31 / 66
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 25, No 6, November/December 2014
AFRICA
281
There are many factors causing epistaxis, including
environmental factors (humidity, temperature), local factors
(inflammation, deviated septum and/or perforation, tumours,
foreign bodies, aneurysm), systemic factors (hypertension,
haematological abnormalities, renal failure, alcoholism,
arteriosclerosis, telangiectasis), andmedications affecting clotting
(anticoagulants, non-steroidal anti-inflammatory drugs).
6
The
literature does not provide a precise definition on the severity
of epistaxis, which is often based on subjective impressions
(subjective evaluation of the volume of bleeding) or anatomical
features, essentially posterior epistaxis.
7
COPD is a known risk factor for morbidity and mortality in
heart surgery. Postoperative complications such as respiratory
failure, prolonged mechanical ventilation and oxygen uptake,
re-intubation, sternal dehiscence, pulmonary infection,
rhythm disturbances and prolonged hospital stays are known
complications in COPD patients after CABG.
2
We could not find any literature on epistaxis in patients
with COPD undergoing CABG surgery. In COPD patients,
drying and thinning of the nasal mucosa due to long-term nasal
oxygen uptake or nebulised use of corticosteroids may cause
epistaxis.
8
Irritation by the endotracheal tube in the pulmonary
system induces the cough reflex and coughing may cause sudden
hypertension in the blood vessels in the nasal cavity. However we
do not believe that in our cases, these factors were the cause of
excessive nasal bleeding after CABG.
Hypertension and antiplatelet therapy may be a predisposing
factor for nasal bleeding in COPD patients post CABG. Aspirin
is thought to be a risk factor for epistaxis.
3
The relationship
between hypertension and epistaxis is unclear.
4
In our study,
neither hypertension nor aspirin were found to be independent
risk factors for epistaxis.
However the presence of COPD in all patients (100%) with
epistaxis, requiring surgical intervention and blood transfusion,
induced us to conduct this study. Profuse nasal bleeding was seen
if the patients had both COPD and hypertension. This analysis
was conducted in our setting to identify the aetiological profile
and to determine the outcome of treatment for epistaxis after
CABG surgery. The results of this study may provide a basis for
the planning of preventive strategies and the establishment of
treatment guidelines.
There was profuse nasal bleeding requiring surgical
intervention in all patients in group 3. Both COPD and
hypertension were diagnosed in all four of these patients.
Although there was no statistically meaningful results for nasal
bleeding in these patients because of the low number of cases (
p
=
0.415), there was an interesting connection between COPD and
hypertension after CABG surgery. Our results showed that both
COPD and hypertension were present in patients with serious
nasal bleeding after CABG surgery.
A limitation of this study was that the incidence of epistaxis
in the early postoperative period after CABG was low. In our
study, only 27 patients had epistaxis. These patients were divided
into three groups according to the amount of nasal bleeding
and the type of treatment, and each group contained only a few
patients. There are also many causes of epistaxis after CABG.
Conclusion
Epistaxis is a co-morbid factor in a small number of patients
with COPD after CABG. It may result in a serious clinical
situation with regard to the amount of nasal bleeding when
seen in patients with COPD alone or with both COPD and
hypertension. From to our results, we recommend that when
COPD and hypertension coincide, cardiac surgeons should
keep in their mind that serious nasal bleeding may occur in
these patients after CABG surgery. If so, they should be sent
immediately to an ENT specialist for appropriate treatment.
References
1.
Willems PWA, Farb RI, Agid R. Endovascular treatment of epistaxis.
Am J Neuroradiol
2009:
30
; 1637–1645.
2.
Bingol H, Cingoz F, Balkan A,
et al
. The effect of oral prednisolone
with chronic obstructive pulmonary disease undergoing coronary artery
bypasses surgery.
J Card Surg
2005;
20
: 252–256.
3.
Tay H, Evans J, McMahon A,
et al
. Aspirin, nonsteroidal anti-inflam-
matory drugs, and epistaxis. A regional record linkage case control
study.
Ann Otol Rhinol Laryngol
1998;
107
: 671–674.
4.
Herkner H, Laggner AN, Mullner M,
et al
. Hypertension in patients
presenting with epistaxis.
Ann Emerg Med
2000;
35
: 126–130.
5.
Pope LER, Hobbs CGL. Epistaxis: an update on current management.
Postgrad Med J
2005;
81
: 309–314.
6.
Tan LK, Calhoun KH. Epistaxis.
Med Clin North Am
1999;
83
: 43–56.
7.
Viducich RA, Blanda MP, Gerson LW. Posterior epistaxis: clinical
features and acute complications.
Ann Emerg Med
1995;
25
: 592–596.
8.
Sastre J, Mosges R. Local and systemic safety of intranasal corticoster-
oids.
J Investig Allergol Clin Immunol
2012;
22
: 1–12.