Peripheral symmetrical gangrene due to severe Plasmodium falciparum malaria: a case report

Case report

An 80-year-old woman presented to our emergency department with high-grade fever associated with chills and rigors for seven days, complicated by a reduced level of consciousness of 24 h. There was no history of seizures, diabetes mellitus, hypertension, old cerebrovascular disease, recent trauma to the limbs, exposure to cold, skin rashes or bleeding from any site.

Her vital signs were stable with an oxygen saturation of 96% on room air. Severe pallor was present. All peripheral pulses were palpable with no radio-radial or radio-femoral delay. She was conscious but drowsy with a Glasgow Coma Score of 12/15, pupils of normal size and normally reacting to light, no neck rigidity and plantar response was bilaterally flexor. She was moving all four limbs. The spleen was just palpable below the left costal margin. On the fourth day of admission, she started developing a bluish-black discoloration of the distal phalanges of the fingers of both hands and over the distal phalanges of the toes of both feet; this continued to progress over the next three days. Eventually, the affected parts became dry, shrunken and dark black with a typical definite line of demarcation (Figure 1). OPEN IN VIEWER

Investigations showed severe anaemia (Hb = 80 g/L), thrombocytopenia (platelet count = 26 × 10⁹/L), leucocytosis (13.7 × 10⁹/L; 80% neutrophils, 18% lymphocytes, 2% monocytes), acute kidney injury (AKI; creatinine = 212.21 µmol/L) and jaundice (total bilirubin/direct bilirubin = 42.7/25.6 µmol/L) but with normal liver enzymes. Arterial blood gas analysis demonstrated compensated metabolic acidosis (pH = 7.35, HCO³= 18.4 mmol/L, pCO₂ = 30 mmHg). Dengue serology was negative, but a quantitative buffy coat showed gametocytes of P. falciparum with a very high level (4+) of parasitaemia. HBsAg, anti HCV antibody and HIV test were negative. Prothrombin time was normal and the activated partial thromboplastin time was slightly elevated. Antinuclear antibody, pANCA and cANCA were within normal range. Cerebrospinal fluid examination was normal and brain imaging was unrevealing. Echocardiography showed no thrombus or valvular vegetations. Colour Doppler of bilateral upper and lower limbs demonstrated normal blood flow in all major arteries with minimal age-related arterial calcification.

Hence the diagnosis of symmetrical peripheral gangrene was confirmed and was attributed to severe P. falciparum malaria.

Treatment with intravenous artesunate 2.4 mg/kg was commenced with supportive care. To prevent the spread of gangrene, unfractionated heparin was administered subcutaneously at 5000 IU subcutaneously twice daily, together with low dose aspirin (75 mg) daily. Consciousness and full orientation resumed; her metabolic derangement likewise AKI, jaundice and acidosis improved. At the two-month follow-up by phone call, she was well and her gangrenous fingers were being self-amputated.

Discussion

Symmetrical peripheral gangrene (SPG) manifests as an acute onset of ischemic damage in two or more extremities without any evidence of obstruction or vasculitis in supplying arteries.¹ It is important to recognise this condition early so that unnecessary surgical intervention can be avoided in these critically ill patients. Efforts should focus on the diagnosis and treatment of the underlying conditions. Any type of septicaemia may cause SPG. Other causes include: asplenia; immunosuppression; diabetes mellitus; renal failure; cold injury to the extremities; myoglobulinaemia; increased sympathetic tone; and the use of vasopressor drugs. SPG may also be a manifestation of multiorgan system failure.

SPG in malaria patients is usually caused by P. falciparum;² very few cases have been reported by vivax³ or by mixed infection.¹ A proposed mechanism for SPG in malaria involves the role of parasitised red cells that initiate intravascular coagulation, leading to the blockage of small capillaries as well as disseminated intravascular coagulation.⁴ However, in our case, the absence of clinical and laboratory evidence of coagulopathy indicate that the interaction between host factors (such as dehydration) and parasitic factors (cytoadherence, rosetting) was likely to have led to SPG.