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Year : 2017  |  Volume : 10  |  Issue : 1  |  Page : 238-240
Symmetric peripheral gangrene: A rare complication of Plasmodium falciparum malaria

Department of Medicine, Government Medical College and Hospital, Nagpur, Maharashtra, India

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Date of Web Publication5-May-2017


Sudden onset of symmetric peripheral gangrene (SPG) is a relatively uncommon clinical entity manifested by distal ischemic damage at two or more sites in the absence of large vessel obstruction. Here, we report a case of a 27-year-old female with complicated falciparum malaria with SPG involving the toes of both the lower limbs.

Keywords: Malaria, Plasmodium falciparum, symmetric peripheral gangrene (SPG)

How to cite this article:
Kumbhalkar S, Aher A, Wanjari S. Symmetric peripheral gangrene: A rare complication of Plasmodium falciparum malaria. Ann Trop Med Public Health 2017;10:238-40

How to cite this URL:
Kumbhalkar S, Aher A, Wanjari S. Symmetric peripheral gangrene: A rare complication of Plasmodium falciparum malaria. Ann Trop Med Public Health [serial online] 2017 [cited 2020 Sep 21];10:238-40. Available from:

   Introduction Top

Symmetric peripheral gangrene (SPG) was initially described in 1981 by Hutchinson.[1] It is defined as a symmetrical distal ischemic damage at two or more sites in the absence of large vessel obstruction. This condition has been described in association with a multitude of medical conditions, the common ones among them being infections, low output states such as myocardial infarction, shock, congestive cardiac failure, or the use of vasopressors such as dopamine. SPG has been rarely reported in falciparum malaria and only a few cases have been reported in the literature till now. We report this case as a rare manifestation of complicated falciparum malaria.

   Case Report Top

A 27-year-old female patient was admitted to the Medicine Ward of Government Medical College (GMC), Nagpur, Maharashtra, India with chief complaints of high-grade fever with chills and rigors since 4 days and had altered sensorium 1 day before the admission. On examination the patient was drowsy, her Glasgow Coma Scale (GCS) was 8/15, she had pallor, and icterus was present. Her pulse was 80 bpm, regular, and all the peripheral pulses were well felt; her blood pressure (BP) was 110/80 mmHg and random blood sugar was 108 mg%. Her cardiovascular, respiratory, and abdominal examinations revealed no clinical abnormality. Peripheral smear showed malarial pigment and gametocytes of falciparum malaria. Histidine-rich protein 2 (HRP 2) was positive. Her hemoglobin was 4.8 g%, total leukocyte count (TLC) 8,000/m3, platelets were 84,000/m 3, and serum bilirubin was 2.1 mg%. The remaining parameters of liver function test (LFT) and kidney function test (KFT) were normal. Her blood culture and urine culture showed no growth. Diagnosis of cerebral malaria was kept and the patient was started on Artesunate injection and Clindamycin injection. The patient regained consciousness on the second day, was responding to oral commands, and no neurological deficit was noted. On the third day of admission, she complained of burning sensation in the toes and dorsum of both lower limbs. On the fourth day of admission, she developed blackish discoloration of the toes of both her lower limbs. On local examination, the toes of both her lower limbs had blackish discoloration, were cold, dry, shrunken, and had a definite line of demarcation [Figure 1] and [Figure 2]. No local ulceration was seen. There was no past history of rash, oral ulceration, joint pain, claudication, Raynaud phenomenon, or any addiction. There was no history of chest pain, palpitation, exertional dyspnea, or neurological weakness and no past history of systemic hypertension and diabetes mellitus. Arterial and venous Doppler of both the lower limbs and coagulation profile revealed no abnormality. However, evidence of disseminated intravascular coagulation was seen in skin biopsies obtained from the junction of the gangrenous skin and the normal skin in the form of fibrin deposits almost occluding the lumen of the dermal vessels, along with perivascular infiltration. Antinuclear antibody (ANA), dsDNA, sickling test, carotid Doppler, 2-D echocardiography, electrocardiogram, computed tomography of the head, rheumatoid factor test, Venereal Disease Research Laboratory (VDRL) test, and Coombs test (direct and indirect) revealed no abnormality. Final diagnosis of complicated malarial fever with falciparum malaria-associated SPG was kept. The patient was then started on aspirin tablet and pentoxifylline tablet, along with antimalarial agents. The patient had symptomatic relief but blackish discoloration of the toes was persistent at the time of her discharge. At follow-up after 1 month, the patient had complete resolution of the symptoms.
Figure 1: Gangrenous changes on the dorsum of both the lower limbs

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Figure 2: Gangrenous changes over the toes

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   Discussion Top

SPG has been associated with a variety of medical conditions including blood stream infections, sepsis, low cardiac output states, use of vasopressors, ergot poisoning but its association with falciparum malaria infection is rare. In our patient, all the possible causes of symmetrical peripheral gangrene other than falciparum malaria were ruled out and the patient was hemodynamically stable throughout the course of the disease. And as our patient improved after receiving antimalarial therapy, it clearly indicates that Plasmodium falciparum infection was the underlying cause of SPG in her case. The underlying mechanisms can be the following:

  1. Microcirculation is compromised in falciparum malaria infection as a result of adhesion of the infected erythrocytes to the vascular endothelium (cytoadherence) and due to rosetting of the uninfected erythrocyte around the parasitized red blood cells.[2] Several vascular receptors for the adhesive surface protein of infected erythrocytes have been identified such as cluster of differentiation 36 (CD 36), intercellular adhesion molecule 1 (ICAM-1), thrombospondin (TSP), vascular cell adhesion molecule-1 (VCAM-1), endothelial leukocyte adhesion molecule-1 (ELAM-1), and HRP.[3]
  2. Disseminated intravascular coagulation: Functionally active but controlled coagulation state exists in falciparum malaria.[4] Heavy parasitemia may alter the lipid distribution across the cell membrane of parasitized erythrocytes resulting in the activation of intrinsic coagulation cascade and complement system. The initial procoagulant stage of disseminated intravascular coagulation is followed by the stage of consumptive coagulopathy with depletion of the platelets, fibrinogen, and other coagulation proteins with widespread bleeding manifestations. Though biochemical evidence of disseminated intravascular coagulation was lacking in our patient, demonstration of the intravascular fibrin deposits in dermal vessels of the affected regions confirm disseminated intravascular coagulation. However, disseminated intravascular coagulation in this case may have been arrested in the initial procoagulant stage by effective management of falciparum infection with artesunate and clindamycin before consumptive coagulopathy could set in. Thus, it may be concluded that this patient had SPG as a complication of Plasmodium falciparum malaria and had complete recovery with effective antimalarial combination therapy.

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Conflicts of interest

There are no conflicts of interest.

   References Top

Molos MA, Hall JC. Symmetrical peripheral gangrene and disseminated intravascular coagulation. Arch Dermatol 1985;121:1057-61.  Back to cited text no. 1
Bradley D, Newbold Cl, Warrel DA. Malaria. In the Oxford Textbook of Medicine. Weatherall DJ, Ledinghan JGG and Warrel DA (Eds). Oxford University press, Third Edition. 1996;1:835-63.  Back to cited text no. 2
White NJ. Malaria. In the Mason's Tropical Disease. In: Cook G, editor. Hospital for Tropical Disease, University of London. 20th ed. 1996. p. 1087-164.  Back to cited text no. 3
Clemens R, Pramoolsinsap C, Lorenz R, Pukrittayakamee S, Bock HL, White NJ. Activation of coagulation cascade in severe falciparum malaria through the intrinsic pathway. Br J Haematol 1984;87:100-5.  Back to cited text no. 4

Correspondence Address:
Dr. Sunita Kumbhalkar
Department of Medicine, Government Medical College and Hospital, Nagpur, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1755-6783.205548

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