Unilateral livedo reticularis in COVID-19 patient: Case with fatal outcome.

To the Editor: Recently, Strom et al described a patient whose initial sign of COVID-19 infection was a reticular skin eruption. Other reports have also indicated that livedoid eruptions in COVID-19 patients are associated with more severe disease and that these skin findings may be a clinical clue to an underlying thrombotic state. In contrast, Manalo et al described transient unilateral livedo reticularis (LR) in 2 patients with mild-to-moderate disease and a favorable outcome. The authors speculated that such manifestations might be associated with low-grade disseminated intravascular coagulation as a possible cause. However, the small number of reported cases and lack of coagulation studies make it difficult to draw definitive conclusions at this time.

We report a case of unilateral LR in a patient, with a fatal outcome, presenting their initial and follow-up clinical and laboratory findings.

A previously healthy 59-year-old woman presented with an 8-day history of dry cough, mild dyspnea, and low-grade fever. Physical examination revealed a body temperature of 37.6°C, blood pressure of 110/70 mmHg, pulse rate of 75 beats/min, and an oxygen saturation of 70% on room air. A chest radiograph demonstrated patchy bilateral lung opacities. COVID-19 was confirmed by polymerase chain reaction.

Her skin examination revealed nonblanching, nontender, and red-to-purple reticular discoloration over the lower portion of her right limb, which persisted for 8 hours (Fig 1). The patient denied sun or heat exposure before the onset of the cutaneous lesions. Within 24 hours after admission, her skin lesions gradually faded.

Fig 1

Unilateral LR in a PCR-confirmed COVID-19 patient. LR, Livedo reticularis; PCR, polymerase chain reaction.

On the second day after admission, the oxygen saturation decreased, and the patient was transferred to the intensive care unit for full ventilatory and inotropic support. Despite intensive treatment, the patient died 12 days after admission. The clinical and laboratory parameters are summarized in the Table I.

Table I

Laboratory results of the patient on different days of hospitalization

Variable	HD1∗	HD2∗	HD3	Extreme values HD4 to HD12	Reference range
WBC109/L	14.0	15.8	16.3	15.7	3.5-10
RBC1012/L	5.06	4.42	4.52	2.75	3.50-5.50
Platelet (×109/L)	210	248	318	51	150-400
D-dimer (ng/mL)	0.95	4.05	2.65	6.57	<0.55
PT (seconds)	12.8	12.5	12.2	14.9	10.3-13.0
LDH (U/L)	464	499	538	750	81-234
Ferritin (μg/L)	438	/	/	/	20-290
CRP (mg/dL)	>201	162	155	280	0-10
SpO2 (%)	70	97	92	88	92-100
pH	/	7.34	7.39	7.52	7.35-7.45
pO2 (mmHg)	/	34	62	41	90-100
Lactates (mmol/L)	/	2.9	1.3	1.6	0.5-2.2
Treatment	AZM 500 mgCFX 2 gMPS 120 mgFraxiparin 0.6 mL × 2	AZM 500 mgCFX 2 gMPS 120 mgFraxiparin 0.6 mL × 2NALopinavir 200 mgRitonavir 50 mgCPAP	AZM 500 mgCFX 2 gMPS 120 mgFraxiparin 0.6 mL × 2NACPAP	Meropenem 1500 mgCFX 2 gMPS 120 mgFraxiparin 0.6 mL × 2NAIMV (IPPV)

AZM, Azythromicin; CFX, ceftriaxone; CRP, C-reactive protein; CPAP, continuous positive airway pressure therapy; IMV, invasive mechanical ventilation; IPPV, intermittent positive-pressure ventilation; LDH, lactate dehydrogenase; MPS, methylprednisolone; HD hospital day; NA, noradrenaline; PT, prothrombin time; RBC, red blood cells; SpO2, oxygen saturation; WBC, white blood cells.

Bold formatting indicates results when livedo reticularis persisted.

A variety of cutaneous manifestations in COVID-19 patients have been described. At present, the potential association between morphological subtypes with different COVID-19–associated syndromes and/or outcomes remains unclear. A reticulated vascular pattern indicates partial or intermittent cutaneous blood flow disturbance. LR is characterized by nonfixed, dusky patches forming complete rings, while livedo racemosa, which is representative of a more significant reduction in blood flow, presents with broken rings, which are persistent but rarely necrotic or ulcerative.

Coagulation disorders in COVID-19–infected patients range from thrombocytopenia, elevated D-dimers, and prolonged prothrombin time to episodes of macro- and microvascular thrombosis. Several mechanisms have been proposed to explain these observations, including (i) disseminated intravascular coagulation, (ii) properties of the virus itself, (iii) antiphospholipid syndrome, (iv) activation of complement cascade, (v) endothelial dysfunction, and (vi) drug interactions.

Similarly to that in the case described by Strom et al, the only parameters that were evident in our patient when LR persisted were the low oxygen saturation and increased lactate levels, and coagulopathy occurred a few days later (Table I).

Therefore, close monitoring is required in patients with COVID-19 and LR to ensure the early detection of disease progression, even in initially asymptomatic or mild-to-moderate cases.