized about 3,000 folks to receive either IJ, subclavian, or femoral TLCs and looked at infection and complication rates. The results may surprise you.

  1. Parienti JJ, Mongardon N, Mégarbane B, Mira JP, Kalfon P, Gros A, Marqué S, Thuong M, Pottier V, Ramakers M, Savary B, Seguin A, Valette X, Terzi N, Sauneuf B, Cattoir V, Mermel LA, du Cheyron D; 3SITES Study Group. Intravascular Complications of Central Venous Catheterization by Insertion Site. N Engl J Med. 2015 Sep 24;373(13):1220-9. doi: 10.1056/NEJMoa150096