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Intraoperative Management of Septic Shock

Bettina Makon, BSN


University of Pennsylvania

Anticipated graduation date: May 2015
Email address: bmakon@nursing.upenn.edu

Keywords: Septic Shock, metabolic acidosis, hemodynamic instability, systemic inflammatory
response syndrome, hypotension, vasopressin, norepinephrine, lactate

Although surgery and anesthesia are ideally postponed until hemodynamic instability with sepsis
is achieved, the underlying cause of sepsis may require urgent surgical intervention. Septic shock
is severe sepsis, acute organ dysfunction secondary to infection, with hypotension not reversed
by fluid resuscitation.
1
Sepsis mounts a systemic inflammatory response syndrome that becomes
exaggerated by activating the complement system and coagulation cascade. Furthermore, it
produces widespread arterial vasodilation and altered capillary permeability.
1
These
abnormalities make it difficult to manage septic patients in the operating room due to
hypotension, lactic acidosis, and hypoxemia.

Case Report

A 68-year old male, 107.3kg and 177cm, presented for an abdominal washout and right hip
incision and drainage with wound vacuum placement. His medical history was significant for
gastroesophageal reflux disease, deep vein thrombosis, right hip septic arthritis, chronic
obstructive pulmonary disease, and diabetes mellitus. His surgical history included right hip
arthroplasty, right hip prosthesis removal related to infection, and spinal surgery for epidural
abscess. None of the previous surgeries were associated with anesthetic complications.

The patient presented to the emergency room with right hip pain and white fluid drainage from
an open wound on the hip. In following days, he was taken to the operating room (OR) for right
hip arthroscopy. In the Post-Anesthesia Care Unit, he became hypotensive 70/50mmHg with a
HR 110bpm and then experienced a pulseless electrical activity arrest, requiring three rounds of
cardiopulmonary resuscitation, reintubation, and stabilization on large doses of norepinephrine
and vasopressin infusions. He was coagulopathic with extensive bleeding from his surgical site
requiring 20units of packed red blood cells (PRBCs) over eight hours post operatively; he had
also developed abdominal compartment syndrome requiring emergency exploratory laprotomy.

The patient was brought back to the OR for a washout of his abdomen and hip, presenting as an
ASA 5E. He came into the OR directly from the Intensive Care Unit (ICU) intubated and
requiring norepinephrine 10mcg/min and vasopressin 0.02units/min. American Society of
Anesthesiologist standard monitors were applied. Bilateral breath sounds were confirmed and the
patient was continued on AC ventilation. General anesthesia was induced with midzolam 2mg
and fentanyl 100mcg. He arrived febrile per core temperature of 39C. The initial arterial blood
gas (ABG) results on arrival were pH=7.25, ionized calcium = 0.8mmol/L, lactate =
13.7mmol/L, hemoglobin = 6.3gm/dL, base excess = -10.5mEq/L.

The case lasted 55 minutes, over which blood loss totaled 1500cc. Intraoperative resuscitation
consisted of PRBCs 6units, fresh flozen plasma (FFP) 2units, bicarbonate 5amps, calcium
chloride 3gm and normal saline 1L. The patients blood pressure was maintained with the
continuous vasopressin infusion and by increasing the norepinephrine infusion to14mcg/min. He
remained hemodynamically unstable post intraoperative resuscitation efforts, with ABG findings
of pH=7.21, ionized calcium = 0.89mmol/L, lactate=12.8mmol/L, hemoglobin = 6.9gm/dL, base
excess = -0.8mEq/L. After wound vacuum placement on the abdomen and hip, the patient was
taken back to the ICU.

Discussion

Urgent surgical intervention is occasionally necessary before stabilization of hemodynamics, as
in patients with septic shock.
2
Intraoperatively, the components of sepsis, such as hypotension,
capillary permeability, and coagulopathy, are potentiated by common hemodynamic anesthetic
changes such as hypotension, bleeding, and cardiovascular surgical stress.
2
Acute management
of septic patients in the operating room becomes challenging.

Septic patients with lactate levels greater than 3mmol/L and hypotension should initially be
treated with crystalloid.
2
Volume resuscitation with crystalloid is recommended over
hydroxyethyl starches (HES).
3
A meta analysis compared the use of crystalloid to HES, found
that there was no difference in mortality when using either; however, there was an increased risk
of acute kidney injury with HES.
4
Additionally, RCT in patients with septic shock compared the
administration of albumin to normal saline found a non-statistically significant reduction in 28-
day mortality in the albumin-receiving group; therefore, supporting the low-level
recommendation for albumin administration in septic shock.
5
Primary resuscitation
intraoperatively of patients with septic shock should be with crystalloid, supported by HESs
associated risks and albumins non-significant benefits.


Fluid administration should be decreased when additional fluid does not improve tissue
perfusion, as evidenced by a continued increase in lactate
.2
Transfusion of red blood cells can be
considered to facilitate oxygen delivery to tissues, hypovolemia, and intraoperative blood loss.
2

This patient arrived to the operating room hypotensive with hgb = 6.3gm/dL. Therefore, PRBCs
and FFP were administered in this case, as the Surviving Sepsis guideline advocates for
administration of blood products for hgb less than 7.0gm/dL.
3
In this case, the patients lactate
concentration was increasing despite crystalloid administration so our resuscitation efforts were
focused on blood product administration. This patient had increasing lactate levels, continued
hypotension and bleeding with a hgb less than 7.0gm/dL, so the administration of blood products
was indicated as per the evidence.

Continued hypotension and hypoperfusion of tissues despite fluid resuscitation contributes to
mortality with sepsis.
6
The addition of vasoactive medications, commonly norepinephine and
vasopressin, may be necessary to maintain adequate perfusion. Norepinephrine is used as a
potent alpha-adrenergic agent. However, it may decrease cardiac output, oxygen delivery, and
blood flow to vulnerable organs despite adequate perfusion pressure.
7
Vasopressin is used to
exogenously restore the relative vasopressin deficiency that occurs in septic shock. Vasopressin
will restore vascular tone and blood pressure, therefore decreasing the required norepinephrine
dose and its deleterious effects.
7
The Vasopressin and Septic Shock Trial found that vasopressin
infusion did not significantly decrease 28-day mortality when compared to norepinephrine
infusion in patients with septic shock.
6
The study did however find that, in patients with less
severe septic shock, requiring norepinephrine infusion 5-15mcg/min, the addition of low dose
vasopressin had a decrease in 28-day mortality, supporting the vasoactive medication
administration in this case.
7


Endogenous steroid administration in septic shock is used to maintain cortisol levels. Cortisol
maintains systemic blood pressure by facilitating conversion of norepinephrine to epinephrine in
the adrenal medulla.
1
Cortisol level becomes depleted in septic shock, so the exogenous
administration may increase levels and help modulate the stress response.

Corticosteroids may have a role when comparing the addition to low-dose vasopressin infusion
versus norepinephrine infusion. The vasopressin group is associated with less organ dysfunction
and increased vasopressin levels; the increase in vasopressin levels does not occur in the
norepinephrine infusion group alone. The increase may not be seen in the norepinephrine group
related to a low endogenous concentration of vasopressin in sepsis.
6
A systemic analysis of 6
RCTs determined that patients with less than 50% predicted mortality rate did not benefit from
hydrocortisone administration, while patients with a predicted mortality of greater than 60%
showed a non-significant trend of lowered mortality related to shock reversal.
3
When the use of
vasopressin and norepinephrine are failing to maintain perfusion, cortiocsteroid administration
may decrease mortality. Therefore, the addition of hydrocortisone 200mg could have been
administered in this case to help obtain hemodynamic stability.
3

In this case, multiple doses of sodium bicarbonate were administered in an attempt to correct
acidosis. The administration of sodium bicarbonate to treat lactic acidosis due to sepsis is not
recommended by the Surviving Sepsis guidelines for a pH above 7.15.
3
The administration of
bicarbonate is associated with increased serum sodium concentrations and fluid overload,
increased lactate, increased PCO
2
, and a decreased ionized calcium. The decrease in ionized
calcium further causes decreased cardiac and vascular contractility and responsiveness to
catecholamines.
8
Also, the acidosis related to lactate will not improve. Bicarbonate will increase
extracellular pH since the negatively charged bicarbonate buffer remains largely extracellular.
Intracellular compartments of organs remain acidotic such that organ function will not be
restored.
8


In conclusion, many research studies exist to guide management of septic shock, however few
articles exist on acute management of septic shock intraoperatively. Acute management of septic
shock and hypotension should mimic standard guidelines for best practice.





References

1. Stoelting RK, Hines RL, Marschall KE. Anesthesia and Co-Existing Diseases. 6th ed.
Philadelphia: Saunders:Elsevier; 2012.
2. Eissa D, Carton EG, Buggy DJ. Anaesthetic management of patients with severe sepsis.
Br J Anaesth. 2010;105(6):734-43. doi:10.1093/bja/aeq305.
3. Dellinger et al. Surviving Sepsis Campaign. Crit Care Med. 2012;41:580-637.
4. Perel P, Roberts I, Ker K. Colloids versus crystalloids for fluid resuscitation in critically
ill patients. Cochrane Database Syst Rev. 2013;2:CD000567. doi:10.1002/14651858.
5. Delaney AP, Dan A, Mccaffrey J, Finfer S. The role of albumin as a resuscitation fluid
for patients with sepsis: A systematic review and meta-analysis. Crit Care Med.
2011;39(2):386-91. doi:10.1097/CCM.0b013e3181ffe217.
6. Russell JA, Walley KR, Gordon AC, et al. Interaction of vasopressin infusion,
corticosteroid treatment, and mortality of septic shock. Crit Care Med. 2009;37(3):811-8.
doi:10.1097/CCM.0b013e3181961ace.
7. Russell JA, Walley KR, Singer J, et al. Vasopressin versus norepinephrine infusion in
patients with septic shock. N Engl J Med. 2008;358(9):877-87.
doi:10.1056/NEJMoa067373.
8. Boyd JH, Walley KR. Is there a role for sodium bicarbonate in treating lactic acidosis
from shock? Curr Opin Crit Care. 2008;14(4):379-83.
doi:10.1097/MCC.0b013e3283069d5c.

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