What are
the complications of laparoscopic surgery?
The complications associated with laparoscopic
surgery are:
· Overall mortality rate 0.1–1.0 per 1,000 cases
· Postoperative nausea and vomiting (40–75% of
patients)
· Shoulder pain
· Bowel perforation 0.06–0.4% with a mortality
rate of 5%
· Bladder/ureter injuries 2 per 10,000 cases
· Vascular injuries
· Gynecologic injuries 0.64%
· Gastrointestinal, urologic injuries 0.03–0.06%
· Significant hemorrhage in 2–9 per 1,000 cases,
often delayed
· Nerve injuries from improper positioning:
peroneal/ femoral neuropathies, meralgia paresthetica
· Subcutaneous emphysema from extraperitoneal
insufflation
· Pneumothorax, pneumomediastinum
· Venous gas embolism
· Volume overload from excessive fluid
administration, decreased insensible losses and decreased urine production
↑ICP
Deep vein thrombosis
·
Increased
risk of regurgitation from ↑IAP along with the Trendelenburg position
Subcutaneous emphysema (SQE) is a known
complica-tion of laparoscopic surgery. It may occur as a result of acci-dental
extraperitoneal insufflation or may be considered unavoidable in certain
laparoscopic procedures that require intentional extraperitoneal insufflation,
such as inguinal her-nia repair. SQE is identified by the development of
crepitus over the abdominal wall, excessive changes in airway pres-sures, or by
increasing ETCO2 concentrations over time.
When SQE does occur, the area for diffusion of
CO2 increases and this may lead to hypercarbia and respiratory
acidosis.
In most cases, no specific intervention is
necessary other than the discontinuation of N2O, if it is being
used. SQE resolves soon after deflation of the abdomen. However, as there
exists a “continuum of fascial planes,” SQE could potentially extend from the
abdomen to the thorax and neck, resulting in pneumothorax or pneumomediastinum.
If SQE is suspected, a chest radiograph should be obtained for confirmation.
Although the treatment may not change, having the diagnosis is important for
future management of untoward events, for example, cardiovascular collapse. The
presence of SQE does not necessarily contraindicate extubation, yet it should
be emphasized that it may predis-pose to laryngeal swelling, difficult
spontaneous respira-tions, and difficult reintubation. It is recommended that
controlled mechanical ventilation be maintained until hypercarbia is corrected
to avoid the increase in work of breathing, especially in compromised patients.
Pneumothorax is a rare yet potentially
life-threatening complication of laparoscopic surgery with increasing
inci-dence over recent years as a result of an increasing number of procedures
involving dissections at the esophageal junc-tion (e.g., Nissen
fundoplication). Pneumothorax occurs when gas traverses into the thorax, either
through a tear in the visceral peritoneum, disruption of the parietal pleura
during dissection around the esophagus, or through a con-genital defect in the
diaphragm. Pneumothorax may be asymptomatic or may be associated with
hypotension or cardiac arrest resulting from the impairment of cardiac filling
and limitation of lung excursion. When CO2 pneumothorax occurs
without pulmonary trauma, spontaneous resolution may occur within 30–60 minutes
after abdominal defla-tion. If the pneumothorax is large or symptomatic,
thora-cocentesis should be performed without delay. N2O, if used,
should be discontinued and the IAP should be reduced. Ventilation should be
adjusted to correct hypox-emia, applying positive end-expiratory pressure
(PEEP) if necessary. If the pneumothorax results from trauma to the lung
itself, PEEP should be avoided.
A rare, yet potentially fatal complication of
laparoscopy is that of venous gas embolism (VGE). The estimated incidence is
0.002–0.08%. When it occurs, it brings with it the potential for significant
hemodynamic compromise. VGE develops most commonly during the first few minutes
after the devel-opment of the pneumoperitoneum. This occurs more frequently in
patients who have had prior abdominal surgery.
Gas bubbles enter the venous system via vessel
tears in the abdominal wall or peritoneum and enter the heart and pulmonary
circulation. When clinically significant, the right ventricular outflow tract
is obstructed, producing a constellation of signs and symptoms: a “mill-wheel
murmur,” sudden hypotension, decrease in cardiac output, tachycardia or other
dysrhythmias, pulmonary edema, hypoxemia, increased airway pressures, and
jugular venous distention and facial plethora/cyanosis from inflow obstruction
to the right heart. The ETCO2 response is biphasic. Firstly, an
initial increase in ETCO2 occurs secondary to the pulmonary
excretion of CO2. Then, a decrease in ETCO2 occurs
because of a decrease in cardiac output and an increase in physiologic dead
space. When this occurs, the N2O should be discontinued (if being
used), and the patient should be placed in the left lateral decubitus position,
with steep head-down tilt to prevent entry of the bubbles into the pulmonary
arterial circulation. The patient should be hyperventilated to eliminate CO2.
If a central venous catheter is in place, it should be aspirated in an attempt
to remove gas emboli. Hyperbaric oxygen, cardiopulmonary bypass, and external
cardiac massage are all measures that may be necessary in extreme situations.
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