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127 Postoperative Fever
441
Scenario 2
A 26-year-old male is admitted to the trauma service after
suffering a motor vehicle crash while intoxicated. His injuries include a chance fracture of T11, fractures of the right
8th to 10th ribs, and a left parietal subarachnoid hematoma.
He is taken to the operating room on hospital day 1 for posterior fusion to repair his spine and returns to the intensive
care unit and is able to be extubated. On hospital day 5, he
spikes a temperature of 101.5°F.He complains of pain in his
left lower leg, and on exam it appears slightly larger than his
right leg.
How toAnswer?
• This case represents a mildly complicated polytrauma
patient with injuries that could each represent a potential
source of fever. An intracranial bleed or spinal cord injury,
if present, could be a source of central fever (this would
be a diagnosis of exclusion).
• He has rib fractures that could certainly precipitate pneumonia, but further information on this is not included in
the stem.
• He had surgery and could have a wound infection. The
main physical exam nding of a swollen, tender leg in a
patient who is postoperative day 4 from a spinal surgery
should set off alarms for deep vein thrombosis.
• Further concerning signs which are not included, but
should be asked for, are other vital signs, evidence of
hypoxia, and EKG ndings, to guide thinking in terms of
PE.
– Workup should include bilateral lower extremity
Doppler ultrasound, as well as consideration of CTA
PE protocol if other concerning signs such as hypoxemia and tachycardia exist.
– However, it is important to keep in mind that this
patient has a contraindication to anticoagulation in
his initial injuries which must not be forgotten when
developing a treatment plan.
– For this patient, if a DVT were present, he would likely
be recommended an IVC lter until therapeutic anticoagulation was deemed safe from a neurosurgical
perspective.
Bonus Points
A mnemonic may be helpful: Wind (lungs: atelectasis vs
pneumonia), Water (UTI), Walking (DVT), Wound, Wonder
(drugs); these represent the more common causes of postoperative fever in the chronological order in which they are
more likely to occur.
Clean Kills
• Failure to consider pneumonia in the workup of postoperative fever
• Failure to consider venous thromboembolism in the
workup of postoperative fever
• Failure to consider urinary tract infection in the workup of
postoperative fever
Words ofWisdom
Postoperative fever is sometimes benign, but it may also be a
harbinger of grave clinical concern. The cause of a fever
may be multifactorial, but always remember to consider
where the hands of the surgeon have been. Also keep in
mind that the elderly and those who are frail, at the extremes
of age, and immunocompromised may not mount a febrile
response. The wording in a question may not necessarily
lead you directly to the source, so maintain a broad, but
focused, differential, and conduct a workup that will narrow
in on the diagnosis and treat the underlying problem. Lastly,
in practice, a 3 degree rise in their baseline temperature,
while not technically a fever, may still be signicant enough
for alarm.
Bibliography
Abdelmaseeh TA, Azmat CE, Oliver TI.Postoperative fever [updated
2023 Jun 4]. In: StatPearls. Treasure Island, FL: StatPearls
Publishing; 2023. https://www.ncbi.nlm.nih.gov/books/
NBK482299/.
Townsend JCM, Beauchamp RD, Evers BM, Mattox KL.Sabiston text-
book of surgery. 20th ed. Elsevier Health Sciences Division; 2016.
Postoperative Myocardial Infarction
KathleenJarrell
128
Way Questions May BeAsked?
A 57-year-old male with past medical history of peripheral
arterial disease, diabetes mellitus type 2, hypertension,
hyperlipidemia, and current tobacco abuse is now on postoperative day 1 status post-left femoral to popliteal artery
bypass with a right saphenous vein conduit. He complains of
dyspnea as well as chest pain with radiation to his left shoulder. What is on your differential? How do you evaluate and
treat?
How toAnswer?
• Start with a complete history and physical exam.
– Focus on prior history of angina, coronary artery inter-
ventions, and other signs and symptoms of vascular
disease. The presence of atherosclerotic vascular disease anywhere in the body—in this case, peripheral
artery disease—means the patient likely has it systemically and is therefore at risk for myocardial infarction
(MI).
• In this patient who recently underwent major vascular
surgery and with multiple underlying medical comorbidities, a postoperative myocardial infarction (MI) should be
high on the differential. The differential should also
include an aortic dissection, pulmonary embolism, heart
failure exacerbation, gastroesophageal reux, and
pericarditis.
What is the initial workup and treatment for chest pain in
a postoperative patient?
• Assess the patient’s stability and vital signs.
K. Jarrell (*)
Department of Surgery, Thomas Jefferson University Hospital,
Philadelphia, PA, USA
e-mail: Kmj009@jefferson.edu
• Review pertinent patient history—previous MI, history of
cardiac conditions/previous cardiac surgery or stenting,
relevant medications.
• Discuss current symptoms—location, character and
severity of pain, any radiation pain, other associated
symptoms (palpitations, diaphoresis, dyspnea, etc.).
• Perform a physical exam—cardiac auscultation.
• Obtain an EKG—assess for ST-segment elevations, ST
depression, T-wave inversions, and Q-waves.
• Send basic labs and trend serial cardiac enzymes—over
the next several hours.
– Troponin—delayed release, will be elevated over
hours to days after an MI.
– CK-MB—quick release, will be elevated earlier on in
the rst few hours of an MI.
– Consult cardiology for further management and pos-
sible intervention.
– If patient is found to have a STEMI or is unstable with
an NSTEMI, likely will proceed to PCI.
Will require aspirin, possibly clopidogrel, and a
heparin drip post-procedure.
– If patient has a stable NSTEMI, treat medically in con-
junction with cardiology.
Oxygen supplementation, aspirin, pain control (IV
morphine), heparin drip if bleeding risk is acceptable; consider starting a beta-blocker (to decrease
cardiac demand), a statin (for plaque stability), and
an ACE-I (to prevent remodeling).
What are common risk factors for postoperative myocar-
dial infarction (MI)?
• Coronary artery disease
• Recent stroke
• Previous MI
• Recent cardiac stenting
• Peripheral arterial disease
• Diabetes mellitus
• Hyperlipidemia
• Hypertension
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2025
M. Neff et al. (eds.), Passing the General Surgery Oral Board Exam, https://doi.org/10.1007/978-3-031-78244-2_128
443
444
K. Jarrell
• Smoking history
• Family history of an MI
• Recent major surgery
What steps can you take to decrease the risk of a postop-
erative MI?
• During the preoperative period, it is important to identify
patients who have risk factors that place them at high risk
for a postoperative MI.These patients should be referred
to cardiology or their primary care physician for preoperative risk stratication. This typically includes the
RCRI scale or others such as the ACS NSQIP Risk
Calculator. Patients who have two or more risk factors on
the RCRI scale are considered to be at high risk for
surgery.
• Close co-management of these patients with their primary care physician and/or cardiologist is important in
the perioperative period. Beta-blockers should generally
be continued in the perioperative period for patients who
were already on them preoperatively. If a patient is
found to have three or more risk factors on the RCRI
scale, they can be considered to be started on a betablocker, at the discretion of their cardiologist. Statins
have been shown to decrease postoperative cardiovascular events and should also be continued in the perioperative period.
• Not recognizing atypical presentations of myocardial
infarction
– Patients with long-standing diabetes mellitus may
have autonomic neuropathy which blocks the typical
sensations of chest pain. Their presenting complaint
may be nausea.
• Failure to consult cardiology and begin treatment in a
timely manner
Words ofWisdom
Postoperative myocardial infarction is a serious complication and can lead to signicant morbidity and mortality for
patients if it is not managed appropriately and expeditiously.
Early diagnosis and a high index of suspicion are critical,
particularly in patients with multiple risk factors. Patients
with a suspected myocardial infarction should be evaluated
promptly: assess for stability; investigate symptoms; obtain
an EKG and cardiac enzymes. General surgeons should
know the initial management steps for myocardial infarction:
supplemental oxygen, aspirin, IV morphine, heparin drip,
and possibly beta-blocker. If the patient is unstable or has a
conrmed STEMI, proceed with urgent cardiology consultation and likely PCI.If they are stable, manage medically with
assistance from cardiology.
Common Curveballs
• Arrhythmias
– May require management with rate control agents
– May require cardioversion in the case of atrial brilla-
tion with hypotension
• Symptoms of heart failure
Clean Kills
• Inadequate workup of a postoperative patient with chest
pain
Bibliography
ACS Risk Calculator—Home Page. https://riskcalculator.facs.org/
RiskCalculator/. Accessed 1 Sept 2023.
Badner NH, Knill RL, Brown JE, Novick TV, Gelb AW.Myocardial infarc-
tion after noncardiac surgery. Anesthesiology. 1998;88(3):572–8.
https://doi.org/10.1097/00000542- 199803000- 00005.
Ruetzler K, Smilowitz NR, Berger JS, Devereaux PJ, Maron BA, Newby
LK, de Jesus Perez V, Sessler DI, Wijeysundera DN.Diagnosis and
management of patients with myocardial injury after noncardiac
surgery: a scientic statement from the American Heart Association.
Circulation. 2021;144(19):e287–305. https://doi.org/10.1161/
CIR.0000000000001024.
Townsend CM Jr, etal., editors. Sabiston textbook of surgery the bio-
logical basis of modern surgical practice. 19th ed. Philadelphia:
Saunders; 2012.
Air Embolism
TylerFox andAnirudhKohli
129
Way Question May BeAsked?
You are called to the ICU to place a central line in an intubated patient. Following dilation of the tract, you hear a rush
of air as you withdraw the dilator over the wire. The patient
becomes tachycardic and their oxygen saturation decreases
from 98% to 86%. Their blood pressure decreases from
120/60 to 88/50 and they are tachycardic to 110. What is the
next best step?
How toAnswer?
• The next best step is to place an occlusive dressing over
the puncture site and place the patient in Trendelenburg
position with their right side up.
• This prevents further air from entering the venous system
and helps sequester air in the right heart within the right
ventricle. This lessens right ventricular outow tract
obstruction and decreases air transit into the lungs.
• Additional management includes temporarily increasing
FiO2 to 100% to aid reabsorption of trapped air by nitrogen displacement.
• Consider imaging (transthoracic echocardiogram) to
assess volume of intracardiac air.
Continued Scenario The patient stabilizes after positioning
and increasing FiO2. Bedside ECHO is performed which
demonstrates a large pocket of air within the RV.What would
be the next step in management?
T. Fox
Department of Surgery, Lankenau Medical Center,
Wynnewood, PA, USA
e-mail: foxt@mlhs.org
A. Kohli (
Department of Surgery, Lankenau Medical Center,
Wynnewood, PA, USA
Division of Acute Care Surgery, Department of Surgery, Thomas
Jefferson University Hospital, Philadelphia, PA, USA
e-mail: anirudh.kohli@jefferson.edu
*)
• You can consider placing a multi-port catheter over the
wire in the neck and attempt aspiration of the intracardiac
air via syringe.
• It should be noted that de novo placement of a catheter is
controversial.
What is a vascular air embolism? (Pathophysiology)
• Intravascular air embolism, divided into either venous gas
embolism (VGE) or arterial gas embolism (AGE), is a
rare and potentially fatal condition in which air within the
intravascular space leads to obstruction of blood ow
resulting in hemodynamic compromise and tissue perfusion decits. The main adverse clinical outcome is endorgan damage secondary to ischemic insult. In addition to
obstruction, air bubbles may directly injure endothelium
of the microvasculature which results in vasospasm and
capillary leak, initiating a local or systemic inammatory
response (Gordy and Rowell 2013; McCarthy etal. 2017).
The severity of symptoms and lethality is determined by
the composition of the gas, the volume of gas instilled,
and the rate of instillation. A small volume of gas may
have no effect. Moderate volumes of gas can result
inlocal inammation and edema (e.g., pulmonary edema)
(Shaikh and Ummunisa 2009). Large volumes of gas
impair hemodynamics. A lethal quantity of air for humans
is believed to be ~3–5 mL/kg (Gordy and Rowell 2013;
McCarthy etal. 2017). If utilizing a 14 gauge needle, this
amount of air can be instilled in <3 s, accounting for standard central venous pressure (CVP) of 5 mmHg
(McCarthy etal. 2017).
What are risk factors and incidence for VGE? For
AGE? (Epidemiology and risk factors)
• Venous gas embolism (VGE) is most commonly an iatrogenic complication in the healthcare setting. Risk varies
with positioning and procedure. Most commonly these
are secondary to central line placement or removal with
incidences reported to be approximately 0.2–1% (Gordy
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2025
M. Neff et al. (eds.), Passing the General Surgery Oral Board Exam, https://doi.org/10.1007/978-3-031-78244-2_129
445
446
T. Fox and A. Kohli
and Rowell 2013; Brunicardi etal. 2014). Additional risk
factors include (Gordy and Rowell 2013; McCarthy etal.
2017):
– Procedures ~5 cm or higher (Shaikh and Ummunisa
2009) above the heart (oral, maxillofacial, ENT, neu-
rosurgical procedures).
– Patient in sitting position:
This increases venous drainage above the heart and
increases the gradient which could draw air intravascularly at a more rapid pace.
Some series place the risk of air embolism in
patients undergoing posterior craniotomies in
seated position as high as 10–80%.
– Cardiac bypass: 0.003–0.007%.
– Percutaneous lung biopsy.
– Cavitation secondary to ablative procedures (tumor,
atrial brillation, etc.).
– Penetrating, blunt, or barometric trauma to the lung,
typically resulting in alveolar rupture and alveolarvascular stula (Shaikh and Ummunisa 2009). Larger,
penetrating injuries may result in larger communications between the endovascular space and the
airway.
– Abdominal insufation (e.g., with use of a Veress nee-
dle) (Powell-Brett etal. 2020).
• Arterial gas embolism (AGE) can result from the conversion of VGE to AGE via right to left shunt, most commonly via a patent foramen ovale (PFO), as up to 9% of
the general population may have a PFO (McCarthy etal.
2017). In one series, PFO was detected in up to 77% of
AGE (McCarthy et al. 2017). Additionally, AGEs may
result from direct arterial catheterization, most commonly
from an “unushed” catheter. Another possible etiology
includes endovascular balloon rupture during vascular
procedures (e.g., angioplasty).
• Outside of the healthcare setting, air emboli are also seen
secondary to decompression during ascent in deep-sea
divers. The soluble quantity of nitrogen gas in the blood
increases with increased pressure as the diver descends.
During ascent these gases dissociate from blood and may
form large bubbles which embolize tissue.
What are the signs and symptoms of VGE/AGE?
(Diagnosis)
• Presentation varies from being asymptomatic to altered
mental status to hypotension and cardiovascular collapse.
Diagnosis is typically based on patient history and temporal relationship of mechanism to onset of symptoms.
Vascular air emboli can share common presentation with
pulmonary emboli if the embolus enters the heart and/or
pulmonary circulation. Such similarities include the following (Brunicardi etal. 2014):
– Air in the pulmonary artery increases pulmonary resis-
tance which causes right heart strain, decreased cardiac output, and even arrhythmias.
– Air in pulmonary microvasculature causes V/Q mis-
match and increased pulmonary dead space. This
results in hypercapnia and hypoxia.
– Air in the left ventricle (LV) may impede LV lling
and thus decrease cardiac output.
– Air in the coronary arteries may result in myocardial
ischemia.
• Other features of presentation vary with the end organ
affected but commonly include a component of acute
altered mental status or even seizures secondary to cerebral air embolus. Air emboli in peripheral tissues can also
cause pain. This is common in decompression in divers
(“bends”) (Shaikh and Ummunisa 2009). Physical exam
ndings may aid in diagnosis. These include (Gordy and
Rowell 2013; McCarthy et al. 2017; Shaikh and
Ummunisa 2009):
– Jugular venous distention secondary to increased right
ventricular (RV) pressures secondary to pulmonary air
embolus
– Classic “mill wheel” murmur over the precordium
– Evidence of right heart strain or arrhythmia on EKG
– Dilated RV on bedside echocardiography
– In the intubated patient: an acute increase in end-tidal
CO
2
– Visible intracardiac air on echocardiogram/bedside
ultrasound
– Large pulmonary or intracardiac air emboli which may
be visible on CXR
– Evidence of peripheral hypoxemia
What is the management of VGE/AGE? (Treatment)
• Monitoring and early recognition during at-risk procedures is critical. Mortality, even with prompt diagnosis
and treatment, may be as high as 20% (McCarthy etal.
2017). It should be noted, however, that many more mild
cases of air embolism may go undiagnosed, thus raising
mortality in reported series (McCarthy etal. 2017).
• The rst step after recognition is stopping further air entry
by closing off portals to the arterial or venous circulation
including capping or removal of central lines, sheaths, or
catheters. Depending on the location of the air, supportive
care may be the only viable option. This includes supplemental 100% O
± hyperbaric oxygen (to decrease frac-
2
tion of nitrogen in embolized gas and speed reabsorption)
as well as circulatory (pressors) and respiratory support
(intubation) as warranted by the patient’s clinical status.
• For air emboli in the central venous system and right
heart, Durant’s maneuver may be utilized. This entails
placing the patient in Trendelenburg with right side up
129 Air Embolism
447
(left lateral decubitus). Air is moved away from the right
ventricular outow tract and trapped in the RV.Aspiration
can be attempted on trapped right ventricular air. The
placement of a de novo catheter remains controversial
(Gordy and Rowell 2013; McCarthy etal. 2017).
• In the setting of pulmonary trauma, cross clamping of
pulmonary hilum to control bleeding may also prevent
return of air to the left atrium from traumatic bronchialvenous stula.
Clean Kills
• Failure to promptly recognize air embolism while performing an at-risk procedure
• Failure to utilize appropriate positioning in suspected
central venous gas embolism
• Failure to recognize potential sites of air entry and close
off to prevent propagation of embolism
Bonus Points
• Use of point of care ultrasound in the periprocedural setting (operating rooms or intensive care units) can help in
diagnosis of large pockets of intracardiac air and hence
may expedite treatment.
Words ofWisdom
• Air embolism as a clinical condition needs a high index of
suspicion, and any change in the clinical status of the
patient that is temporally related to an invasive procedure
should make you pause and strongly consider this
diagnosis.
Bibliography
Brunicardi F, Andersen D, Billiar T, Dunn D, Hunter J, Matthews J,
Pollock R. Schwartz’s principles of surgery. 10th ed. McGrawHill; 2014. p. 1034–99. https://ia600908.us.archive.org/23/items/
SchwartzsPrinciplesOfSurgery10thEdition/Schwartz%27s%20
Principles%20of%20Surgery%2C%2010th%20Edition.pdf.
Accessed 27 Aug 2023.
Gordy S, Rowell S. Vascular air embolism. Int J Crit Illn Inj Sci.
2013;3(1):73.
McCarthy CJ, Behravesh S, Naidu SG, Oklu R.Air embolism: diagno-
sis, clinical management and outcomes. Diagnostics. 2017;7(1):5.
Powell-Brett S, Richardson M, Super P, Singhal R. Veress needle
creation of pneumoperitoneum: a safe technique. Obes Surg.
2020;30:2026–7.
Shaikh N, Ummunisa F.Acute management of vascular air embolism. J
Emerg Trauma Shock. 2009;2(3):180.
Perioperative Care: Recent Myocardial Infarction
SubhadraAcharya
130
Way Question May BeAsked?
A 56-year-old male, heavy smoker, with recent myocardial
infarction (MI) 2 weeks ago, now presents with intractable
right upper quadrant abdominal pain and nausea with imaging concerning for acute cholecystitis.
How toAnswer?
• The example will include some kind of surgical problem
in the setting of a recent MI.
• This could also be presented as a very high risk patient
coming in with an urgent surgical issue who develops cardiac complications after surgery.
• Examinees should consider whether there is any way to
temporize a surgical problem, noting that, ideally, surgery
should be delayed as long as possible (but at least 6
months) after an MI.Usually, the scenario given will be
such that such a delay is not feasible, based on the patient’s
condition or nature of the surgical problem.
• History to elicit:
– Medical history: coronary artery disease, peripheral
vascular disease, hypertension, hyperlipidemia, diabetes mellitus, kidney disease
Including any interventions: coronary artery bypass
graft (CABG), percutaneous coronary intervention
(PCI), etc.
– Family history: MI, CAD
– Social history: smoking, alcohol, use, illicit drug use
• Imaging/labs
– Complete blood count (CBC), basic metabolic panel
(BMP), electrolytes (as abnormalities can increase
arrhythmia risk).
– If there is a concern for congestive heart failure (CHF),
one can add on BMP.
– Add troponins if there is concern for ongoing MI.
S. Acharya (*)
Thomas Jefferson University Hospital, Philadelphia, PA, USA
– Chest X-ray, EKG, echocardiogram (ECHO).
– May require a stress test if there are new or concerning
abnormalities on ECHO.If there are reversible defects
on stress thallium, the patient may need a cardiac
catheterization.
• Other preoperative considerations:
– Admission to a monitored bed.
– Nitroglycerin drip preoperatively.
– Invasive monitoring such as an intra-arterial catheter
for blood pressure.
– Patients with conduction system abnormalities may
require a pacemaker preoperatively.
Risk stratication for a preoperative patient:
Revised Cardiac Risk Index (RCRI)
• Has replaced the Goldman criteria for risk stratication
preoperatively
• Predictors include:
– Type of surgery (intraperitoneal, intrathoracic, supra-
inguinal, vascular)
– History of ischemic cardiac disease
– History of CHF
– History of cerebrovascular disease
– Pre-existing diabetes mellitus that is being treated with
insulin
– Preoperative serum creatinine >2 mg/dL
• Patients are stratied based on the number of predictors
they have:
– Class I [0 predictors] correlates with a 0.4% 30-day
risk of death, myocardial ischemia (MI), or cardiac
arrest (CA).
– Class II [1 predictor] correlates with a 0.9% 30-day
risk of death, MI, or CA.
– Class III [2 predictors] correlates with a 6.6% 30-day
risk of death, MI, or CA.
– Class IV [greater than or equal to 3 predictors] corre-
lates with a more than 11% 30-day risk of death, MI,
or CA.
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2025
M. Neff et al. (eds.), Passing the General Surgery Oral Board Exam, https://doi.org/10.1007/978-3-031-78244-2_130
449
450
S. Acharya
Other considerations:
• All anesthetic agents (local, epidural, or general) can pose
cardiac risks and cause cardiac depression; therefore,
there is risk with any anesthesia modality.
• Do not forget postoperative management. High-risk
patients should get a post-op EKG and should be monitored closely.
Way Question May BeAsked?
A 70-year-old male with known atrial brillation, coronary
artery disease, and congestive heart failure with ejection
fraction (EF) of 25% on preoperative echocardiogram is
now POD 0 from a laparoscopic right hemicolectomy for an
ascending colon mass. As he is brought from PACU to his
oor bed, he complains of chest tightness and shortness of
breath.
How toAnswer?
• Main thing to remember is to adequately work up these
problems.
• History to elicit:
– Onset, inciting factors, relieving factors of the pain,
presence of dyspnea
– Prior episodes of similar symptoms
• Labs/imaging:
– CBC, BMP, electrolytes
– Troponin, BMP
– EKG
– CXR
– Depending on above, may need ECHO or further inter-
vention such as cardiac catheterization
• Other considerations:
– Monitored bed/telemetry
– Medication optimization
Restart patients’ home medications, such as betablockers and diuretics as appropriate.
Common Curveballs
• Intraoperative ischemic event
• Intraoperative arrhythmias
• Post-op ischemia
• Post-op arrhythmias (Especially A-b, do not forget your
ACLS algorithms!)
• Post-op pulmonary edema
• Preoperative management of patients with recent cardiac
events
Clean Kills
• Not knowing any criteria that would make patient high
risk via RCRI
• Not adequately working up the patient preoperatively
• Forgetting about intraoperative monitoring
• Believing one type of anesthesia superior to another (risk
itself is just anesthesia, so do the surgery you need to do)
• Not appropriately working up or treating postoperative
complications
Words ofWisdom
Oral board scenarios, involving recent MI, intraoperative or
immediately postoperative MI, or other cardiac conditions,
are common because they are relatively common and challenging in real practice. Surgeons should have a basic understanding of the cardiac risk stratication tools, steps to take
to assist in perioperative monitoring and support, and initial
treatment of MI in the immediate postoperative period.
Bibliography
Barker SJ, Gamel DM, Tremper KK.Cardiovascular effects of anesthe-
sia and operation. Crit Care Clin. 1987;3:251–68.
Bonaccorsi HA, Burns B.Perioperative cardiac management [updated
2023 Apr 17]. https://www.ncbi.nlm.nih.gov/books/NBK493196/.
Brown KN, Cascella M.Goldman risk indices [updated 2023 Feb 13].
https://www.ncbi.nlm.nih.gov/books/NBK546604/.
Acute Kidney Injury
JoelB.Durinka andJoshuaA.Marks
131
Way Question May BeAsked?
Did the patient have a bowel preparation preoperatively, i.e., was the patient dry to begin the case?
A 52-year-old obese (BMI 41) female presents for colon
resection for a third episode of diverticulitis. Preoperative
colonoscopy showed diverticulosis with a sigmoid stricture.
The patient undergoes a laparoscopic converted to open sigmoidectomy due to the complexity of the dissection. On the
morning of postoperative day 1, her urine output is marginal
and her creatinine has bumped from a baseline of 0.95–1.58.
Was there a degree of obstruction from the stricture
too that led to a further dehydrated state?
What was the estimated blood loss (EBL) and how
much resuscitation did the patient receive
intraoperatively?
– Consider why the procedure was converted to open
and whether you have any anatomical concerns such as
a ureteral injury.
– What interventions would you try and what would be
How toAnswer?
the expected outcome?
– Suppose you give two liters of lactated Ringer’s solu-
• History and physical examination should focus on risk
factors for AKI (Table131.1).
• Examinees should try to think through the following
questions as they prepare to answer:
– What are the likely causes of oliguria in this patient?
tion and the patient’s urine output does not increase
and the creatinine continues to rise, what would you do
next?
– What if the closed suction drain output also was
increasing?
– What is the patient’s volume status and what operative
data points would you want?
Table 131.1 Risk factors for developing AKI: Risk factors for developing postoperative acute kidney injury
Prerenal Renal Postrenal Type of surgery Patient factors
Hypovolemia Nephrotoxic medication
– Aminoglycosides
– Amphotericin
B-NSAIDS
Hemorrhage Radiocontrast media (?) Cell debris Major vascular surgery Obesity
Third space loss Rhabdomyolysis BPH Emergency surgery High ASA class
Hypotension Neurogenic bladder Laparoscopic surgery Underlying renal insufciency
RAAS blockers Diabetes
Increased intra-abdominal
pressure
Stones Cardiac surgery Age
Foley obstruction Impaired cardiac function
Anemia
Chronic liver disease
Preexistent Essential
Hypertension
J. B. Durinka · J. A. Marks (*)
Division of Acute Care Surgery, Department of Surgery, Thomas
Jefferson University, Philadelphia, PA, USA
e-mail: Joel.Durinka@jefferson.edu; joshua.marks@jefferson.edu
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2025
M. Neff et al. (eds.), Passing the General Surgery Oral Board Exam, https://doi.org/10.1007/978-3-031-78244-2_131
451
452
J. B. Durinka and J. A. Marks
Alternate Scenario
A 64-year-old male undergoes an open abdominal aortic
aneurysm (AAA) repair and is admitted to the SICU postoperatively. He remains intubated and sedated. In the early
postoperative period, his urine output is robust but then
drops off precipitously. He is now 12h postoperative and the
nurse is calling and saying the patient is oliguric and his
creatinine has doubled since surgery.
How toAnswer?
• It is important to think about possible etiologies and
develop a focused differential diagnosis specic to the
scenario.
– Hypovolemia: What was the EBL? Is he bleeding?
Check hemoglobin and hematocrit.
– Hypoperfusion/hypotension: What are his current
hemodynamics? What is his baseline blood pressure?
What was his pressure throughout the case?
– Medications: What does he take at home? What has he
received? For example, does he take an ACE inhibitor
and did he take it the morning of surgery?
– Pulmonary mechanics: Is he stable on the ventilator?
What are his peak airway pressures?
– Abdominal exam: Is he distended or taut? Are you
concerned about intra-abdominal hypertension? Check
the urinary catheter and measure bladder pressure.
• Consider the index operation, what was done, and what
technical factors could be contributing.
– Why was the AAA done open as opposed to an endo-
vascular approach? Was the AAA juxta-renal? Were
the renal arteries manipulated, covered, or
reimplanted?
– Was there a suprarenal or supra-celiac clamp placed to
sew the proximal anastomosis? If so, what was the
cross-clamp time? Was furosemide or mannitol given
intraoperatively prior to the cross-clamp to “protect”
the kidneys, and was the initial robust urine output a
byproduct of that?
• Volume resuscitate and reassess whether the intervention
has the desired effect. Always reassess any intervention
and reevaluate as time passes and new information such
as labs and vitals becomes available.
The pathophysiology of AKI can generally be character-
ized as prerenal, intrinsic renal, or postrenal. Assessments
of volume status as well as analysis of urine and serum electrolytes may help distinguish between the likely causes
(Table131.2).
Table 131.2 Denitions and staging of acute kidney injury
Denition of acute kidney injury
Increase in serum creatinine by ≥0.3mg/dL within 48h
or
Increase in serum creatinine to ≥1.5 times baseline, which is known
or presumed to have occurred within the prior 7 days
or
Urine volume <0.5mL/kg/h for 6h
Staging of acute kidney injury
Serum creatinine Urine output
Stage 1
1.5–1.9 times baseline
or
≥0.3mg/dL increase
Stage 2
2.0–2.9 times baseline
Stage 3
3 times baseline
or
Increase in serum creatinine to ≥4.0mg/
dL
or
Initiation of renal replacement therapy
or
In patients <18 years, decrease in eGFR
to <35mL/min/1.73m
2
<0.5mL/kg/h for 6–12h
<0.5mL/kg/h for ≥12h
• Prerenal: hypovolemia. Decrease in circulating intravas-
cular volume from bleeding or dehydration. It may also
be caused by medications that affect regulation of the
renin-angiotensin-aldosterone system (RAAS) or impair
the normal regulatory mechanisms of afferent and efferent arterioles, such as vasodilatation from inammation,
sepsis, or anesthetic agents.
• Intrinsic renal: acute tubular necrosis (ATN). In surgical
patients, this is often from the effects of sustained hypoperfusion. Intrinsic renal injury though may also be
caused by medications or chemicals that are directly toxic
to the kidney such as nonsteroidal anti-inammatory
drugs (NSAIDs), aminoglycosides, and amphotericin
B.Trauma patients with crush injuries or impaired blood
supply to the extremities may also develop rhabdomyolysis, and the release of myoglobin from injured muscle
may cause kidney injury by renal vasoconstriction, the
formation of tubular casts caused by myoglobin precipitation, or injury of tubular cells by free oxygen radicals.
The use of contrast media in radiographic imaging is
another commonly discussed cause of AKI in surgical
patients, although whether contrast-induced nephropathy
truly exists as a real entity with modern contrast media is
debatable. The proposed mechanisms of contrast mediainduced AKI were thought to involve a combination of
medullary vasoconstriction/ischemia and direct injury/
cytotoxicity to tubular epithelial cells.