Information regarding factors predictive of morbidity and mortality in patients with COVID-19 has surfaced such as laboratory findings indicative of coagulopathy or systemic inflammation. These indicators include thrombocytopenia, prolonged prothrombin time or partial thromboplastin time, elevated D-dimer, and increased ferritin1-6. Here, we present a case of acute compartment syndrome (ACS) of the left hand in a COVID-19-positive patient with associated pneumonia, acute kidney injury, coagulopathy, and multiple cocomorbidities.
At the time of this submission, the patient remained intubated and partially sedated. His family provided informed consent for submission of his clinical presentation and treatment.
A 58-year-old man with hypertension, type II diabetes mellitus, congestive heart failure, and chronic kidney disease presented to the emergency department (ED) in early April 2020 with acute onset dyspnea, oxygen desaturation, hypotension, and hypothermia. He subsequently tested positive for COVID-19 and was diagnosed with acute respiratory distress syndrome (ARDS). He was intubated in the ED and admitted to the intensive care unit (ICU). On hospital day (HD) 2, he developed an acute kidney injury and was started on dialysis. His coagulation panel at this time revealed thrombocytopenia with a platelet count ranging from 35 to 83 × 103/μL (normal limit [nl]: 160-420 × 103/μL), an elevated activated partial thromboplastin time of 40.1 seconds (nl: 21.0-32.0 seconds), an elevated fibrinogen of 852 mg/dL (nl: 180-460 mg/dL), and an elevated D-dimer of 1.56 mg/L (nl: 0.0-0.59 mg/L). He was started on 25,000 units of intravenous (IV) heparin, quaque die.
An arterial line was placed in the patient's left upper extremity to monitor his blood gases and severe hypotension. He required 16 mg of IV norepinephrine and 40 units (2 mL) of IV vasopressin from admission. He was successfully weaned off vasopressors by HD 2. On HD 3, he was found to have extravasation with an associated hematoma at the arterial line site. It was not patent and was removed. Over the course of the next 26 hours, the development and worsening of diffuse swelling to this extremity prompted a consult to the orthopaedic service with a concern for ACS. The clinical course obtained from the treatment team revealed no inciting trauma, infectious etiology, or medication reaction. On the initial physical examination per orthopaedic surgery, the patient was intubated and partially sedated with propofol. He was minimally responsive to auditory stimuli and demonstrated spontaneous motion of the right upper extremity but not of the left. His left hand was positioned in an intrinsic minus position. He had significant edema of the distal forearm and hand with multiple large, tense serous bullae most prominent on the dorsal aspect of his left hand. In addition, a large hematoma was present on the volar aspect of the left forearm (Fig. 1). The left hand compartments were firm. The left forearm compartments were compressible proximally; however, increased pressure was noted in the distal volar forearm. Radial and ulnar pulses were palpable, and there was brisk capillary refill to all fingers. There was no marked temperature change of the left upper extremity. Noteworthy laboratory results at the time included a platelet count of 52 × 103/μL (nl: 150-420 × 103/μL), ferritin of 665.0 ng/mL (nl: 23-338 ng/mL), albumin of 1.7 g/dL (nl: 3.4-5.0 g/dL), and total protein of 6.2 g/dL (nl: 6.3-8.2 g/dL).
Clinical photographs of patient's left hand. Note intrinsic minus positioning with a large hematoma over the volar forearm (Fig. 1-A) and diffuse bullae dorsally (Fig. 1-B).
The senior author (F.H.S.), the attending on call, performed a secondary examination and found that the left upper extremity edema had worsened over 30 minutes. The clinical diagnosis of ACS of the hand was made. Because of operational changes due to the ongoing pandemic, it was anticipated that preparing an operating room (OR) for compartment release would have caused a significant delay in treatment that likely would have threatened the long-term functionality or viability of this patient's extremity. Given the urgent nature of the diagnosis, a bedside 10-compartment decompression of the left hand with volar forearm compartment release and carpal tunnel release was performed.
The procedure was performed with a prepackaged sterile laceration tray, an additional 11 blade knife, Metzenbaum scissors, ChloraPrep, and povidone-iodine. The 2 operating surgeons donned appropriate personal protective equipment per the standards of the ICU including N95 masks, an outer mask, eye protection, sterile gloves, and gowns. The operative extremity was prepped with chlorhexidine and draped, creating a sterile field. One-centimeter longitudinal incisions centered over the second and fourth metacarpal; thenar and hypothenar compartments were used to access all 10 compartments for decompression (Fig. 2). After the hand compartment release, which yielded copious fluid, the patient had significant improvement in his passive range of motion and clinical appearance of his left hand (Fig. 3). A volar approach was then performed to release the carpal tunnel and the volar compartment of the forearm yielding significant hematoma. Loose approximation of the incisions was performed without tying knots for planned advancement of skin edges as the edema improved. The hand was then cleaned and irrigated, dressed with xeroform, sterile gauze, and wrapped with a Kerlix without tension.
Dorsal (Fig. 3-A) and volar (Fig. 3-B) clinical photographs of patient's left-hand demonstrating improved clinical appearance after compartment release.
Postprocedure, the patient had significant improvement in swelling and passive range of motion. Radial and ulnar pulses remained intact. Urine myoglobin remained within normal limits at 3 ng/mL (nl: 0-13 ng/mL). In the following days, the edema improved significantly, and the compartments remained soft and compressible. Radiographs of the extremity showed no acute fracture and no abnormalities were found on venous and arterial ultrasounds.
The classical signs of ACS include pain, pallor, poikilothermia, paresthesia, pulselessness, and paralysis7,8. However, these signs are much more likely to go unnoticed in unconscious or sedated patients who cannot volunteer such symptoms to the care team9. An intracompartmental pressure greater than 30 mm Hg may result in tissue injury. When intracompartmental pressure increases to within 10 to 30 mm Hg of the patient's diastolic blood pressure, this indicates inadequate perfusion and relative ischemia of the involved extremity10. Although the measurement of intracompartmental pressures may have helped in decision-making, clinical diagnosis of ACS was made and further testing would have delayed the procedure. Therefore, pressures were not measured.
The coagulopathy associated with COVID-19 has prompted recommendations from the American Society of Hematology and the International Society of Thrombosis and Haemostasis for prophylactic treatment of abnormal clotting in these patients. These societies likened the abnormalities to coagulation profiles seen in disseminated intravascular coagulopathy1,3. Consistent with these observations, our patient had an elevated fibrinogen and D-dimer level. Zhang et al.2 proposed another pathway for coagulopathy in a case series of 3 COVID-19-positive patients in Wuhan, China, who presented with combinations of cerebral infarcts and evidence of ischemia in limbs. In all of these patients, serologic tests were positive for anticardiolipin immunoglobulin (Ig) A antibodies and anti-β2-glycoprotein I IgA/IgG antibodies. Although these antibodies tend to be the hallmark of antiphospholipid syndrome, they can be transiently present in patients with critical illness and may lead to thrombotic events that may be difficult to distinguish from other multifocal thrombosis presentations11.
Although the etiology of this patient's compartment syndrome is unclear, several factors could have contributed. The patient was placed in precautionary 2-point restraints of the arms while intubated prompting concern for added constriction at the site of the restraints. In addition, he had an arterial line in his left arm, which has been associated with the development of ACS12. The arterial line may have damaged the vessel; in the setting of coagulopathy, this may have led to extravasation of blood into the volar compartment12. The patient also had low serum protein levels. Decreased plasma oncotic pressure could have resulted in increased capillary leak, thereby contributing to increased compartment pressures. Finally, the patient's blood pressure was volatile, ranging from approximately 110 to 180 mm Hg systolic and approximately 60 to 90 mm Hg diastolic. It is possible that these wide fluctuations in blood pressure compounded with the other factors contributed to repeated cycles of ischemia and reperfusion within the patient's affected extremity leading to ACS.
In our hospital system, similar to many others, cases have been limited to only urgent and emergent cases as directed by the Louisiana Department of Health13,14. In light of these measures, the available operative staff has been significantly decreased and a delay was anticipated in preparing an OR with the appropriate staff and instruments for the procedure. Furthermore, in an effort to preserve personal protective equipment and reduce the risk of SARS-CoV-2 exposure for other patients, staff, and doctors, it was deemed the safest course of action was to pursue a bedside fasciotomy to avoid transporting the patient to the OR through high-traffic areas of the hospital. A 2012 study performed at the University of Toledo reviewed the outcomes of 34 patients who had undergone bedside fasciotomies of the upper and lower extremities concluding that in extraordinary circumstances; bedside fasciotomies can be an effective and safe choice for treating ACS15.
This case report adds to the relatively scarce body of literature regarding orthopaedic complications related to the COVID-19 pandemic. This case highlights the importance of effective interdisciplinary communication and teamwork and heightened vigilance in the ICU with sedated and mechanically ventilated patients. If ACS is diagnosed, immediate decompression is indicated and may require bedside treatment if logistical or public health challenges preclude rapid transport to an OR.
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