fever above 38° C (100.4°F) is common in the first few days after surgery, and does not usually
signal infection
fever that develops 48 hours after surgery often represents a nosocomial infection
fever results from cytokine release from tissue trauma or from bacterial endotoxins and exotoxins
Timing of Fever
Immediate
develops in the OR or within hours of surgery
may result from infections that were present before the operation (appendicitis, peritonitis) or from
increased cytokine release following surgery
adverse drug reactions or transfusion reactions are less common causes
malignant hyperthermia is a very rare cause of immediate fever, and typically presents
within 30 minutes of administering a triggering agent like succinylcholine or an
inhalational anesthetic
Acute
fever develops within the first week of surgery
nosocomial infections are the most common cause: pneumonia, UTIs, wound infections,
anastomotic leaks, intraabdominal abscesses, central line infections
noninfectious causes include pancreatitis, DVT or pulmonary embolism, alcohol withdrawal,
acute gout
Subacute
occurs from one to four weeks after surgery
wound infections or deep space abscesses are the most common causes
C. difficile infections often occur during this time period
infections in long-term central lines are another culprit
Delayed
occur later than one month from surgery
often result from infected mesh or implanted grafts
although very rare now, viral infections (hepatitis B and C, HIV) from blood transfusions
can present in this time period
Management
Evaluation
the workup of the febrile postop patient will be guided by the timing of the fever, the
underlying disease process, the surgery performed, and the relevant exam findings
chest x-ray, urinalysis, blood cultures are not routinely necessary unless clinical suspicion is high,
especially within the first several days of surgery
abdominal surgery patients will often require a CT scan to look for an abscess or leak,
if there is no other obvious cause for the fever
Treatment
all unnecessary medications, lines, and tubes should be removed, if possible
wound infections are managed by opening the wound
most intraabdominal abscesses can be percutaneously drained, although re-exploration is
sometimes necessary
Tylenol is only necessary to treat highly symptomatic fevers
antibiotics should be targeted to the likely infectious cause of the fever
Cardiac Complications
Ischemia and Infarction
Etiology
30% of patients undergoing surgery have coronary artery disease
mortality associated with post-op MI is 30%
myocardial ischemia most commonly results from an imbalance between
myocardial oxygen supply and demand without atherothrombotic plaque rupture (type II myocardial infarction)
stress response of surgery increases myocardial oxygen demand
hypotension, hypoxia, and anemia all decrease myocardial oxygen delivery
Presentation
risk is greatest within the first 48 hours after surgery
classic symptoms of cardiac ischemia are often absent or masked by analgesic/anesthetic/amnestic drugs,
and can also be confused with normal postoperative pain
symptoms/signs include dyspnea, tachycardia or arrhythmia, hypotension
Diagnosis
primarily made by elevation of a biomarker for myocardial necrosis (usually troponin)
cardiac troponins may remain elevated for 5 – 14 days
ischemic EKG changes are present in a minority of patients (35%)
ischemic EKG changes include ST-segment elevation, pathologic Q waves, new left bundle
branch block
Management
continuous EKG monitoring in ICU setting (defibrillator available)
oxygen, morphine for pain and anxiety
nitroglycerin
beta-blockers, unless contraindicated by hypotension or bradycardia
systemic heparin or LMWH unless contraindicated
aspirin, statin
STEMI
fibrinolytic therapy is usually contraindicated because of the recent surgery
emergency angioplasty or stent placement is the primary treatment
Plavix is usually started after stent placement, unless the postoperative bleeding
risk is prohibitive
NSTEMI
coronary angiography in unstable patients or those with recurrent ischemia
Cardiogenic Shock
Etiology
usually results from a post-op MI
other causes include a ruptured papillary muscle, aortic valve insufficiency, mitral
regurgitation
hypotension and respiratory failure are the primary symptoms
Management
mechanical ventilation
consider Swan-Ganz catheter monitoring
vasodilators: IV nitroglycerin or nipride – reduce preload, afterload
atrial fibrillation or atrial flutter occurs most commonly in patients with
electrolyte abnormalities, history of atrial fibrillation, and chronic COPD
combined with fluid overload
Ventricular Tachycardia
usually managed with lidocaine, procainamide, or amiodarone
postoperative risk factors include hypoxemia, hypokalemia, and hypercapnia
Bradyarrhythmias
transient runs require no specific treatment
ustained runs, especially if they cause hypotension, require treatment with atropine or a beta agonist
Heart block
persistent high-grade second-degree or third-degree block will require the insertion
of a permanent pacemaker
CXR will often show pulmonary edema, cardiomegaly (ratio of heart to thoracic cavity diameter > 0.5),
or a pleural effusion
echocardiogram assesses ventricular function, regional wall motion, valve function
Management
diuretics to reduce volume overload and pulmonary congestion
afterload reduction with ACE inhibitors is the primary treatment
preload reduction with nitrates is valuable in patients who can’t tolerate an ACE inhibitor
beta blockers also reduce mortality in patients with ischemic and nonischemic heart failure
inotropes increase cardiac contractility in critically ill patients
Pulmonary Complications
Atelectasis
Etiology
results from alveolar collapse as a result of anesthesia, abdominal incisions, post-op
narcotics
hypoxia can then result from a pulmonary shunt (perfusion of non-ventilated alveoli)
buildup of secretions also occurs, which can lead to secondary infection with bacteria, resulting
in pneumonia
Diagnosis
diminished breath sounds in the lower lung fields
most commonly occurs within 48 hours of the procedure
Management
preoperative preparation is key by optimizing patients with COPD, asthma, CHF
smoking cessation at least one week before surgery may minimize secretions
postoperatively, good pain control allows earlier mobilization, more use of incentive
spirometry, and better pulmonary hygiene (deep breathing and coughing)
Pneumonia
Etiology
most common nosocomial infection
multiple risk factors. including age, immune status, nutrition, smoking, length of hospital
stay, prior antibiotic therapy
aspiration of oropharyngeal and gastric secretions play a major role in hospital-acquired
pneumonia
NG and endotracheal tubes serve as conduits for bacteria to migrate into the lower
respiratory tract
PPIs increase colonization of the stomach with pathogenic bacteria
Prevention
chlorhexidine rinse reduces the rate of ventilator-associated pneumonia in the ICU
proper endotracheal tube care
frequent suctioning and medical management of copious secretions
sucralfate, rather than PPIs, in patients at low risk for stress ulceration
minimize duration of mechanical ventilation
Diagnosis
high fever, thick secretions, ↑WBC, infiltrates on CXR
induced sputum cultures, blind tracheobronchial aspiration, or BAL for culture and
sensitivity
Management
aggressive pulmonary toilet
empiric antibiotics until cultures available
Aspiration Pneumonitis
Etiology
acute lung injury that results from the inhalation of regurgitated acidic gastric contents
chemical pneumonitis
predisposing risk factors include gastric or bowel stasis leading to a full stomach,
depressed level of consciousness (narcotics, CVA) leading to impairment of laryngeal
reflexes, impairment of esophageal sphincters, supine position, emergency intubation
Presentation
often associated with vomiting
urgent intubation and extubation are high-risk times
cough, wheezing, shortness of breath
diffuse, bilateral interstitial infiltrates (fluffy) on CXR
may progress to ARDS or bacterial pneumonia
Prevention
reduce gastric contents (NPO for at least 6 hours before elective surgery, NG tubes in
vomiting patients)
awake fiberoptic intubation is recommended for difficult airways in the OR
cricoid pressure during emergent rapid-sequence intubations
post-op: avoid over-sedation, initiate early mobilization, cautiously feed an obtunded
or debilitated patient, and attempt to minimize the development of delirium
Management
oxygen
clinical deterioration mandates intubation
suctioning to remove particulate matter
empiric antibiotics for most, especially if the stomach is colonized
DVT/PE
Etiology
responsible for 5 – 10% of hospital deaths
results from a triad of intimal injury, stasis of blood flow, and a hypercoagulable state
most PEs originate from DVTs in the iliofemoral veins
fat embolism from long bone fractures and air embolism from central lines or operative
procedures may rarely cause PE
general risk factors include age and poor mobility
inherited hypercoagulable states include protein C and S deficiency, antithrombin III
deficiency
acquired hypercoagulable states include malignancy, inflammatory bowel disease, trauma,
major surgery (especially orthopedic), pregnancy, prior history of VTE
Presentation
> 50% of DVTs are silent, and PE may be the first sign of the disease
pleuritic chest pain, sudden dyspnea, hemoptysis, tachycardia are common symptoms of PE
5 – 10% of PEs are massive and present with shock or death
Diagnosis
CXR
main value is to rule out other pulmonary causes of the patient’s respiratory symptoms
Spiral CT Scan
CT pulmonary angiography
high specificity (92%) and sensitivity (86%) for central PE
drawbacks: requires IV contrast, requires a cooperative patient, may miss emboli in sub-segmental arteries
(20% of PEs), and not always available after hours
inconclusive in 10%
Pulmonary Angiography
gold standard
detects intravascular filling defects
drawbacks: requires contrast, invasive, limited after hours availability
Echocardiography
shows the hemodynamic consequences of PE – right ventricular overload
useful for ruling out cardiac tamponade as a cause of shock
D-Dimer
degradation product of a cross-linked fibrin blood clot
negative D-dimer excludes PE, but a positive test does not rule in the diagnosis
Venous Ultrasound
indirect test for diagnosing PE
positive in 80% of PEs
Management
Prophylaxis
majority of PEs originate from pre-existing deep leg vein clots
intensity of prophylaxis must match the risk of PE
low-dose heparin or LMWH are the agents of choice, but are contraindicated in
thrombocytopenic or overtly bleeding patients
SCDs/TEDs provide good risk reduction in high-risk patients, and may also be
combined with pharmacologic prophylaxis in very high-risk patients
Anticoagulation
prevents clot propagation and allows fibrinolysis to dissolve the clot
initial treatment is with LMWH, UFH, or fondaparinux, followed by Coumadin for
3 - 6 months (INR goal of 2.5)
if anticoagulation is contraindicated, IVC filter protects against recurrent PE
Massive PE
goal is to maintain hemodynamic stability and minimize right ventricular ischemia
thrombolytic therapy dissolves clot rapidly, with rapid improvement in
pulmonary perfusion, gas exchange, and right ventricular function
thrombolytic therapy may be contraindicated in fresh post-op patients
transcatheter embolectomy can be combined with thrombolytic therapy
role of surgical embolectomy is controversial with extremely high mortality
Renal Complications
Urinary Retention
Causes
common post-op problem, especially after hernia operations, perianal procedures, and spinal
anesthetics
may also occur after a low anterior resection or APR as a result of injury to the pelvic hypogastric nerves
most common etiology is pain causing discoordination between the trigone and detrusor
muscles of the bladder
BPH may also be the cause of urinary retention; rarely a urethral stricture
Management
prevention: adequate pain control, minimize IV fluids especially in high-risk patients
in outpatient surgery, high-risk patients should void before discharge
straight catheterization or Foley placement if the patient doesn’t void within 6 – 8 hours
after surgery
Acute Kidney Injury (AKI)
Etiology
associated with significant mortality in post-op patients
commonly classified into 2 types: oliguric (<500 ccs/day) and non-oliguric
causes include prerenal (inflow), renal (parenchymal), or postrenal (outflow)
prerenal: hypovolemia, sepsis
renal: nephrotoxic drugs, IV contrast agents
postrenal: tubular obstruction from myoglobin or cellular debris, ureteral obstruction from
injury, Foley catheter obstruction or kinking (assess with bladder scanning)
Prevention
identify patients with pre-existing renal dysfunction
avoid hypovolemia, hypotension
avoid nephrotoxic drugs if possible
adjust drug doses
avoid IV contrast in at risk patients, or pretreat with a free radical scavenger
(N-acetylcysteine)
Presentation
Anuria
if there is no pre-existing renal disease, the cause is postrenal until proven
otherwise
again, check for a kinked or obstructed Foley
if patient has had major pelvic surgery, then consider ureteral ligation and get an
ultrasound or CT scan to look for hydronephrosis or free intraabdominal fluid
AKI
diagnosed by a rising BUN/Cr and declining urine output
in most surgical patients, it is reasonable to first consider hypovolemia as the
primary cause
best test for distinguishing between prerenal and renal etiologies is the FENA
FENA < 1% = prerenal; FENA > 3% = renal
Management
fluid resuscitation in the hypovolemic patient
if the ultrasound shows hydronephrosis, then surgical repair of an injured ureter is indicated
monitor electrolytes, especially potassium
avoid nephrotoxic drugs
renal dosing of renally excreted drugs
Indications for Dialysis
uremic symptoms (encephalopathy)
BUN > 80 – 90
volume overload
potassium > 5.5
Neurologic Complications
Delirium
Etiology
state of acute confusion common after surgery
multiple risk factors are implicated:
advanced age
alcohol or drug abuse
psychiatric disorders
stroke
pre-existing dementia
post-op narcotics
ICU psychosis
hypoxia
must rule out organic causes such as hypoxia, hypoglycemia, electrolyte disorders, sepsis,
hypovolemia
Presentation
patient becomes acutely confused, agitated or combative
hallucinations are common, but hypoactive delirium also exists
in particular, psychiatric patients may become withdrawn, noncommunicative, or depressed