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248 D. T. Bennett et al.
Mediastinitis
• The most common causes of mediastinitis are infections related to sternotomy
incisions or esophageal perforations. A rarer entity, descending necrotizing
mediastinitis (DNM), has a more subtle presentation and devastating outcomes if not managed promptly.
• DNM carries a mortality rate of 20–40%. DNM typically arises from an oro-
pharyngeal or cervical infection. Presentation of DNM includes neck
swelling, dysphagia and pyrexia. It is generally associated with elevated
WBC and CRP. The most commonly involved organisms are streptococcus
species and anaerobes.
• Diagnosis is confirmed by presence of neck and mediastinal fluid collections or
abscesses identified on computed tomography. DNM is classified as follows:
(1) Type I — localization to mediastinum above the carina; (2) Type IIA —
extension from neck to anterior mediastinum; and (3) Type IIB — extension
from neck to anterior and posterior mediastinum.
• Immediate treatment includes prompt administration of broad-spectrum anti-
biotics followed by surgical debridement. Cervical debridement and drainage
is achieved with parallel, horizontal collar incisions down to infected tissue,
leaving passive (Penrose) drains in place. The mediastinum is generally
accessed through a right-sided anterolateral thoracotomy. All necrotic tissue
is aggressively debrided and the pleural space and mediastinum is copiously
irrigated with saline. The left side is avoided as the aortic arch may prohibit
mediastinal debridement. After debridement thoracostomy tubes are placed in
the mediastinum as well as apicoposteriorly in the pleural cavities.
• Postoperatively, the mediastinal tubes are irrigated with 1–2 liters of saline
twice daily with drainage allowed through the pleural thoracostomy tubes.
This is continued until pleural drainage is culture-negative for three consecutive days. In several studies, duration of drainage averaged 21 days with a
range of 9 to 69 days. Antibiotics should be tailored to address sensitivities of
the organisms involved.
• Serial CT scans are necessary to ensure all abscesses have been adequately
drained. Undrained abscesses require further operative debridement.
Pleural Space and Mediastinum 249
Practical Algorithm(s)/Diagrams
Fig. 1. Algorithm for management of pleural effusions. (Image reproduced from
Moore et al. J Trauma Acute Care Surg 2012; 73: 1372–1379).
Review of Current Literature with References
• The MIST2 trial was a multicenter randomized controlled trial of 210 patients
published in 2011. It utilized a 2 × 2 factorial design where patients with an
infected pleural effusion were given one of four treatments: double placebo,
DNase plus placebo, t-PA plus placebo, or DNase plus t-PA. DNase (5 mg),
t-PA (10 mg) or placebo were administered to the appropriate cohorts via thoracostomy tube twice daily, and the tube was clamped for 1 hour post-administration. In the DNase-t-PA group, the authors identifi ed a statistically signifi cant reduction in: (1) Hospital length of stay; (2) Referral for surgery; and (3)
250 D. T. Bennett et al.
Size of effusion relative to placebo. (Rahman et al. Intrapleural use of tissue
plasminogen activator and DNase in pleural infection. N Engl J Med 2011;
365: 518–526)
• DNM is a rare entity with mortality rates up to 40%. Iwata and colleagues
describe their management of 10 patients experiencing 20% mortality. CT
scan confi rms diagnosis. Immediate broad-spectrum antibiotics and surgical
debridement and drainage of both the neck and mediastinum are performed.
Postoperatively, the mediastinum is irrigated daily with normal saline and
drained via pleural thoracostomy tubes. Drainage is continued until pleural drainage is culture-negative for 3 days. (Iwata T et al. Early open thora-
cotomy and mediastinopleural irrigation for severe descending necrotizing
mediastinitis. Eur J of Cardio-thorac Surg 2005; 28: 384–388)
• Tong and colleagues retrospectively reviewed prospectively collected data from
420 consecutive patients undergoing VATS (326 patients) or open (94 patients)
decortication. They evaluated outcomes between the groups in an intention
to treat analysis with 11.4% conversion rate from VATS to open. The authors
found the VATS group to have signifi cantly shorter operative time and hospital length of stay. The VATS group also demonstrated signifi cant reduction
in prolonged air leak, ventilator dependence, number of tracheostomies, sepsis
and 30-day mortality. (Ann Thorac Surg 2010; 89: 220–225)
• Meyer and colleagues performed a prospective randomized trial of 39 patients
comparing early VATS drainage (15 patients) to second tube thoracostomy
(24 patients) in stable patients with retained hemothorax from trauma within
72 hours of initial presentation. They found a signifi cant reduction in duration of tube drainage, hospital length of stay and hospital costs for patients
undergoing early VATS drainage compared to management with second tube
thoracostomy. Furthermore, 42% of patients failed management with second
tube thoracostomy and ultimately required surgery. (Ann Thorac Surg 1997;
64: 1396–1401)
7. Renal
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Chapter 7-(i)
Acute Renal Insufficiency and Failure
Max Wohlauer, MD*
*Surgical Resident, University of Colorado School of Medicine
Take Home Points
• Although comprising 2% of the body’s mass, the kidneys receive 25% of
cardiac output.
• Acute renal failure (ARF), also called acute kidney injury (AKI), remains a
major clinical challenge.
• AKI is characterized by the loss of the kidney’s ability to eliminate waste,
regulate acid base status, and regulate extracellular volume.
• Treatment is aimed at identification of high-risk patients and to treat under-
lying causes of renal dysfunction.
Background
• Acute kidney injury (AKI) is an abrupt decrease in renal function that leads
to the buildup of nitrogenous waste and uremic toxins.
• AKI is an important complication of surgery and trauma with a high associ-
ated mortality.
Contact information: Denver Health Medical Center, 777 Bannock St., Denver, CO 80204;
Email: Max.wohlauer@gmail.com
253
254 M. Wohlauer
• AKI is defined as an elevation of serum creatinine of 0.5 mg/dL from baseline
or need for acute renal replacement therapy.
• Glomerular filtration (GFR) is usually regulated between a wide range of
systolic blood pressures (80–180 mmHg).
• GFR is used as an estimate of renal function and renal drug clearance. The
Cockcroft-Gault estimates creatinine clearance and is frequently used to
calculate the GFR. Patients with Stage IV CKD (estimated GFR < 30 mL/
min/1.73 m2) should consider initiating hemodialysis or undergoing renal
transplantation. Additionally, many medications need to be dose-adjusted
with GFR < 30.
• Three classifications of acute renal failure: pre-renal, renal, and post-renal.
• Despite availability of renal replacement therapy (RRT), mortality in the
critically ill population exceeds 60%. Although many advocate for continuous
hemofiltration, others have shown intermittent hemodialysis (HD) to be less
expensive and more effective.
Main Body
• Classification of AKI:
{ Pre-renal: low cardiac output, decreased intravascular volume, renal
vascular disease.
{ Renal: glomerulonephritis, acute tubular necrosis (ATN), acute interstitial
nephritis (AIN), hemolytic uremic syndrome (HUS), embolism, trauma.
{ Post-renal: obstruction of ureter, bladder, or urethra.
• Other scenarios:
{ Hepatorenal syndrome (HRS): acute renal failure in the setting of liver
impairment usually due to cirrhosis. Systemic vasodilation leads to profound renal vasoconstriction. HRS is multifactorial and thought to be
related to activation of the renal-aldosterone-angiotensin system in
response to hypotension. These patients often have severe hyponatremia,
volume overload, and low urine sodium concentration (<10 mEq/L).
{ Rhabdomyolysis: When muscle is damaged, a protein pigment called
myoglobin is released into the bloodstream. This compound is normally
filtered out of the bloodstream by the kidneys; however, in large amounts
myoglobin may block the structures of the kidney, causing damage
resulting in acute tubular necrosis or kidney failure. Following injury,
damaged muscle tissue may lead to an excessive amount of myoglobin and
other cellular breakdown products to be released into the bloodstream.
Acute Renal Insufficiency and Failure 255
This process is often compounded by a shock state and reduced blood flow
to the kidneys. Early and aggressive hydration may prevent kidney damage
by rapidly flushing myoglobin out of the kidneys. In severe cases, rhabdomyolysis may lead to acute tubular necrosis or acute renal failure and
patients may need hemodialysis. Management includes fluid resuscitation
to maintain adequate urine output and treatment of the underlying cause;
there is no role for alkalization of the urine in treatment of rhabdomyolysis.
{ Contrast-induced nephropathy (CIN): Serum creatinine usually peaks
three days post-injury and returns to baseline in seven days, although the
injury is sometimes irreversible. Several techniques are in use to prevent
CIN; however, there are no compelling data to support routine use of any
medication in preventing contrast nephropathy. Studies suggest that
N-actetylcysteine may help reduce the severity of contrast nephropathy.
{ Drug-induced AKI: Drugs are an important contributor nephrotoxicity in
the surgical ICU. Patients are maintained on medications at home that
may be nephrotoxic (i.e. cyclosporine, tacrolimus). Antibiotics are a common culprit. Aminoglycosides (i.e. gentamycin) are nephrotoxic and
penicillins can cause AIN. Drugs with renal excretion. Vancomycin is
excreted in the urine and can reach toxic concentrations in renal insufficiency. Concentrations of nephrotoxic drugs should be closely monitored
and dose-adjusted according to GFR.
• Lab tests and diagnostic work-up: Serum creatinine, urinalysis, fen, creatine
kinase, urine eosinophils for AIN, renal ultrasound, and renal biopsy.
• Management: Identification of high-risk patients may help the physician pre-
vent AKI via close monitoring of volume status to prevent hypovolemia and
avoiding contrast agents and other nephrotoxins. Early identification and
treatment remains the hallmark of treating AKI. Treatment of prerenal causes
of AKI, i.e. in trauma, stopping the hemorrhage will help restore intravascular
volume, as will resuscitation from septic shock. A CT scan ordered during a
trauma workup, or antibiotics ordered for treatment of sepsis can lead to
intrinsic renal injury in the aforementioned patients; however, highlighting
the complexities of AKI management. AKI that leads to anuria requires renal
replacement therapy, which will be discussed in a separate chapter.
256 M. Wohlauer
Practical Algorithm(s) / Diagrams
Fig. 1. Classification of AKI.
Fig. 2. RIFLE Criteria.
Review of Current Literature with References
• A randomized controlled trial of 83 patients with chronic renal insuffi ciency
evaluated the role of acetylcysteine in protecting against contrast nephropathy.
Ten out of the 83 patients (12%) developed contrast nephropathy, 1/41 (2%) in
the acetylcysteine group compared to 9/42 (21%) of patients in the saline-only
control group (p = 0.01). The authors concluded that prophylactic oral administration of acetylcysteine (600 mg twice daily the day before and on the day of
contrast agent administration, when coupled with IV saline administration)
Acute Renal Insufficiency and Failure 257
prevented contrast nephropathy, although this should be taken with a grain
of salt due to the small sample size (Tepel M, van Der Giet M, Schwarzfeld
C, Laufer U, Liermann D, Zidek W. Prevention of radiographic-contrastagent-induced reductions in renal function by acetylcysteine. N Engl J Med
2000; 343: 180–184).
• Role of loop diuretics in oliguric AKI: Cantarovich et al. performed a random-
ized control trial evaluating the role of furosemide in AKI. The concept of
converting oliguric AKI to non-oliguric AKI is appealing because of several
reasons including: (1) loop diuretics protect the loop of Henle from ischemia
via inhibition of the Na
+-K+
-2Cl− pump in the loop of Henle and (2) inducing
polyuria may help treat volume overload in this high-risk patient population.
Although in this study, high doses of the loop diuretic helped to maintain
urine output, it did not improve survival or hasten renal recovery (Cantarovich F, Rangoonwala B, Lorenz H, Verho M, Esnault VL. High-dose furosemide for established ARF: a prospective, randomized, double-blind, placebocontrolled, multicenter trial. Am J Kidney Dis 2004; 44: 402–409).
• A single institution retrospective review of 2,157 trauma patients investigated
the prognostic signifi cance of early AKI. The authors showed that early AKI,
with a prevalence of 2%, had a strong association with the development of
MOF. The majority of the 154 renal failure cases (82%) evolved to MOF.
Isolated kidney failure on day 2 (creatinine >1.8 mg/dL) was a rare event,
but when it occurred, renal failure had a very high likelihood of progression
to MOF (Wohlauer MV, Sauaia A, Moore EE, Burlew CC, Banerjee A, Johnson J. Acute kidney injury and posttrauma multiple organ failure: the canary
in the coal mine. J Trauma Acute Care Surg 2012; 72: 373–378; discussion
379–380).
• Determining the time to initiate dialysis has been a topic of considerable in-
terest lately, and studies have shown that early initiation of dialysis is associated with improved outcomes. A multicenter prospective observational study
evaluated 98 patients undergoing major abdominal surgery who developed
AKI requiring renal replacement therapy (RRT) found that patients who underwent RRT earlier in their course [RIFLE 0 and R, early dialysis (ED)] had
improved outcomes compared to patients initiating dialysis after the kidney
injury who had progressed to injury or failure [RIFLE I-F, late dialysis (LD)].
Although serum creatinine and albumin levels were not statistically different between ED and LD groups upon ICU admission and before RRT initiation, the study is limited due to small sample size and possibly selection bias
(Shiao CC, Wu VC, Li WY et al. Late initiation of renal replacement therapy
is associated with worse outcomes in acute kidney injury after major abdominal surgery. Crit Care 2009; 13: R171).