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Superficial skin ulcers: Histopathological analysis and review of the literature.

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 Superficial skin ulcers 26

SUPERFICIAL SKIN ULCERS: HISTOPATHOLOGICAL ANALYSIS AND

REVIEW OF THE LITERATURE

Oluwole OP1*, Taiwo JO2, Awani KU2, Adeniran JO3

1. Department of Pathology/Forensic Medicine, University of Abuja Teaching Hospital,

Gwagwalada, Abuja, Abuja, F.C.T, Nigeria
2. Paediatric Surgery Unit, Department of Surgery, Federal Medical Centre, Lokoja, Kogi
State, Nigeria
3. Paediatric Surgery Unit, Department of Surgery, University of Ilorin Teaching
Hospital, Ilorin, Kwara State, Nigeria

Correspondence:
Dr Olabode Peter Oluwole. Department of Pathology/Forensic Medicine University of
Abuja Teaching Hospital, Gwagwalada, Abuja, Abuja, F.C.T. Nigeria
E-mail: olabode166@gmail.com

Oluwole OP, Taiwo JO, Awani KU, Adeniran JO. Superficial skin ulcers:
histopathological analysis and review of the literature. Adv Lab Med Int. 2016; 6(2): 26 -
30.

ABSTRACT

Superficial skin ulcers are common clinical problems in the tropics and these pose a
major diagnostic challenge to both clinicians and pathologists. The objective of this study
is to determine the histological pattern of superficial skin ulcer in our environment. This
is a 2-year retrospective histopathological analysis of superficial skin ulcers diagnosed at
the Histopathological Unit of Federal Medical Centre, Lokoja, Nigeria, between August
2007 and July 2009. Clinical information and biodata were extracted from histopathology
request cards. Histology slides stained with haematoxylin and eosin (H&E) was retrieved.
Periodic acid Schiff, Gomori methenamine silver and Ziehl Neelson stains were done for
cases of chronic granulomatous inflammation to exclude fungal or mycobacterial
infection. A total of 19 cases of superficial skin ulcers were analyzed. The age range was
20-69 years with the mean age of 44.5 years. There were 16 males and 3 females. The
peak age frequency was in the third decade (20-29 years). The spectrum of lesions in this
analysis was categorized into inflammatory, infections, benign and malignant diseases. A
total of 6 (31.5%) cases of granulomatous inflammation, two (10.5%) non-specific
inflammation, lobular capillary haemangioma 3 (15.8%) and one (5.3%) intermediate
mesenchymal tumour- dermatofibrosarcoma protuberans were found. The most common
malignant tumour was squamous cell carcinoma 5 (26.3%); this was followed by one
(5.3%) case each of malignant melanoma and basal cell carcinoma. Superficial skin
ulcers are common in the tropics and could undergo malignant transformation, if medical
intervention is not sought early. So there is need for a high index of suspicion, adequate
tissue biopsy and early histopathological diagnosis.

Key words: Superficial skin ulcers, Squamous cell carcinoma, malignant melanoma

Advance Laboratory Medicine International 2016; 6(1): 26 - 30 26

 Superficial skin ulcers 27

INTRODUCTION

The skin is a complex organ with many functions and is exposed to environmental
elements, the most important being long time exposure to ultraviolent light, trauma and
infections1.
Ulcers can be defined as wounds with complete loss of the epidermis and often portions
dermis with subcutaneous fat that has a slow healing tendency2.
The incidence of ulceration is rising as a result of the ageing population and increased
risk factors for atherosclerotic occlusion such as smoking, obesity and diabetes2.
In general, the slow healing tendency is not simply explained by depth and size, but
caused by an underlying pathogenetic factor that needs to be removed to before healing
can be induced2.
The probable causes are exposure to extremes of temperature, venous valve insufficiency
and lower extremity arterial disease like atherosclerosis and diabetes. Other less frequent
conditions are infections, vasculitis, hypercoagulability, skin malignancies and ulcerating
skin diseases such as pyoderma gangrenosum2.

MATERIALS AND METHODS

This is a 2-year retrospective histopathological analysis of superficial skin ulcers

diagnosed in the Histopathological Unit of Federal Medical Centre, Lokoja, Nigeria,
between August 2007 and July 2009. Clinical information and biodata were extracted
from histopathology request cards.
Histology slides stained with haematoxylin and eosin (H&E) was retrieved. In cases of
chronic granulomatous inflammation, Periodic acid schiff and Gomori methenamine
silver stains were used to exclude fungal infection, while Ziehl Neelson stain was used to
exclude mycobacterial infection.

RESULTS

A total of 19 cases of superficial skin ulcers were analyzed. The age range was 20-69
years with the mean age of 44.5 years. There were 16 males and 3 females. The peak age
frequency was in the third decade (20-29 years). The spectrum of lesions in this analysis
was categorized into inflammatory, benign and malignant diseases.
A total of 6 (31.5%) cases of granulomatous inflammation were observed; four were
confirmed to be mycobacterial tuberculosis and two fungal infections by Gomori
methenamine silver stain. There were two (10.2%) cases of non-specific inflammation,
three cases (15.8%) of lobular capillary haemangiomas and one (5.2%) mesenchymal
tumour of intermediate malignancy- dermatofibrosarcoma protuberance.
The most common malignant lesion was squamous cell carcinoma 5 (26.3%); this was
followed by one (5.2%) case each of malignant melanoma and basal cell carcinoma.

Advance Laboratory Medicine International 2016; 6(1): 26 - 30 27

 Superficial skin ulcers 28

DISCUSSION

Various definitions of the term ulcer exist but the two main criteria postulated are
involvement of the full thickness of the lining epithelium- epidermis, dermis and portions
of subcutaneous tissue; which implies that there are no sources for re-epithelialisation left
in the centre of the ulcer, and a slow healing tendency. In most definitions, slow healing
is further specified by defining a time frame (present for more than 4 weeks) to separate
chronic ulcers from acute wounds2.
In general, the slow healing tendency is not simply explained by depth and size, but
caused by an underlying pathogenetic factor that needs to be removed before healing can
be induced. Prevalence numbers (all skin ulcers) range from 1% in the adult population to
3–5% in the population over 65 years of age3. In Western countries, the incidence of
chronic skin ulcers is rising as a result of the ageing population, and increased risk factors
for atherosclerotic occlusion such as smoking, obesity and diabetes4.
Nineteen patients were analysed in this study. The age range was between 20-69 years,
the mean age was 44.5 years. The peak age frequency was in the third decade (20-29)
years. There was male preponderance with the ratio 16:3 (5.1:1). This finding differs
from the findings of a study done in Zaria by Samaila et al5. Their peak age was in the
fifth and sixth decades, but there was male preponderance as was observed in this
analysis.
Six (31.5%) of the patients had granulomatous inflammation; four were confirmed to be
mycobacterial tuberculosis by Ziehl Neelson’s stain and two fungal infections by Gomori
methamine silver stain. Two (10.2%) patients had non-specific chronic inflammation.
This differs from a similar study done in Zaria5. Though their series had a larger number
of patients than ours, they recorded 51% categorized as non-specific lesions (chronic
inflammation, granulation tissue and pseudoepitheliomatous hyperplasia).
Three (15.8%) cases of lobular capillary haemangiomas, a benign lobular vascular
tumour was observed. These were located in the digits of both right and left hands. One
(5.2%) case of dermatofibrosarcoma protuberans, a mesenchymal tumour of intermediate
grade malignancy was found. This differs from the findings of studies from Kano6 and
Zaria5 that recorded 8.8% and 0.6% in their malignant series, though they had large
number of patients.
The predominant malignant tumour was squamous cell carcinoma 5(26.3%), this was
followed by a case (5.2%) each of malignant melanoma and basal cell carcinoma. This is
in concordance with studies from Nigeria5-7 and other parts of Africa8 where squamous
cell carcinoma constituted the largest number of carcinomas seen.
In the past, some of these observed phenomena, such as shunting of blood near ulcers, the
fibrin cuff, iron accumulation, white cell accumulation, decreased fibrinolytic activity,
binding of transforming growth factor-beta9 and other growth factors by macromolecules
such as fibrin or alpha-macroglobulin; and various inflammatory responses to the
vascular damage, were believed to contribute to ulceration. To date, it is still not clear
whether they represent causative factors.
Most authors believe that the haemodynamic changes at the microvascular level are
sufficient to explain ulceration10-11.
Many factors such as impaired blood supply, jaundice; vascular insufficiency-
atherosclerosis, anaemia, macronutrients and micronutrient deficiencies,

Advance Laboratory Medicine International 2016; 6(1): 26 - 30 28

 Superficial skin ulcers 29

immunosuppression, presence of foreign body, bony deformities and diabetes mellitus

were among the causes of impaired wound healing12 - 13. However, some of the co-
morbidities mentioned above were not found in our patients.

CONCLUSION

In conclusion, superficial skin ulcers may herald an underlying disease in the tropics
ranging from benign to malignant diseases. Thus a high index of suspicion, good clinical
history, physical examination along with adequate biopsy and up to date knowledge of
pathology can help to arrive at a definitive diagnosis.

COMPETING INTERESTS

The authors declare no competing interest.

REFERENCES

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treatment of leg ulceration. Br J Dermatol. 2003;148:388 – 401.
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Epidemiology of chronic venous ulcers. Br J Surg. 1991;78: 864 – 7.
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10. Vanscheidt W, Laaff H, Weiss J. Immunohistochemical investigation of dermal
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11. Mekkes JR, Westerhof W. Venous ulceration. Lancet. 1993; 342: 121 – 2.

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12. American Diabetes Association Preventive Foot Care in People with Diabetes.
Diabetes Care. 1999; 22: 54 - 5.
13. Bergfelt L, Larko O, Blohme I. Skin disease in immunosuppressed patients in
relation to epidermal Langerhans cells. Acta Dermatol Venerol (Stockholm).
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