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Net Letter
ARTICLE IN PRESS
doi:
10.25259/IJDVL_1273_20

Neonatal purpura fulminans caused by Acinetobacter baumannii: Unusual occurrence of three coincident cases

Department of Dermatology and STD, University College of Medical Sciences and GTB Hospital, University of Delhi, Delhi, India
Corresponding author: Dr. (Prof.) Archana Singal, Department of Dermatology and STD, University College of Medical Sciences and GTB Hospital, University of Delhi, Delhi, India. archanasingal@hotmail.com
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How to cite this article: Singal A, Dhir B. Neonatal purpura fulminans caused by Acinetobacter baumannii: Unusual occurrence of three coincident cases. Indian J Dermatol Venereol Leprol, doi: 10.25259/IJDVL_1273_20

Sir,

Neonatal purpura fulminans is a potentially lethal disorder, characterized by disseminated intravascular coagulation triggering dermal thrombosis, which leads to progressive hemorrhagic necrosis of the skin in the newborn.1 Neonatal purpura fulminans may be congenital, caused by protein C and protein S deficiency or acquired, resulting from septicemia caused by Group B Streptococcus and Gram-negative organisms.

Three full-term neonates, born within 12 hours in a tertiary care facility, developed multiple hemorrhagic blisters and ecchymosis over acral areas and thighs within 12–36 hours of birth. All three were born healthy with a normal Apgar score. There was no family history of coagulation disorders.The third neonate was born to consanguineous parents.

In the first neonate, the acral bullous lesions turned necrotic and hemorrhagic within a day with evident gangrenous changes by day three. These lesions rapidly progressed to involve thighs and toes [Figure 1] and were associated with systemic features of neonatal sepsis like lethargy, fever, tachycardia and poor feeding. By day five, he worsened and developed acute respiratory distress. The other two neonates had a relatively less fulminant progression, with acral hemorrhagic bullae turning necrotic [Figures 2 and 3] within 24 hours followed by the development of gangrene. No new lesions appeared after 72 hours of disease onset. Clinical features and clustering of cases led to the diagnosis of neonatal purpura fulminans secondary to sepsis The differential diagnoses of meningococcemia/septic vasculitis and thrombotic thrombocytopenic purpura were also considered. Relevant investigations were undertaken summarized in Table 1. All neonates were managed in the neonatal intensive care unit. In addition to the general care and intravenous fluids (as per clinical assessment), all the neonates were administered parenteral antibiotics and fresh frozen plasma. While the first neonate succumbed to septicemia by day seven, the other two neonates showed progressive improvement with healing of skin lesions. The course of their stay in the hospital and the treatment offered have been tabulated [Table 2]. Multiple swabs from the concerned health care workers, instruments and surfaces of the labor room failed to reveal any pathogens. Furthermore, detailed evaluation (history and clinical examination) of the mothers failed to reveal any focus of infection. The labor room was disinfected as per hospital infection control committee guidelines and no further cases were reported.

Figure 1:: First neonate with acral lesions at day two
Figure 2:: Second neonate with acral blisters at day two
Figure 3:: Third neonate with acral blisters and purpura at day five
Table 1:: Summary of investigations
Investigations Neonate 1 Neonate 2 Neonate 3
TLC(109/L) 26 15.8 32.1
Platelet count (109/L) 440 354 420
FDP (mg/L) 5-20 5-20 5-20
d-dimer (ng/L) normal range (<250 ng/mL) 1943 783→481 2249→1715
PT/ APTT/INR§(s) 12/33/1.0 12/26/1.1 11/29/1.0
Protein C and S levels WNL WNL WNL
CRP (mg/L) Range >0.6 <0.6 <0.6
Blood culture and sensitivity Acinetobacterbaumannii; sensitive to meropenem, vancomycin, piperacillin Acinetobacter baumannii; sensitive to ampicillin, amoxycillin/clavulanic acid, gentamycin, vancomycin, colistin Acinetobacter baumannii; sensitive to meropenem, vancomycin, teicoplanin
Pus culture and sensitivity Acinetobacter baumannii; sensitive to cefepime, meropenem, vancomycin, trimethoprim/sulfamethoxazole No growth Acinetobacter baumannii; sensitive to cefepime, meropenem, vancomycin, ciprofloxacin
Necrosis progression +++ ++ ++
New lesions after a week +++ No lesions No lesions
TLC: Total leukocyte count, WNL: Within normal limits, N.A: Not available, FDP: Fibrin degradation product, CRP: C-reactive protein, §PT/APTT: Prothrombin time/activated prothrombin time. INR-International Normalised Ratio
Table 2:: Course during hospital stay and treatment
Neonate 1 Neonate 2 Neonate 3
Inj. meropenem + Inj. vancomycin

three units FFP over three days

Worsened by day five
Intubated and put on mechanical ventilation

Further deterioration and patient expired on day seven
Inj. amoxicillin + clavulanic acid and inj. amikacin

one unit FFP on day two

Clinical improvement on day four

Significant improvement by day seven
Inj. meropenem + Inj. vancomycin

three units FFP on day two

TLC reduced to 13×109/L (from 32)

Clinical improvement by day four/five
As per weight, FFP: Fresh frozen plasma; TLC_Total Leukocyte Count

Neonatal purpura fulminans generally presents 2-12 hours after birth as ecchymotic lesions over perineum, thighs and abdomen that turn rapidly into purpuric papules, bullae and hemorrhagic necrosis, the latter being the hallmark of the condition.2 Acquired neonatal purpura fulminans is mainly due to severe infections with Streptococcus, Escherichia coli, varicella, meningococcus and pneumococcus. Recently, Klebsiella oxytoca and Citrobacter have been reported to cause neonatal purpura fulminans.3 We report here Acinetobacter baumannii, a Gram-negative coccobacillus, as the causative organism for neonatal purpura fulminans. It accounts for 2-10% of Gram-negative hospital infections. It has been labeled by Infectious Diseases Society of America as one of the six most important multidrug-resistant microorganisms in hospitals worldwide.4 Even though Acinetobacter infections are more frequent in immunocompromised individuals, no such immunosuppressed state was noted in any of the neonates.

During the acute phase of neonatal purpura fulminans, laboratory findings are of disseminated intravascular coagulation including thrombocytopenia, increased fibrin degradation products, d-dimer, prolonged prothrombin time and activated partial thromboplastin time. Proteins C and S levels may be reduced in both acquired and inherited cases.

In such a scenario, testing of parents is recommended. Confirmatory testing at three and six months of age is vital in neonates.

In the management of neonatal purpura fulminans, the goal is to maintain platelet count above 50,000/mm3 and fibrinogen levels less than 1 g/L. Early empiric broad-spectrum antibiotic therapy covering the reported pathogens is paramount. It may be modified based on the sensitivity of isolates. Fresh frozen plasma (at a dose of 10–20 mL/kg every 6–12 hours) has a critical role in replacing the depleted levels of proteins C and S and preventing the progression of the disease.5 With strict aseptic precautions followed in obstetric and neonatal care, neonatal purpura fulminans is becoming a rare entity. However, a high index of suspicion for neonatal purpura fulminans should be kept for newborns presenting with hemorrhagic cutaneous necrosis.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

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  2. , , , . Neonatal purpura fulminans due to methicillin resistant Staphylococcus aureus. Pediatr Dermatol. 2013;30:266-7.
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  3. , , . Sepsis-associated purpura fulminans due to Klebsiella oxytoca. Dtsch Arztebl Int. 2018;115:784.
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  4. , , . Acinetobacter baumannii: Evolution of a global pathogen. Pathog Dis. 2014;71:292-301.
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  5. , . Management of septic skin necroses. Eur J Pediatr Surg. 2013;23:349-58.
    [CrossRef] [Google Scholar]

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