Acute compartment syndrome is the physiologic consequence of increasing pressures within an enclosed anatomic space; if left untreated, it can subsequently cause irreversible necrosis, nerve injury, and tissue damage. A number of iatrogenic causes have been reported in the literature; however, to the best of our knowledge, there are no prior reports of upper extremity compartment syndrome in orthotopic liver transplant following arterial line placement. Here, we report a 52-year-old male with a history of end-stage liver disease secondary to primary sclerosing cholangitis who presented for orthotopic liver transplant. A radial arterial line with 20-gauge catheter was placed atraumatically without complication. Intraoperatively, the patient developed severe coagulopathy. The cause was likely multifactorial, including dilution of factors from the massive blood loss during the dissection phase, a prolonged anhepatic period, and delayed graft function, resulting in decreased production of coagulation factors. This consumptive process likely subjected minor vascular injury to potential bleeding and caused a slow cumulative bleed into the right forearm, resulting in compartment syndrome. This case exemplifies the complications that can occur from arterial line placement in a liver transplant recipient who develops severe intraoperative coagulopathy. This can arguably be extrapolated to any situation caused by significant dilutional coagulopathy or a consumptive process, such as disseminated intravascular coagulation. As such, when large-volume blood transfusions are anticipated, we recommend that all central venous and arterial accesses be obtained under ultrasonographic guidance and that frequent extremity physical examinations should be performed at a minimum of every hour. Correcting the underlying coagulopathy is imperative to resolve ongoing bleeding, a high index of suspicion is warranted, and immediate diagnosis and therapy are integral to improving patient outcomes.
Key words : Acute compartment syndrome, Coagulopathy, Delayed graft function, End-stage liver disease
Acute compartment syndrome (ACS) is a condition that occurs when increased pressure accumulates in a confined space, causing circulatory compromise and potentially irreversible tissue and nerve injury.1,2 Although typically associated with trauma, there have been numerous case reports of spontaneous compartment syndrome occurring in anticoagulated patients as well as after venipuncture or arterial line placement in anticoagulated patients.3-9 Coagulation derangements are a known consequence of end-stage liver disease and liver transplant.10,11 Despite this, to the best of our knowledge, there are no prior reports of upper extremity compartment syndrome in orthotopic liver transplant following arterial line placement.
A 52-year-old male with a history of end-stage liver disease secondary to primary sclerosing cholangitis, ulcerative colitis status after previous hepaticojejunostomy for stricture of the common bile duct, nonbleeding varices, and portal hypertension with mild intrahepatic shunt presented for orthotopic liver transplant with piggyback technique. His Model for End-Stage Liver Disease score was 17 (bilirubin level of 2.3 mg/dL, international normalized ratio of 1.7, and creatinine level of 0.7 mg/dL). The patient was positioned supine with arms padded and secured on arm boards at less than 90 degrees. After induction of anesthesia, the following venous and arterial accesses were obtained atraumatically, under ultrasonographic guidance without complication: left radial arterial line with 20-gauge catheter, 8.5-gauge rapid infusion catheter in a left antecubital vein, advanced venous access multilumen central venous catheter, and Swan-Ganz catheter in the right internal jugular vein. Of note, there were 2 attempts to place the right arterial line before a third successful attempt. Ultrasonographic guidance was not used, no hematoma was appreciated, and there were no complications noted.
Surgical dissection was complicated by multiple adhesions from prior surgeries and took approximately 2.5 hours. During dissection, the patient experienced episodes of hypotension, and transesophageal echocardiography was utilized to rule out cardiogenic causes. The transesophageal echocardiogram probe was left in place. The patient was anhepatic for approximately 2 hours. Approximately 45 minutes into the anhepatic phase, the right arterial line tracing disappeared, as well as the ability to obtain blood return despite saline flushes.
One hour after going into the anhepatic phase, approximately 200 cm3 of blood was suctioned from the oral cavity; it was also noticed that the urine was now blood tinged. Furthermore, the patient was developing significantly worsening coagulopathy during this time (Table 1). The transesophageal echocardiogram probe was removed. Following hepatic recirculation, continued oropharyngeal bleeding necessitated a gastroenterology consult. Intraoperative esophagogastroduodenoscopy identified bleeding varices, and 2 gastric bands were placed.
Immediately after completion of the procedure and removal of drapes, the patient had noticeable hard edema of the right upper extremity without palpable radial pulse. Forearm compartment pressures were measured above 30 mm Hg. The arterial line was removed, and immediate right forearm anterior compartment and right hand intermetacarpal compartment release were performed. During the fasciotomy, the patient had ongoing worsening coagulopathy, increased blood pressure support requirements, declining venous hemoglobin oxygen saturation, and increased drain output, prompting abdominal washout. No significant intra-abdominal arterial or venous bleeding was identified; however, there was ongoing ooze. Therefore, the surgical team electively packed the abdomen and placed a temporary abdominal closure with the intent of returning to the operating room to close the abdomen after improvement in coagulopathy. Coagulopathy and resuscitation were performed from initiation of surgery until the patient was transferred to the intensive care unit with a total product count as follows: 48 U of packed red blood cells, 33 U of fresh frozen plasma, 16 U of platelets, 17 U of cryoprecipitate, 14 400 cm3 of cell savers, and 7 L of 5% albumin.
On postoperative day 1, international normalized ratio improved to 1.4, and the patient underwent a second abdominal washout and wound closure. The patient had a fascial dehiscence on postoperative day 2, which required an exploratory laparotomy with abdominal washout and subsequent closure. The patient underwent a right forearm complex wound closure, measuring 16 cm, which was performed by plastic surgery on postoperative day 25. The patient was discharged home on postoperative day 28 with full range of motion and functionality of the right forearm and hand.
Acute compartment syndrome is the physiologic consequence of increasing pressures within an enclosed anatomic space. As the pressures within this space continue to rise, perfusion pressure decreases distally. If left untreated, it can subsequently cause irreversible necrosis, nerve injury, and tissue damage.1,2 Although typically caused by trauma, there are also a number of iatrogenic causes, including external compression, extravasation of medications, hyperosmolar or hypertonic solutions, pressurized intravenous infiltration, Bier block, inadvertent injection of hypertonic saline for nerve blocks, faulty blood pressure cuffs, and attempts at cannulating veins and arteries in an anticoagulated patient.12 It can also occur spontaneously in patients taking systemic anticoagulants or thrombolytic agents.12 The pathognomonic presentation of ACS in order of symptom occurrence includes “the 5 P’s”: pain, paresthesias, pallor, pulselessness, and paralysis.1 However, in a patient under general anesthesia, these symptoms are impossible to ascertain. Therefore, a diagnosis is dependent on clinical examinations and measurements of compartment pressures. Generally, a difference between the diastolic blood pressure and the compartment pressure of < 30 mm Hg or a measured compartment pressure of > 30 mm Hg is strongly suggestive of ACS.13
Treatment of ACS involves immediate consultation of surgical services, with the definitive treatment being decompressive fasciotomy (Figure 1). Temporizing measures include removing any external pressure on the extremity; the limb should remain level with the heart to avoid decreases in arterial flow or increases in venous congestion. Optimization of physiologic parameters, including oxygenation, hemoglobin concentration, and blood pressure, should be targeted. In the setting of fluid or medication extravasation, subcutaneous hyaluronidase can increase absorption and dispersion.1,2,13 When available, hyperbaric oxygen therapy has also been utilized as an adjunctive measure.14
Arterial lines are a necessity during liver transplant procedures due to labile blood pressures, frequent blood draws, and, in cases without pulmonary artery catheterization, cardiac output and stroke volume measurements.10,11 In 19 617 radial, 3899 femoral, and 1989 axillary artery catheterizations, Scheer and associates reported an incidence of < 1% for major complications.15 Common iatrogenic complications can include thrombosis, embolism, infection, and air embolism.7 Compartment syndrome is a rare and infrequent consequence of arterial cannulization; however, it can occur in anticoagulated patients.3-9
Although our patient was not on preoperative anticoagulation, he did develop severe intraoperative coagulopathy and treatment was guided by thromboelastography. His coagulopathy likely developed for a number of reasons, including dilutional causes from the massive blood loss during the dissection phase, a prolonged anhepatic period complicated by delayed graft function resulting in decreased production of coagulation factors, and a resultant imbalance between procoagulant and anticoagulant factors. This coagulopathy manifested clinically as serosal oozing in the surgical field and gastrointestinal and urologic bleeding. This consumptive process likely subjected minor vascular injury to potential bleeding. Although there were no signs that indicated injury after right radial arterial line placement, the ensuing coagulopathy likely led to a slow cumulative bleed into a confined space. We believe that bleeding occurred solely from the right radial arterial line, as this was the only line that had multiple attempts.
This case exemplifies complications that can occur from arterial line placement
in a liver transplant recipient who develops severe intraoperative coagulopathy.
This can arguably be extrapolated to any situation caused by significant
dilutional coagulopathy or consumptive process, such as disseminated
intravascular coagulation. As such, when large-volume blood transfusions are
anticipated, we recommend that all central venous and arterial accesses be
obtained under ultrasonographic guidance to ensure unnecessary vascular injury.
Furthermore, even if access is obtained without complications, frequent
extremity physical examinations should be performed at a minimum of every hour.
If compartment syndrome occurs, decompressive fasciotomy is the definitive
treatment. Correcting the underlying coagulopathy is imperative to improve the
ongoing bleeding. However, in this case presentation, despite providing maximal
blood products, the coagulopathy did not resolve.
In such situations, a high index of suspicion is warranted, and immediate diagnosis and therapy are integral to improving patient outcomes.
Volume : 19
Issue : 9
Pages : 986 - 989
DOI : 10.6002/ect.2017.0339
From the Department of Anesthesiology, Mayo Clinic, Jacksonville, Florida, USA
Acknowledgements: The authors have no sources of funding for this study and have no conflicts of interest to declare.
Corresponding author: Stephen Aniskevich, Department of Anesthesiology, Mayo Clinic Jacksonville, 4500 San Pablo Rd, Jacksonville, FL 32224, USA
Phone: +1 904 953 2000
Table 1. Coagulation Trends During the Intraoperative Course of Orthotopic Liver Transplant
Figure 1. Right Forearm Wound on Postoperative Day 10 Showing Right Forearm Anterior Compartment and Right Hand Intermetacarpal Compartment Release Secondary to Spontaneous Compartment Syndrome