Acute upper limb ischemia in a patient with COVID-19: A case report

Abstract

The novel pandemic of coronavirus infection (COVID-19) has been linked with coagulopathy and thromboembolic events, causing limb loss and finally death. The present report describes a case of upper limb ischemia in a patient with COVID-19 infection, who lacked conventional risk factors for acute limb ischemia (ALI).mAn 83 year-old man with intraluminal thrombus and the occlusion of the axillary and brachial arteries, ceasing blood supply to the distal part of the body, was tested positive for the COVID-19 infection. The patient received therapeutic anticoagulation and underwent open thromboembolectomy, which failed to save the patient's life. The link between COVID-19 and thromboembolism remains unknown and needs further studies to be disclosed.

The novel coronavirus infection (COVID-19) can be associated with coagulopathy, which may cause thromboembolic events.¹ The COVID-19 disease is an emerging threat due to the risk of thrombosis in microvascular, venous, and arterial beds. Moreover, thrombosis in patients with the COVID-19 infection may also be more extensive, leading to limb loss and death.² Acute limb ischemia (ALI) is characterized with an abrupt decrease in the arterial perfusion of a limb, threatening its viability and integrity.³ The present report describes a patient developing upper-ALI, without any conventional risk factor for ALI, in a patient with confirmed COVID-19 infection.

CASE REPORT

An 83 year-old Iranian man came to our hospital with the symptoms of sudden pallor, pain, and paresthesia in his left upper limb in the past 10 hrs. He also reported a history of illness, fever, and dyspnea in the past week. He had no previous medical history and was not taking any drug. Examining his vital signs showed low blood pressure (BP = 90/60 mmHg), fever (40°C), tachycardia (heart rate = 110), tachypnea (respiratory rate = 30 cycles per minute), and the peripheral oxygen saturation of 75% while breathing in the ambient air.

On examination, there were bilateral coarse crackles in lungs. His hand and forearm were mottled and cold with motor and sensory loss on physical examination. His radial, ulnar, brachial, and axillary pulses were absent. The Doppler ultrasound of the left arm showed intraluminal thrombus with an occlusion of the axillary and brachial arteries without any blood supply to the distal (Fig. 1 ). Transthoracic echocardiogram (TTE) showed a left ventricular ejection fraction (LVEF) of 55% and no intracardiac thrombus. He was evaluated for the COVID-19 infection by pulmonary computed tomography (PCT) and reverse-transcriptase polymerase chain reaction (RT-PCR). Other routine blood tests were also performed. In chest CT-scan, round-glass opacities were seen in both lungs, suggesting COVID-19 (Fig. 2 ). Laboratory findings presented elevated WBC, LDH, and CPK, and negative troponin I (Table I ).

Fig. 1.

Doppler ultrasound showing intraluminal thrombus.

Fig. 2.

The chest CT-scan of a COVID-19 patient, showing round-glass opacities in both lungs.

Table I.

The laboratory findings of the patient

Parameters	Result	Normal range	Unit
Red blood cell count	5.75	4.70-6.10	10*6/μL
Hemoglobin	17.5	12-16	g/dL
Hematocrit	50.4	41-52	%
White blood cell count	30	4.50-11	10*3/μL
Lymphocyte	89.7	20-50	%
Neutrophil	4.6	35-70	%
Platelet count	237	150-450	10*3/μL
Glucose	103	70-100	mg/dL
Sodium	140	135-145	mmol/L
Potassium	3.9	3.5-5.1	mmol/L
Troponin	0.01	0-0.8	ng/mL
D-dimer	>20	0-0.45	ug/mL
C-reactive protein	26	Less than1.0	mg/dL
Blood urea nitrogen	230	12-45	mg/dL
Creatinine	3.1	05-1.20	mg/dL
Aspartate transaminase	125	17-60	U/L
Alanine aminotransferase	150	0-49	U/L
Alkaline Phosphatase	244	80-200	U/L
CPK	3300	20-200	U/L
Lactate dehydrogenase	700	120-246	U/L

The patient was treated with anticoagulation therapies and underwent open thromboembolectomy, but unfortunately, he died before undergoing the surgical operation.

DISCUSSION

Despite being initially a respiratory infection, several studies have reported other complications for COVID-19, including cardiovascular problems, renal insufficiency, liver failure, and thromboembolic events, whose occurrence has been associated with a poor prognosis.^{4 , 5} The prevalence of thromboembolic events among patients with COVID-19 has not been determined, yet a number of studies have shown a strong association between COVID-19 and thromboembolic events. Most studies focus on hospitalized COVID-19 patients who are likely to have comorbidities, and a few reports have noted that acute thrombotic events can be among initial manifestations.^{2 , 6}

Thromboembolic events mainly manifest as venous thromboembolism (VTE), and peripheral arterial involvement is actually rare.^{7 , 8} Acute limb ischemia is characterized with a sudden decrease in the arterial perfusion of an extremity, which compromises its viability and integrity. According to the definition, in patients with ALI, the duration of symptoms is less than two weeks.³ The etiologies of ALI include embolization from proximal sources, in situ thrombosis due to atherosclerotic plaques, traumatic arterial injuries, and iatrogenic thromboembolism.³ Recently, COVID-19 has also been reported to be a possible cause of this phenomenon.8., 9., 10., 11. The deregulated hyper-inflammatory response may be responsible for the occurrence of arterial thromboembolism in patients with COVID-19;10., 11., 12. however, a combination of mechanisms may be involved in the incidence of arterial thromboembolism in these patients. Our patient demonstrated acute unilateral upper extremity ischemia, which was an unusual event.

The COVID-19 causative agent can predispose individuals to thromboembolic events by deranging the factors involved in blood coagulation regulation.⁷ Evidence suggests that in COVID-19 patients, the pathogenesis of arterial thrombosis is different from that of the classical arterial thrombosis,¹² and COVID-19 patients may present with acute non-atherosclerotic thrombosis.⁸ Further studies are required to divulge the mechanisms involved in the development of thromboembolism in COVID-19 patients.