Key Clinical Massage
Immunocompromised patients are subjected to life-threatening unusual
infections, early diagnosis, and thorough investigations should be done
to identify the underlying cause and offending organism concomitant with
empiric treatment.
BackgroundAspergillosis referred to a spectrum of diseases caused by the
aspergillus fungi species 1, aspergillus causes a wide
array of diseases ranging from allergic conditions to invasive
life-threatening diseases 2 as in patients with acute
leukemia and recipients of allogeneic hematopoietic stem-cell
transplants 3, Invasive pulmonary disease is the most
common invasive disease as candida get inhaled 4.
Meanwhile, cutaneous aspergillosis tends to occur less frequently; the
infection can be a primary infection at the site of skin trauma,
surgery, burn, occlusive dressing or at the site of intravenous access5,6, Secondary infection as a result of blood
dissemination or through the direct extension of infection from
contaminated nearby structures as sinuses 7,8.
Mortality and morbidity due to invasive aspergillosis are increasing due
to the increasing number of patients with malignancies being treated
with immunosuppressive therapy along with the survival of aggressive
bacterial infections due to antibacterial therapy4,Virulence and extent of the disease determined by
host factors and microbial factors, with neutrophils play an essential
role in host defense against filamentous fungi hence patients with
neutropenia rendered more vulnerable to invasive disease caused byAspergillus 1.
The most prevalent species causing invasive aspergillosis in
immunocompromised patients is Aspergillus fumigatus6, followed by A. flavus then A. nigeras showed in a multicentric study in 218 patients with invasive
aspergillosis 4.
Lesions of cutaneous aspergillosis can present as erythematous lesions,
macules, papules, nodules, plaques, pustules, or lesions with purulent
discharge, type of the lesion depends on the source of infection as
disseminated blood infections are different for others caused by an
occlusive dressing which tends to present as hemorrhagic bulla6.
Diagnosis of cutaneous aspergillus requires identification of the
organism either directly by Potassium Hydroxide (KOH) preparation or
through skin biopsy and identification of the aspergillus through
culture and histopathologic examination 4,6,
Galactomannan antigen detection implemented in the diagnosis of invasive
aspergillosis in areas where there is a high chance of specimen
contamination as blood and bronchoalveolar lavage (BAL) is expected9.
Case PresentationA 53-year-old female patient who was diagnosed with frontotemporal
anaplastic astrocytoma (WHO grade IV); the patient operated and started
on post-operative radiotherapy and temozolomide; later admitted to the
hospital multiple times for side effects related to her disease and
chemoradiotherapy.
Patient suffered from saddle pulmonary embolism, received a full dose of
heparin and respiratory support until her condition stabilized, later
patient presented to the emergency department (ED) with heparin-induced
thrombocytopenia; platelets 3000 (reference range 150000 – 400000/uL)
and leukopenia WBC (White blood cells 1, Absolute Neutrophils count
0.4), heparin withheld, the patient admitted and started on aztreonam 2g
Q8hours and vancomycin 20mg/kg Q8hours then shifted to cefepime 2 grams
Q8hours as culture growth showed Pseudomonas for treatment of
axillary cellulitis until resolved, temozolomide stopped.
Two days later, the patient developed a lesion near the ala of the left
nostril and swelling of the left side of the face, ENT team consulted,
the lesion was erythematous, hyperemic, and tender, nasal examination
was limited due to tenderness elicited by exam maneuvers, clear
discharge noted from the left nostril.
Sinus computed tomography (CT) scan with contrast done and showed clear
paranasal sinuses, partial opacification of left maxillary and ethmoidal
sinuses with left facial edema with no clear evidence of fungal
sinusitis (Figure 1).
Patient started on empiric therapy set by the infectious medicine (ID)
team with liposomal amphotericin B 3mg/kg Q24hours, tigecycline 100mg
given as a loading dose followed by 50mg Q12hours, and ciprofloxacin
400mg Q8hours.
The patient did not show any signs of improvement and the lesion evolved
into a black lesion with a central area of necrosis (figure 2) ,
biopsy taken and culture growth showed Aspergillus flavismeanwhile blood culture showed (Stenotrophomonas maltophilia,
Achromobacter xylosoxidans and Enterococcus casseliflavus ), plan of
care discussed with the multi-disciplinary team (MDT) and the decision
was to go for surgical debridement and endoscopic exploration of
paranasal sinuses, but due patient electrolyte imbalance (Na 148, and K
5.5) abnormal coagulation profile (PT 16.7, INR 1.6 APTT 42.8) and low
platelets (Plt 1000/uL)) surgery was delayed until normalization of
patient lab values.
The patient received Granulocyte colony-stimulating factor (G-CSF);
filgrastim 300mcg and platelets transfusion, patient received 6 units
daily for 5 days but no significant improvement of platelets count as
the count did not exceed 40000/uL.
The patient was taken into the theater, wide local excision of the
lesion with 5 mm safety margin (Figure 3) and endoscopic
exploration of the sinuses done which showed clear osteo-meatal complex
and ethmoid air cells with no clear evidence of fungal sinusitis; the
patient was planned for a frontonasal local flap, but due to patient
abnormal coagulation profile plan was postponed until the patient
condition improves.
The patient received 10 units of platelets on the day of surgery and
continued empiric antimicrobial therapy with antifungal treatment and
daily dressing on the surgical site; due to low platelet count patient
tends to develop blood oozing from the surgical site, for that pressure
dressing with hemostatic materials was done.
Unfortunately, the Patient had poor survival rate due to her disease,
later she died of systemic complications of her primary disease.