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Feeding cats might be dangerous: penetrating orbital and brain injury without neurological deficits
  1. F Knerlich,
  2. R Verheggen
  1. University Hospital of Göttingen, Göttingen, Germany
  1. Correspondence to:
 R Verheggen
 Department of Neurosurgery, University hospital, Georg-August-University of Göttingen, Göttingen, 37075, Germany; raphaela.verheggenmed.uni-goettingen.de

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A 67 year old alcoholised woman stumbled over an unevenness, lost her balance, and fell into an ordinary butterknife while preparing cat food.

Initially the woman was awake with a Glasgow coma scale (GCS) of 9. On hospital admission, she was intubated, sedated, the pupils were equal and reactive to light, the eyeballs were both intact, and there was no neurological deficit. The handle of the knife was protruding from the right orbit. There was a leakage of bloody cerebrospinal fluid (CSF) out of the inner right canthus.

X ray and computed tomography (CT) demonstrated the blade penetrating the medial part of the right orbit—gyrus rectus extending to the anterior horn of the right lateral ventricle (fig 1). Beside there was an old infarction area due to the right medial cerebral artery. After exclusion of a space occupying intracerebral haemorrhage the knife was pulled out in the operating theatre. After removing the knife a control CT was performed revealing only a minimal traumatic subarachnoid haemorrhage (tSAH) (fig 2). Thereafter, the right canthus was microsurgically sutured.

Figure 1

 CT with bone algorithm: butterknife penetrating through the orbit, frontal cranial base, and frontal lobe.

Figure 2

 Postoperative native CT demonstrating tSAH. Note the defect zone resulting from an ischaemic infarct.

Postoperative contrast-enhanced, T1 and T2 weighted magnetic resonance images revealed minimal tSAH and a slight defect zone in the right gyrus rectus (fig 3). Hypothalamus, pituitary gland, and optic nerve were completely unaffected. Initially, CSF analysis indicated massive erythrocytes (due to the tSAH), a disturbed blood-brain-barrier function, and a total cell count of 38/mm3. Hormonal testing was inconspicious including prolactin, follicle-stimulating hormone, lutheinizing hormone, growth hormone, thyrotropin, and corticotropin. Electrolytes were normal and the patient did not develop a syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Neuroophtalmologic investigation revealed no loss of visual acuity and full ocular motility.

Figure 3

 Postoperative magnetic resonance images (left T1 sagittal, right T2 coronal): beside tSAH there was a slight defect zone in the right gyrus rectus. No lesions became obvious in the hypothalamus, pituitary gland, and optic nerve.

She received a prophylactc antibiotic therapy including amoxicillin/clavulanate (3×2.2 g), ciprofloxacin (2×0.5 g), and metronidazole (2×0.4 g). Through the clinical course the patient showed no signs of infection. As an independent complication she developed a crural thrombosis and was discharged on day 37 after initial trauma.

Penetrating orbital trauma should alert the clinician because of potentially devastating consequences. Even an intact orbital globe does not exclude intracranial trauma. The high mortality rate associated with cranial penetration injuries is mainly a result of intracranial suppuration.1–3 Therefore, an appropriate, broad spectrum antimicrobial therapy is inevitable. Considering the serious injury the patient’s course was remarkably inconspicuous.

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Footnotes

  • Competing interests: none declared

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