Keywords
intracerebral abscess - transorbital injury - intracranial penetrating injury - meat hook - occult transorbital injury
Introduction
Penetrating orbital injuries is a significant threat to orbital and, often, cranial contents. Transorbital injuries represent up to 24% and 45% of all penetrating head injuries in adults and children, respectively.[1] Transorbital orbitofrontal penetrating injury by a foreign body is infrequent, approximately 0.4% of all head injuries.[2] It may present dramatically, with a severe large gaping wound or as subtle, innocuous, and initially occult injury. This occult injury may fail to be recognized initially, especially when the penetrating foreign object was removed, resulting in delayed presentation. Trivial-appearing eyelid lacerations may camouflage occult deep penetrations, which are frequently sutured without further investigation.[3] This occult injury is more dangerous, as it can be easily missed and may present later with potentially life-threatening complications.[4]
[5] In this article, a case of a meat hook causing occult transorbital orbitofrontal penetrating injury, resulting in brain abscess was described and literature reviewed.
Case Report
A 33-year-old male patient had suffered atypical transorbital penetrating injury when he suddenly lost his balance due to a slip while standing in the meat shop in front of meat hooks and his head accidentally plunged into the sharp/pointed arm of an S-shaped bare meat suspension hook. The meat hook penetrated his orbit through a small cut over his right eyebrow, and he immediately experienced severe pain. He grabbed the hook with his hands, balanced and adjusted himself, and gently pulled out the meat hook on his own. He took an analgesic medication and did not pay much attention to it. The next morning, he discovered swelling in his right eyelid and diffuse redness in his right eye, so he consulted an ophthalmologist who prescribed him oral analgesic and antibiotic eyedrops and oral antibiotics for 5 days. Within the next 3 to 4 days, he had no pain, redness in his right eye disappeared, and the eyelid swelling reduced. He had no further consultation. Three weeks after his initial injury, he presented with severe progressive holocranial, dull-aching, continuous headache for 2 to 3 days along with giddiness. On examination, he was drowsy but easily arousable. His Glasgow coma scale (GCS) score was approximately 14/15 (E3M6V5). Plantars were extensor on the left side and flexor on right side. Ophthalmological examination revealed right upper eyelid swelling and right conjunctival congestion. Both pupils were of normal size, isochoric, and reacting normally to light. His visual acuity and extraocular movements were normal. He had a small, healed wound over the right eyelid ([Fig. 1]). He received a tetanus toxoid injection along with intravenous (IV) antibiotics and antiepileptic medications. The CT scan brain revealed right frontal lobe edema. CT scan of orbit revealed minimally displaced fracture of the roof of the right orbit with mild angulation of the fractured fragment and periorbital edema. Contrast-enhanced CT scan of the brain and orbit revealed a peripheral irregular ring-enhancing lesion of approximately 3.1 × 4.4 × 5.3 cm size in the right frontal lobe with perilesional edema. The lesion was communicating with the orbit through a bony defect in the orbital roof ([Fig. 2A], [2B], [2C], [2D]). MRI of the brain with orbit revealed 3.2 × 4.6 × 5.2 cm size peripheral rim-enhancing mass lesion over right frontal lobe, communicating with an orbit which was isointense on T1-weighted images and hyperintense on T2-weighted image with moderate perifocal vasogenic edema ([Fig. 3A], [3B], [3C], [3D]).
Fig. 1 Clinical photograph showing right eyelid edema, redness and small healed punctured wound over upper eyelid just below lateral one third of right eyebrow.
Fig. 2 CT scan of brain showing right frontal cystic lesion with perilesional edema (A). Lesion was enhancing after intravenous (IV) contrast administration (B). CT scan brain and orbit, coronal view showing cystic cavity just above fractured orbital roof (D), and bone window showing right orbital roof fracture (C).
Fig. 3 MRI of brain showing right frontal cystic lesion on axial T1-weighted image (A) and T2-weighted image (B) with perilesional edema with mass effect. Lesion showing peripheral rim of contrast enhancement (C). Postcontrast coronal view image showing right frontal contrast-enhancing lesion communicating with orbit (D).
The patient underwent a right frontal craniotomy. The dura mater was tense and brain wall full. Via the anterior part of the middle frontal gyrus, a lesion entered. Brownish, viscous, nonfoul-smelling pus of approximately 30 ml aspirated and cyst wall excised. Subsequently, the brain became lax. Part of the frontal lobe just above the anterior part of the orbital roof was adherent to it. On gentle separation of frontal lobe from the orbital roof, a 15 × 8 mm size defect was found in the basal frontal dura and orbital roof. Two free bony fragments adjacent and superior to the orbital roof were also found along with granulation tissue and pus. Free-floating bony fragments, granulation tissue, along with the pus, were removed and cavities thoroughly irrigated with antibiotic solutions. The dural defect over the orbital roof was closed with a temporalis fascia graft.
The postoperative course was uneventful. Headache completely disappeared. Right eyelid swelling also subsided within 4 to 5 days. The patient was empirically started on broad-spectrum antibiotics (IV vancomycin, cephalosporin, and metronidazole). He also received antiepileptic (phenytoin) in the postoperative period. Postoperative contrast-enhanced CT scan revealed no residue of the abscess, disappearance of ring-like enhancement and decreased brain edema. The microbial culture of the pus from the brain abscess grew colonies of Staphylococcus aureus, sensitive to vancomycin. The patient was discharged on the seventh postoperative day without any neurological deficit. He received IV antibiotics for 2 weeks and oral antibiotics for 4 weeks. He received oral anticonvulsants for 3 months.
At 3 months follow-up, the patient was completely asymptomatic. His visual acuity and fields of vision were completely normal. Follow-up MRI images revealed complete resolution of an abscess on postgadolinium administration ([Fig. 4A], [4B], [4C], [4D]).
Fig. 4 MRI of brain showing complete resolution of right frontal lesion on T1-weighted axial mage (A), T2-weighted axial (B) and coronal image (D). Very subtle enhancement was seen after intravenous (IV) contrast administration (C).
Discussion
The bony cranium can be entered through the orbit via its weak walls. The most common route of entry is a thin orbital roof.[1] Superior orbital fissure is the second most frequent site through which foreign bodies occasionally reach the brain stem via cavernous sinus, resulting in a severe injury.[6] A third, rarer avenue of penetration is the optic canal, where the object is directed into the suprasellar cistern, close to the optic nerve and internal carotid artery.[7] Turbin and colleagues analyzed transorbital intracranial injury patterns and divided the orbital surface into different zones.[1] Balasubramanian and colleagues classified transorbital penetrating injury, based on the orbital bone's anatomy and the associated injury.[8] This analysis of injury patterns could help one tailor the management and surgical approach, and anticipate the potential type and sites of intracranial complications related to foreign body penetration.
Orbital injuries can cause vision loss by damaging the orbital contents or optic nerve. Bilateral vision loss in unilateral orbital injury due to direct chiasmal and indirect ischemic vascular injuries has also been described.[9] Penetrating orbital injury gives rise to severe brain injury when the foreign object enters the cranium, leading to both orbital and cerebral complications. Because of the small entry point, incomplete history, and trivial nature of the injury, caregivers easily overlook it.[1] In such cases, eyelid laceration is sutured without further investigation and these patients present with delayed complications like rhinorrhea, orbital cellulitis, eyelid abscess, cerebritis, subdural empyema, recurrent meningitis, encephalitis, cerebral and intraorbital abscesses, pseudoaneurysm, and posttraumatic arteriovenous malformation.[4]
[10]
[11]
Brain abscess following transorbital orbitofrontal injuries is rare. In literature review, we found about 10 cases.[12]
[13]
[14]
[15]
[16]
[17]
[18]
[19]
[20]
[21]
[Table 1] summarizes the studies of transorbital craniocerebral penetrating injuries complicated by an intracerebral abscess.
Table 1
Summary of selected studies for occult transorbital craniocerebral penetrating injuries complicated by intracerebral infection
|
Author (year)
|
Age (y)
|
Sex
|
Route of entry into cranial cavity
|
Foreign body type
|
Cerebral abscess location and infection type
|
Organism isolated /antibiotics received
|
Surgical approach
|
Outcome findings
|
|
Abbreviation: CFS, chronic fatigue syndrome (CFS); IV, intravenous.
|
|
Amano and Kamano[12]
|
7
|
M
|
Superior orbital fissure
|
Bamboo stem
|
Meningitis and right cerebellar abscess
|
Escherichia coli from CFS/no details
|
No surgery only antibiotics
|
Gradual reduction of the cerebellar abscess size
|
|
Mutlukanet al[13]
|
41
|
M
|
Orbital roof
|
Splinters of wood
|
Right frontal lobe abscess
|
Bacteroides asaccharolyticus
and small numbers of anaerobes/no details
|
Right frontal craniotomy, right optic canal decompression, and exploration of the right orbit
|
Postoperative seizures; loss of vision in the right eye
|
|
Bert et al1[4]
|
57
|
M
|
Orbital roof
|
Thuja hedge
–
|
Right frontal abscess
|
Bacillus macerans/IV amoxicillin (12 g/day) and metronidazole (1.5 g/day
|
Right frontal craniotomy and excision of abscess
|
Death
|
|
Potapov et al[15]
|
26
|
M
|
Medial orbital wall
|
Wooden foreign body
|
Right temporal lobe abscess
|
No growth/cefotaxime,
amikacin, metronidazole
|
Fronto-temporal craniotomy
|
Loss of visual function; right sided ptosis
|
|
di Roio et al[16]
|
6
|
M
|
Orbital roof
|
Chopstick
|
Left frontal lobe abscess
|
Staphylococcus cohnii and Enterococcus faecalis/penicillin-G and amoxicillin
|
Abscess aspiration
|
No documented abnormalities
|
|
Maruya et al[17]
|
56
|
F
|
Lateral orbital wall
|
Bamboo fragments
|
Left temporal lobe abscess
|
No growth/antibiotics for 5 weeks
|
Left fronto-temporal craniotomy and orbito-zygomatic osteotomy
|
Slight left-eye lateral gaze limitation
|
|
Nishio et a[18]
|
13
|
F
|
Orbital roof
|
Chop stick
|
Right frontal
|
Streptococcus mitis and Staphylococcus hominis/IV
cefoperazone, amoxicillin, sulbactum 2 weeks
|
Craniotomy and excision of abscess
|
Recovered without neurological deficit
|
|
Seider et al[19]
|
1
|
M
|
Orbital roof
|
Pencil tip (made of graphite)
|
Frontal lobe abscess
|
Alpha-hemolytic streptococci/IV ceftriaxone and metronidazole for 6 weeks
|
Frontal burr hole and orbitotomy
|
Right upper eyelid ptosis
|
|
Abdulbaki et al[20]
|
5
|
F
|
Orbital roof
|
Pen
|
Frontal lobe abscess
|
No growth/vancomycin, ceftazidime, and metronidazole.
|
Transcutaneous upper eyelid approach
|
Mild right eye ptosis
|
|
Mulla et al[21]
|
70
|
M
|
Orbital roof
|
Bamboo fragments
|
Frontal lobe abscess
|
No growth/antibiotics for 6 weeks
|
Right frontal Craniotomy
|
No neurological deficits
|
|
Present case
|
33
|
M
|
Orbital roof
|
Meat hook
|
Frontal lobe abscess
|
Staphylococcus aureus/2 weeks IV and 4 weeks oral antibiotics
|
Left frontal craniotomy
|
No neurological deficit
|
The brain abscesses may result from either the foreign body's presence or the bone fragments from a skull fracture that have been driven further into the cranial tissue. Organisms present on the surface of foreign objects and bacteria present on the skin at the site of impact can be transported not only to the orbit but also to the cranium when there is an orbital roof fracture. Therefore, such an injury may cause severe infectious complications from days to years after the initial injury. Following transorbital transcranial injury, the patient can develop eyelid abscess within 3 weeks and brain abscess within a few weeks to months.[14] Formation of brain abscess runs through four radiological and histopathological stages: early cerebritis (1–4 days), late cerebritis (4–10 days), early capsule formation (11–14 days), and late capsule formation (> 14 days).[22] Early cerebritis is an early stage of infection with coagulative necrosis. It progresses to late cerebritis with mainly liquefactive type of necrosis. Cerebritis may progress and organize to form an abscess. Early capsule stage has a very thin capsule of granulation tissue around a central necrotic material. It appears as a discrete lesion with thin enhancing rim on imaging. Late encapsulation is a process where the central necrosis progresses further, the cavity shrinks, and edema decreases. In our case, the patient presented with brain abscess symptoms after 21 days of the injury. Brain abscess occurs in 50% of intracranial injuries following a periorbital wound.[23] The duration required for brain abscess development depends on the potency, infectivity, and virulence of a particular organism.[24] In our case, the patient developed brain abscess, possibly due to direct implantation of the infecting organism (S. aureus based on microbial cultures) by the meat hook, although there was no retained foreign body in the orbit or cranium.
The management of penetrating transorbital craniocerebral head injuries depends on the presence/absence and foreign body location, its tract in the orbit and cranium, associated bony or neural injuries, intracranial complications, and the time interval between initial injury and treatment.[1]
[21] The clinical goals of such operations include preventing infection, decreasing the possibility of epilepsy (by giving antiepileptic medications), controlling bleeding from affected cerebral vessels, and preventing cerebrospinal fluid (CSF) fistula and brain abscess.
Initial empirical antimicrobial therapy should be based on the suspected organisms, underlying predisposing conditions, and expected source of infection. Broad-spectrum parenteral antibiotics which can cross blood-brain barrier (BBB) and blood-CSF barrier, and can accumulate in the abscess cavity in bactericidal concentrations, are chosen. Cephalosporins are the most preferred antibiotics.[9] In abscesses due to trauma or neurosurgical procedures, combination of the vancomycin, third- or fourth-generation cephalosporin and metronidazole is recommended.[25] In immunosuppressed patients, therapies for Nocardia (trimethoprim-sulfamethoxazole), Aspergillus (voriconazole), or Toxoplasma (pyrimethamine-sulfadiazine) can be added.[26] Once the pus is drained and the antibiotic culture and sensitivity report is available, patients are started on specific bactericidal agents. If the culture is negative for any organism, the empirically given broad-spectrum antibiotics can be continued. According to the British Society for Antimicrobial Chemotherapy, only 1 to 2 weeks of IV therapy is recommended.[27] The recommended duration of IV antimicrobial therapy in other studies varies widely from 2 weeks to 8 weeks. Dattatraya et al suggested “triple high dose” antibiotics IV for 2 weeks, followed by four weeks of oral therapy.[22] Agrawal et al recommend appropriate IV antibiotics administered for 3 weeks, followed by oral antibiotics for another 3 weeks.[28] Some suggest IV antibiotic therapy for 6 to 8 weeks, followed by a course of an oral agent. Common oral treatment regimens include ciprofloxacin, metronidazole, and amoxicillin. In general, antibiotic treatment is generally advised as long as the abscess cavity is visible on cranial MRI.[26] Intraventricular antimicrobials are recommended after intraventricular rupture of brain abscess. Opportunistic organisms may need longer, 3 to 12 months, antibiotic courses.[22] Surgical treatment includes evacuation of the cavity by aspiration of its contents, debridement of the path, excision of the abscess wall, removing the foreign body, and any retained bone fragments.[18]
[29]
[30]
Conclusions
Transorbital transcranial penetrating injuries are uncommon injuries and can be life-threatening if not diagnosed and treated appropriately on time. These injuries can easily be missed when periorbital swelling is present and the foreign body is not visible outside. Appropriate radiological imaging can lead to an earlier and accurate diagnosis and prevent delayed sequelae like brain abscess.
