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Documentation Tip of the Week: Shock

Posted on Wed, Sep 09, 2015
Documentation Tip of the Week: Shock

Our weekly feature of documentation tips for clinicians.

By Timothy Brundage, MD

Shock is typically associated with evidence of inadequate tissue per fusion on physical examination

  • Skin - Degree of cutaneous perfusion
  • Kidneys - Urine output
  • Brain - Mental status

The presence of low blood pressure should not be a prerequisite for defining shock: compensatory mechanisms may preserve blood pressure through vasoconstriction, while tissue perfusion and oxygenation are already decreased significantly.

The definition of circulatory shock emerging from this consensus conference does not require the presence of hypotension.

Consensus on circulatory shock 2014

Timothy Brundage

Dr. Timothy Brundage is a hospitalist for EmCare at St. Petersburg General Hospital in St. Petersburg, Fla. Dr. Brundage earned his bachelor’s degree in chemistry and molecular biology at the University of Michigan, his M.D. at the Wayne State University School of Medicine and completed his residency in internal medicine at the University of South Florida College of Medicine. Subscribe to Dr. Brundage’s weekly documentation tips, or ask him about specific documentation issues, by emailing him at DrBrundage@gmail.com.

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Documentation Tip of the Week: Shock v. Septic Shock

Posted on Wed, Jul 29, 2015
Documentation Tip of the Week: Shock v. Septic Shock

Our weekly feature of documentation tips for clinicians.

Shock:

  • Defined as a life-threatening, generalized maldistribution of blood flow resulting in failure to deliver and/or utilize adequate amounts of oxygen, leading to tissue dysoxia
  • Hypotension (SBP < 90, SBP decrease of 40 mmHg from baseline, or mean arterial pressure (MAP <65), while commonly present, should NOT be required to define shock
  • In the absence of hypotension, when shock is suggested by history and physical examination, we recommend that a marker of inadequate perfusion be measured (decreased ScvO2, SvO2, increased blood lactate, increased base deficit, perfusion-related low pH)
Septic Shock: Sepsis with Hypotension
  • If hypotension resolves after recommended 30 cc/kg fluid bolus then diagnose severe sepsis
  • If hypotension persists after recommended 30 cc/kg fluid bolus then diagnose septic shock and begin Levophed (preferred pressor)
  • If Lactic acid > 4.0 with sepsis then diagnose septic shock and treat as septic shock Reference




 

Timothy Brundage, MD, is a hospitalist for EmCare at St. Petersburg General Hospital in St. Petersburg, Fla. Dr. Brundage earned his bachelor’s degree in chemistry and molecular biology at the University of Michigan, his medical degree at the Wayne State University School of Medicine and completed his residency in internal medicine at the University of South Florida College of Medicine. Subscribe to Dr. Brundage’s weekly documentation tips or ask him about specific documentation issues by emailing him at DrBrundage@gmail.com.

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Clinical Hot Topics: Hypotensive Resuscitation in Hemorrhagic Shock: The Science So Far

Posted on Wed, Nov 12, 2014
Clinical Hot Topics: Hypotensive Resuscitation in Hemorrhagic Shock: The Science So Far

Hosted by Al Sacchetti, MD, FACEP as moderator, Don’t Blink or You Will Miss It - Clinical Hot Topics can feel much like the “speed dating” of training presentations. The 12 hyper-paced presentations covered a wealth of information for the 2014 EmCare Leadership Conference attendees.  Each week, we’ll publish highlights from select clinical hot topics presented at the conference.

Hypotensive Resuscitation in Hemorrhagic Shock: The Science So Far
by Matthew M. Carrick MD, FACS

“Shock” has been called the “Rude Unhinging of the Machine of Life” (Samuel V. Gross, 1892).

Hemorrhagic shock is a leading cause of death following trauma. (Kauvar DS et al. Impact of Hemorrhage on Trauma Outcome: An Overview of Epidemiologic, Clinical, and Therapeutic Considerations: J Trauma 2006; 60: S3‐S11)

So, it’s pretty bad. What do we do?

In 1918, Walter Cannon stated “inaccessible or uncontrolled sources of blood loss should not be treated with intravenous fluids until the time of surgical control.” With each new generation of physicians and technology, the recommendations changed based on new theories. The process of aggressive crystalloid resuscitation began around the time of the Vietnam era. However, the effects of aggressive fluid resuscitation exacerbated the “Lethal Triad” – Acidemia, Hypothermia and Coagulopathy. Over time, it was learned that the effects of resuscitation were not as clear cut as previously thought. All currently available fluid preparations contribute in varying degrees to the development of MSOF and ARDS. At elevated blood pressures, blood clots become dislodged.

How does the clinician balance the risk of resuscitation with the risk of circulatory collapse? Can we withhold all fluid resuscitation?

Dr. Carrick provided data as the participants compared clinical trials on animals testing the approach of fluids versus no fluids for a massive hemorrhage and then for a small volume hemorrhage. (Mapstone J et al., Fluid Resuscitation Strategies: A systemic Review of Animal Trials. J Trauma. 2003; 55:571‐589) Among the human patients who received delayed fluid resuscitation, 70 percent survived as compared with 62 percent who received immediate fluid resuscitation (P = 0.04).
So what’s the verdict?

Ultimately the current conclusion is that for hypotensive patients with penetrating torso injuries, delay aggressive fluid resuscitation until operative intervention improves the outcome.

It seems the recommendations have gone full circle leaving Mr. Cannon to respond simply… “told you so!” 

  1. Cannon W.B, Faser J., Collew E.M: The preventive treatment of wound shock. JAMA 47. 618.1918.
  2. Matthew M. Carrick MD FACS International Symposium on ... (n.d.). Retrieved from http://www.iscb2013.dk/presentations2009/Session%207_Carrick_.pdf_br

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