Burns constitute one of the severest forms of trauma that can be sustained
by individuals. Causes of burns include chemical, electrical, industrial
and thermal agents. The injury occurs both in children and adults. In
Nigeria, burn injuries have been reported from the use of contaminated
kerosene, high voltage electricity, use of sitz bath, petrol pipeline
explosions and from fire therapy in convulsing children (Adesunkanmi and
Oyelami, 1994; Ameh and AbdulWahab, 2000; Oduwole et al., 2003;
Fadeyibi et al., 2006). Burns injuries may occur sporadically or
and in disasters involving mass casualties. In recent years, petroleum
products fires have caused mass casualties in Nigeria due to arson and
use of contaminated petroleum products.
The injury is accompanied by both local and massive systemic inflammatory
responses. The local inflammatory response at the site of injury is initiated
almost immediately. The systemic responses however progress with time,
usually reaching the peak by one week after the sustenance of the injury
(Youn et al., 1992). The series of events involving various tissue
structures and leukocyte subsets such as neutrophils, macrophages, mast
cells and lymphocytes are aimed at tissue repair and wound healing (Martin
and Leibouich, 2005). Various inflammatory and growth promoting cytokines
are involved (Friedl et al., 1969; Fong et al., 1990;
Trautmann et al., 2000). The cytokines are both pro and anti-inflammatory.
Low molecular weight compounds from degranulating platelets and mast cells
are also released (Jurjus et al., 2007). The systemic response
is shown by marked hypermetabolism and accentuated response to further
assaults (Wilmore et al., 1975; Munster et al., 1986).
Some of the cytokines that are associated with hypermetabolism and catabolic
systemic effects include Tumor Necrosis Factor (TNF), Interleukin-1 and
Interleukin-2 (Fong et al., 1990). Oxygen radicals have also been
associated with both local and systemic responses in burn injury (Sasaki
et al., 1987).
Hypermetabolism that is readily observable in burns patients is one of
the forms of the various altered physiologic responses that develop (Oluwasanmi,
The physiologic alterations may cause functional impairment in several
systems including the cardiovascular, respiratory, gastrointestinal and
immune systems. Tissue growth and repair may also be affected.
Sequel to these pathophysiologic changes in major burns injury, various
complications including hypovolaemic shock, gastrointestinal, cardiorespiratory,
vascular and psychiatric problems have been documented (Oluwasanmi, 1986;
Studies of the effects of burns on the male reproductive system are relatively
few in the literature. Most reported studies are also focused on cases
of direct heat or burns in the scrotal and perineal areas (Choudhary and
Steinberger, 1970; Rommerts et al., 1980; Gavetz et al.,
2000). Not much has been documented on the pathophysiological effects
of major burns on the testes when the perineum is not directly involved
in the burns. The aim of present study therefore is to investigate the
testicular histopathological changes of adult patients that died from
major burns not involving the perineum.
MATERIALS AND METHODS
The study population consisted of adult patients who died after having
been managed for major burns injury at the Burns Center of the LASUTH,
Ikeja Nigeria between January and December 2007. Both institutional and
the patient relatives consents were sought and obtained before caring
out the study.
All patients with burns injury were assessed on arrival at the Surgical
Emergency Section of the hospital and those with major burns (>20%)
were admitted into the Burns wards.
Fluid resuscitation with Ringer`s lactate was commenced on all patients
at the rate corresponding to the percentage Total Body Surface Area (TBSA)
involved multiplied by body weight (kilogram) multiplied by 4. Adjustments
to the calculated fluid requirement were made based on the hourly urinary
output, sensorium assessment and other vital signs. Prophylactic antibiotics
were administered on all the patients based on the results from the Microbial
Surveillances of the wards and house staff. Closed wound management was
observed in all the patients. All patients received tetanus toxoid. The
anatomic distribution of the burns injuries was charted in all the patients
while the pre-burn injury medical history was noted.
During the post mortem examination of the burns patients from the
wards, the charts for the anatomic distribution of wounds were reviewed.
All the male adult patients with injuries not involving the perineum were
recruited into the study. The pre-burns medical histories of the recruited
patients were also reviewed. All the patients with history of diabetes
mellitus, goitre, sexually transmitted diseases, tuberculosis, mumps and
hypertensive heart diseases were excluded.
The testes of the patients that satisfied the inclusion criteria underwent
the histopathologic investigations. Specimens were collected from patients
as soon as postmortem examinations were concluded and preserved in Bouins
fluid. These specimens were then processed on glass slides after cutting
and fixing. Staining was done with Haematoxylin and Eosin stains. The
prepared slides were examined with phase-contrast light microscope CETI
at x100 and x 400 magnifications.
One hundred and five patients were seen with major burns during the study
period. The total number of deaths among this category of patients was
36 given a mortality rate of 34.3%.
As shown in Table 1, ten of the deaths satisfied the
inclusion criteria are were recruited for the study.
The age range of the patients was 17-50 years with a mean of 34.1 years.
The range of Total Body Surface Area (TBSA) involved in the burns was
60-83% and mean of 67.9%.
The weights of the testes examined were between 15 and 26 g with a mean
of 22.1 g. The period of admission for the patients ranged from 6-15 days
with a mean of 10.0 days.
Mild to moderate interstitial oedema was observed. Fibrous and Cellular
components were clearly delineable.
The Leydig cells were few in number but morphologically normal (Fig.
The general outline appeared normal with empty ad-luminal space. The
deep cell layers were detached from the basement membrane in some areas
and broken- up in others (Fig. 2). On higher magnification
the epithelium was detached from the basement membrane and broken-up.
Cells of the spermatogenic series, spermatogonia (types A and B), primary
and secondary spermatids appear normal and in the different stages of
the spermatogenic cycle.
Cells of spermiogenic series which include cells from the level of the
elongating spermatids to mature spermatozoa were scanty. In deed matured
were not seen in all the specimens (Fig. 3).
Sertoli cells were very few however they appeared normal morphologically
|| Patients characteristics
||Stromal oedema and detachment of deep cell layers form
the basement membrane (H and E x400)
||Seminiferous tubules containing cells of the spermatogenic
series. Scanty cells of the spermiogenic series (H and E x400)
||Sertoli cells arising from the basement membrane these
are few but morphologically normal (H and E x400)
The plethora of pathophysiological changes that accompany major burns
injury are determined by the extent of burn, the age of the patient and
the depth of injury (Oluwasanmi, 1986; Heimbach et al., 1992; Press,
1997). Other factors that are important include the types of first-aid
management, interval between the onset of injury and the commencement
of appropriate therapy and of course availability of the treatment facilities
including the experience of the management personnel (Adesunkanmi and
Oyelami, 1994; Ameh and AbdulWahab, 2000; Oduwole et al., 2003;
Fadeyibi et al., 2006).
With the appropriate knowledge of the dynamics of fluid changes in major
burns and control of sepsis, more patients survive burns injury (Moore,
1970; Pruitt et al., 1971; Pruitt and McManus, 1992). Many of the
hitherto possible complications of burns are now becoming important with
the increased chance of survival.
Major burn is characterized by a hypermetabolic state. Massive amounts
of oxidants, arachidonic acid, metabolites proteases, cytokines and interleukins
are released (Friedl et al., 1969; Fong et al., 1990; Trautmann
et al., 2000). These can cause both local and systemic inflammation
induced tissue damages (Goris et al., 1985). Soon after major burns
injury, there is hemodynamic instability and blood flow redistribution.
Blood flow is shunted away from non-vital to vital organs of the body
(Pruitt et al., 1971). The effect may consequently result in severe
organ dysfunction later.
In this study, oedema was demonstrated in all the testes (Fig.
1). This is in agreement with the concept of post-burn inflammatory
disease (Ganong, 2001). Generalised tissue inflammation will be found
in uninjured organs within hours. Cytokines produced primarily by macrophages
and lymphocytes, with other products from the keratinocytes, endothelium
and parenchymal cells in the body are thought to be responsible for this
(Youn et al., 1992).
The persistence of certain factors including delayed and inappropriate
management and sepsis, may however lead to stimulation of primed macrophages
with hyperactive response. This will cause further release of inflammatory
mediators with the consequent further damages to tissues (Youn et al.,
1992). The persistent activity of TNF has been shown to be one of the
factors responsible for the multiple organ failure syndromes (Youn et
The detachment of the epithelium from the basement membrane of the seminiferous
tubules and the physical disintegration of the cells may be a consequence
of the ischaemic effects of the hemodynamic instability and blood flow
maldistribution occurring after major burns (Fig. 2).
Cell to cell interaction is important in the stages of spermatogenesis
The testes have dual functions; (a) gametogenesis and (b) sex hormones
production. Large amounts of androgens, mostly testosterone, a steroid
sex hormone is produced. Little amount of oestrogens and other polypeptides
including inhibin, are also produced. Spermatozoa are equally produced
by the testes. The gametogenic and secretory functions of the testes depend
on the production of the anterior pituitary gonadotrophins-.Follicle Stimulating
Hormones (FSH) and Leutenizing Hormones (LH) (Ganong, 2001).
The Interstitial cells of Leydig secrete testosterone into the blood
stream. Proteins pass from Sertoli cells to Leydig cells in paracrine
fashion for the co-ordination of spermatogenesis. Spermatogenesis is the
process of cell division from the primitive germ cells to the secondary
spermatocytes and then spermatids. This process is androgen independent.
The process is dependent on the secretions of anterior pituitary-gonadotrophins.
Maturation from spermatids to spermatozoa depends on androgens acting
on the Sertoli cells (Ganong, 2001).
Follicle Stimulating Hormones (FSH) acts on the Sertoli cells to facilitate
the last stages of spermatids maturation. It also promote the production
of Androgen Binding Protein (ABP) by the Sertoli cells The ABP is important
because maturing spermatids develop in the deep folds of the cytoplasm
of the Sertoli cells (Fornes et al., 1993).
In this study the average weight of the testes that were studied was
slightly above the range for an adult testis. The range for the adult
testis is between 15 and 19 g (Ackermans, 1996). The increase may be due
to the oedema that was noticeable in all the slide preparations. No mature
spermatozoa were found in all the specimens. From the physiology of spermatogenesis;
the relative absence of both the Leydig and Sertoli cells may be responsible
for this. Also Seminiferous tubules and spermatogenesis in mammals have
been shown to be susceptible to toxic damages from a variety of chemicals
and physical insults. Free oxygen radicals have been implicated as the
common pathway for toxic damages caused by many of these substances and
conditions (Fornes et al., 1993). The cause of the paucity of Sertoli
and Leydig cells is uncertain. It may be due to the cytotoxic effects
of the mediators released after the injury or the relative increased sensitivity
of these cell lines to the tissue ischaemia resulting from the hemodynamic
changes. It is however important to know that the products of early stages
of spermatogenesis that are independent of these cells were found in all
In conclusion it could be stated that major burns result in indirect
derangement in the testicular morphology. The possibility of toxigenic
agents with selective affinity for the more mature adluminal cells of
the seminiferous tubules needs to be explored. Studies are also required
to elucidate the mechanisms by which the testicular damages are produced.