Download Clinical management of hyphaema

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Clinical management
of hyphaema
Mathebula SD,
Department of Optometry, University of Limpopo
Correspondence to: Dr Mathebula, e-mail: [email protected]
Introduction
Hyphaema is the presence of red
blood cells in the anterior chamber.15
A minimal amount of tiny red blood
cells suspended in the aqueous
humour is termed a microhyphaema.
Microhyphaema may be visible only
with the slit lamp, in the form of erythrocytes floating and circulating in
the aqueous humour. Slightly larger
amounts of red blood cells settle
as variously shaped masses on the
surface of the iris, lens or vitreous.
Still larger volume of red blood cells
gravitates to the anterior aspect of the
interior chamber, producing a grossly
visible layered hyphaema, which may
be partial or complete.
The management of hyphaema
can present a challenge to a clinician,
because medical treatment is of little
value for hyphaema itself but is useful
for complications.
Traumatic hyphaema
The vast majority of cases occur as a
result of significant blunt trauma to the
eye, although a hyphaema can still
occur because of a seemingly trivial
injury.1-4 Common causes include airbag injuries, blows to the eye during
fist, belt or stick fights. Projectiles to
the orbit, such as baseballs, stones,
explosions and other small objects
are other common agents of injury.
Ocular trauma is a major cause for
monocular vision impairment and
blindness worldwide.2-4
Spontaneous hyphaema
Hyphaemas that occur with no obvious history of trauma are known as
spontaneous hyphemas.5 It can be
caused by vascular abnormalities,
inflammatory processes, vascular
erosions, haematological disorders or
following surgery.
Symptoms
The symptoms of a hyphaema vary
depending on the severity.6,7 Patients
may present with blurred vision, pain,
60
photophobia, lacrimation, headache,
vomiting, nausea and somnolence/
lethargy.
Classification
Description and classification of hyphaema in terms of several variables
are important in evaluating severity, monitoring and management. A
general classification system exists
that has universal acceptance which
is best classified according to the
amount of red blood cells in the anterior chamber.1-6 It consists of grading
the amount of blood layering present.
Documentation of blood layering is
made by drawing the hyphaema,
recording the percentage of layering
or by direct measurement (in mm) of
the layering from the lower limbus. A
grade may then be assigned according to the following guidelines:
Grade 0 : microhyphaemal, circulating red blood cells only
Grade1 : less than 1⁄4 of anterior
chamber
Grade 2 : more than 1⁄4 to 1⁄2 of anterior
chamber
Grade 3 : more than 1⁄2 to 3⁄4 of anterior
chamber
Grade 4 : total filling or “eight-ball”
hyphaema
Patient’s history
The ophthalmic examination focusing
on hyphaema should begin with a
complete history. Circumstances surrounding the event, current medications, past medical history and previous ocular history must be addressed.
Bleeding in the eye warrants questioning concerning systemic blood disorders (haemoglobinopathies) such as
sickle cell anaemia, haemophilia and
von Willebrand’s disease (vascular
haemophilia), because they may affect the course of the hyphaema, its
management and the long term outcome.8,9 Unreliable historians should
be screened for coagulopathic disorders with appropriate testing (sickle
prep or dex, prothrombin time (PT)
and partial thromboplastin time (PTT).
Examination
Inspection for gross ocular injury,
evaluation of the adnexae and the assessment of visual acuity, visual fields,
pupillary function, ocular motility and
the position of the globes should be
undertaken.
Perform uncorrected,
corrected and pinhole (if indicated)
visual acuities depending on the extent of the hyphaema and other ocular
injuries that may affect vision. Pupil
evaluation will help determine the
extent of any traumatic injury to the
surrounding adnexae. Ecchymosis
and lid oedema often accompany
contusion injuries to the eye. Disproportionate conjunctival edema or
haemorrhage may indicate a scleral
rupture, and restriction in ocular
motility may suggest an orbital blow
out fructure.10 For unknown reasons,
many patients diagnosed with traumatic hyphaema may appear drowsy,
thus the mechanism of injury should
be clearly established so that a head
injury will not go undiagnosed.
Management
The overall management for hyphaema should be directed toward minimizing secondary haemorrhage and
reducing the incidence of secondary
glaucoma. Many different supportive
therapeutic and medical regimens
continue to be tried in an attempt to
avoid complications and promote
hyphaema restoration. Clinicians
should not feel obliged to use ritualistic therapy that they consider to be of
uncertain value.
The conventional treatment of patients with traumatic hyphaema has
included hospitalization, bed rest,
bilateral eye patching, sedation and
avoidance of any strenuous activity.35
Although most patients and families
prefer outpatient care for the management of hyphaema, the decision to
hospitalize should be based on cliniSA Fam Pract 2006:48(10)
Review
cian preference. Several authors4,5
have recommended hospitalization
for patients with rebleeding, positive
sickle cell trait or anaemia, hyphaema greater than 50%, sever loss or
decrease in vision or noncompliant
patients.
Advantages of hospitalization are
the ease of follow-up examination,
medical compliance and early diagnosis of complications.1-4 The outpatient management safety depends on
compliance with activity restrictions,
medical delivery and ability to return
for initial daily follow-up.1
In case of traumatic hyphaema,
the injured globe requires adequate
protection with a patch and shield10.
If the patch promotes bacterial
growth by raising the temperature in
the conjunctional sac, topical antibiotic application may be indicated.
Elevating the head of the bed 30-40
degrees while at rest facilitates settling and layering of the hyphaema in
the inferior anterior chamber. Sedation should be recommended only for
the extremely apprehensive (agitated,
hyperactive or anxious) individuals. If
analgesics are required for pain relief,
narcotic analgesics are preferred.10,11
The antiplatelet effect of aspirin tends
to increase the incidence of rebleeding in patients with traumatic hyphaema. This also includes non-steroidal
anti-inflammatory medications, such
as naproxen (Aleve®), ibuprofen
(Motrin®) or mefenamic acid (Ponstel®).
Cycloplegics, miotics, corticosteroids, beta-adrenergic antagonists,
carbonic anhydrase inhibitors and hyper osmotic agents have all been advocated individually or in combination
to increase patient comfort, reduce
intraocular inflammation, decrease
the incidence of secondary haemorrhage, reduce intraocular pressure
(IOP) and promote clearance of traumatic hyphema.2,3
Drops of 1% topical atropine, an
antimuscarinic cycloplegic, in the
affected globe result in mydriasis
and cycloplegia, thereby increasing
patient comfort by reducing ciliary
spasm.10
Published data show that patient
treated with systemic steroids had an
incident of secondary haemorrhage
equal to that of patients treated with
systemic aminocaproic acid.2,12 Topical aminocapraic acid use does not
produce the side effects typically associated with systemic aminocapraic
acid or tranexamic acid, such as nausea, vomiting and hypotension. 2
Conclusion
The eye is an organ that represents
only 0.3% of the total surface area of
the human body. However, loss of
vision in one or both eyes has been
classified as 24% or 85% whole person impairment or disability, respectively.10 Obtain complete ocular and
medical history. Evaluate the entire
eye in an organised manner. Rule out
ruptured globe, orbital fracture, retinal
TARGET
TARGET
TARGET
detachment and systemic bleeding
disorders..
P This article has been peer reviewed
References
1. Rocha KM, Martins EN, Melo LAS, et al. Outpatient management of traumatic hyphema in children: prospective evaluation. J AAPOS 2004; 8:
357 – 361.
2. Nirmalan PK, Katz J, Tielsch JM, et al. Ocular
trauma in a rural South Indian population. The
Aravird comprehensive eye survey. Ophthalmol
2004; 111: 1778 – 1781.
3. Calzada JI and Kerr NC. Traumatic hyphemas in
children secondary to corporal punishment with
a belt. Am J Ophthalmol 2003; 135: 719 – 720.
4. Walton W, Van Hagen SV, Grigorian R and
Zorbin M. Management of traumatic hyphema.
Surv Ophthalmol 2002; 47: 297 – 334.
5. Demeo ML. Management of spontaneous hyphema in a patient with sickle cell trait: A case
report. Clin Eye Vis Care 1998; 10: 141 – 145.
6. Walton W, Hagen SV, Grigorian R, et al. Management of traumatic hyphema. Surv Ophthalmol
2002; 47: 297 – 334.
7. Brandt MT and Haung RH. Traumatic hyphema:
a comprehensive review. J Oral Maxillofac Surg
2001; 59: 1462 – 1470.
8. Hallet D, Willoughby C and Shafiq A. Pitfalls in
the management of a child with mild haemophilia
and a traumatic hyphema. Haemophillia 2000; 6:
118 - 122.
9. Nasrullah A and Kerr NC. Sickle cell trait as a risk
factor for secondary hemorrhae in children with
traumatic hyphema. Am J Ophthalmol 1997; 123:
783 - 785.
10. Mathebula SD. Sports related traumatic hyphema. S Afr Optom 2005; 64: 76-77.
11. Crawford JS, Lewandowski RL and Chan W. The
effect of aspirin on rebleeding in traumatic hyphema. Am J Ophthalmol 1975; 80: 543 – 545.
12. Forber MD, Fiscella R and Goldberg MF. Aminocaproic acid versus Prednisone for the treatment
of traumatic hyphema. Ophthalmol 1991; 98: 279
- 305.
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