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Show J. Oi". Nrwro·ophtha/mol. 4: 155-158. 1984. Occipital Cortical Infarction Complicating Respiratory Failure GEORGE T. FRANGIEH, M.D. EUAS I. TRABOULSI, M.D. BISHARA M. FARlS, M.D. Abstr..ct We deKriM the occurr~nc~of bil~tuu occipit~1 corticAl infuction following r6pir~tory f~ilur~ in two p~ti~nl5 of diff~ring .grt. Th~ pr«ipiuting factors, clinical m.nif6lations, .J.nd ophth.lmologic findings also differed, but the hypoxic dfects on the cortu were Ih~ 5.J.me u evidenced by the IT Kanning studies. Introduction Conditions that compromise the blood supply to both OCcipital cortices may result in transient (W permanent bilateral homonymous hemianopia with or without associated neurologic deficits. I Anoxia to a border zone circulation area with high oxygen requirement has been incriminated 01$ the major etiologic factor.~ We describe two instances in which respiratory failure, a rare cause of cortical blindness,I.) resulted in infarction of both. occipital cortices. Computed tomographic s.ludles confirmed the clinical diagnosis in the (Irst case and were the only diagnostic tools in the second case. The danger of abrupl weaning of mechanical ventilation in the elderly with a compromised circulation is stressed, and the selective vulnerability of the occipital cortex to acute hypoxic injuries is noted. Case Reports Cast 1 A 69·year-old diabetic woman was admitted to our hospital with acute asthmatic attack. She was • known asthmatic for the last 15 years and a type II diabetic, on erratic oral hypoglycemic treatment for the last 20 years. After 3 days of mechanical ventilation and intensive bronchodiI~ tor and antibiotic therapy. her condition stabihzed. She was tried on spontaneous breathing. ~ 1t'1l' Dq:I.rtmnll ~ Oph1mIIl'dosY. Arneric.ln Univer$ If)' 01 ~n,ll Mftik.1 Cmlt'!". 8t1rut. leb.non Septembtor 1984 which she could not tolerate for more than 10 minutes. She sustained a respiratory arrest. was reintubated promptly, and put back on the respirator. On regaining consciousness. the patient claimed complete loss of vision. The general physical examination revealed no other neurologic deficits and an ophthalmologic consultation was requested. The eye examination performed at the bedside revealed no light perception in both eyes, with absent opticokinetic reflex and no response to threatening stimuli. The comeae were dear, the anterior chambers were deep. and the pupils were round and reacted equally well to direct and consensual light stimulation. The lenses showed incipient cataracts and a dilated fundus examination revealed a normal vasculature and optic discs with no norid diabetic changes and no macular lesions. A diagnosis of cortical blindness was made, and a CT scan of the brain was performed which revealed bilateral occipital cortical infarction (Figs. 1 and 2). Case 2 A 3-month-old girl suffocated when her mother fell asleep while breastfeeding her. She was found cyanosed and unresponsive and was admitted to our hopsital where mechanical ven! i1ation was instilutl'd. The physical examination In the emergency room revealed a comatose child with .bulg!n~ fontanelles responsive only 10 painful shmull With movements of all four extremities. The baby convulsed several times with uprolling of the eyeballs and smacking of the lips. Ophthal. m~opr revealed se\'ere optic disc swelling with penpapillary and nerve fiber layer hemorrhages. A CT scan of the brain (Figs_ 3 and 4), revealed extensive ~nrarct!on of the OCcipital and temporal lobes. A diagnosIS of severe brain edema secondary to tissue infarction was made and mannitol and steroid therapy was instituted immediately. Discussion . ~es~iratory arrest has been cited as a rafe preapltatmg factor fOf cortical blindness. I It occurred 155 Occipital Cortical Infarction Figure 1. CT ~"n showing hypodcnse "Tea of infarction in right occipital cortex (with enhancem('nt). Figure 2. CT ~an showing hypodense area of infarction in l('ft occipital cott'), (with enhancement). 156 Figure 3. CT ~ar\ showing hypodense areas of extensive infarction in both occipital poles and temporal lobes (without enhancement), in three of the six children reported by Barnet) and to our knowledge has not been known to occur in an adult. Hoyt and Walsh~ discussed the h,Pothesis first revealed by Lindenberg and Spatz' in 1939. that the border zone regions between the distribution of the three major cerebral arteries suffer most in transient cerebral hypotensive episodes. and that in these areas a relatively more severe tissue hypoxia might be expected. The occipital pole and the striate cortex are such a border zone between the carotid (middle cerebral artery) and the basilar (posterior cerebral artery via its calcarine branch) circulations (Fig. 5). The brain is known to have a high requirement for metabolic energy when compared to other organs of the body.~ It consumes 20% of the oxygen and 70% of the glucose in an adult man although it constitutes only 2% of the total body weight. The effects of ischemia take place very quickly and if it is prolonged beyond a period of a few minutes, the cells will be irreversibly damaged or infarcted. The usual manifestation of striate cortical infarction is a variable loss of visual field in the Journal of Clinical Neuro-ophthalmology Figur~ 4. CT scan showing hypodense areas of e~tensi ...e infarction in both occipitill poles and temporal lobes (with enhancement), Frangieh, Traboulsi, FiUis form of unilateral or bilateral homonymous hemianopsia with or without macular sparing. This defect is usually transient and has been reported to occur after trauma, epilepsy, meningitis, multiple sclerosis, cardiac arrest, and a number of other conditions. l Marquis7 described the essential features of cortical blindness_ These features are: 1) complete loss of all visual sensation including all appreciation of light and dark; 2) loss of reflex lid closure to bright illumination and to threatening gestures; 3) retention of the reflex constriction of the pupils to illumination and to convergence movements; 4) normal-looking retinas by ophthalmoscopy; 5) retention of full extraocular movements of the eyes; and 6) presence or absence of associated neurologic deficits, i.e., hemiplegia, sensory disorders, aphasia, or disorientation. Our case 1 fulfills all the criteria listed by Marquis, and the CT scan documented the extensive infarction of the visual cortex. Many factors seem to have contributed to the development of occipital infarction in case 1. Chronic lung disease with resultant hypoxia and the small vessel affection secondary to diabetes mellitus are possible predisposing factors. It is worthwhile to note that the mechanical ventilation instituted in case I may mildly decrease the oxygen supely to the brain by reducing the cardiac output. Finally, the respiratory arrest tipped off the balance to infarct an area of the brain PCA September 1984 Figurt' 5. Circle showing border zone circulation in occipital cortex, ACA '"' anterior cerebral artery (dasht'd lines); MCA ,. middle cerebral artery: PCA '" posterior cerebral artery_ 157 Ckcipilal Corlicallnfarction whose circulation is anatomically and functionally compromised. At the other extreme of the clinical picture is case 2, where acute respiratory failure and severe hypoxemia with no preexisting pulmonary, vascular, or CNS disease resulted in occipital infarction. The infarction in this case also involved the temporal lobes, and this suggests a failure of the middle and posterior cerebral circulation in addition to the classical watershed area at the tip of the occipital lobe. It is known that the immature brain of young animals resists anoxia more than the mature brain.o Even if this were true for human beings, it seems that the hypoxic insult in case 2 was prolonged enough following respiratory arrest to be beyond the tolerance of the cortical cells to oxygen depletion. CNS factors in the form of vasomotor or neuronal instability have been postulated to playa role in the predisposition to transient cerebral blindness,Q particularly in patients with epilepsy and migraine, which were not noted in our patients. The CT scan in case 1 did not reveal any plaque of multiple sclerosis which is known to cause visual field defects,lo.11 and in case 2, no evidence of tumor or trauma was demonstrated. It appears as if the respiratory failure in both cases was the direct cause of the occipital infarction. CT scanning proved to be of valuable help in assisting to or in making the diagnosis. We would recommend that patients with chronic hypoxic brain injury, even at a subclinical level as in case 1, be closely monitored in acute respiratory failure and be cautiously weaned off mechanical ventilation if its use is unavoidable. Occipital infarction can occur in infants with normal cerebral vascular tree and no associated diseases, and a prolonged hypoxic state would damage this area of the cortex preferentially. References 1. Miller, N.R.: Topical diagnosis of lesions in the visual sensory pathway. In Walsh and Hoyt's: 158 Clinical Neuro-Opllthalmology. Williams & Wilkins, Baltimore, 1982, pp. 140-144. 2. Lindenberg, R.: Compression of brain arteries as pathogenic factor for tissue necrosis and their areas of predilection. I. Neuropalhol. Exp. Nturol. 14: 223243, 1955. 3. Barnet, A.B., Manson, J.I., and Wilner, E.: Acute cerebral blindness in childhood. Nturology 20: 1147-1156,1970. 4. Hoyt, W.F., and Walsh, F.B.: Cortical blindness with partial recovery following acute cerebral anoxia (rom cardiac arrest. Arch. Ophthalmol. 60: 1061-1069,1958. 5. Lindenberg, R., and Spatz, H.: Uber die Thromboendarteritis obliterans der hingefasse. Virchows Arcl1. (Pal/wi. Allat.) 305: 531-557, 1939. 6. Swanson, P.O.: The metabolism of the brain and related disorders. In llltroduclioll to Basic Nturology, H.D. Patlon, J.W. Sundsten, W.E. Crill, and P.O. Swanson, Eds. W.B. Saunders Co., Philadelphia, 1976, pp. 362-373. 7. Marquis, D.G.: Effects of removal of visual cortex in mammals with observations on the retention of light discrimination in dogs. In Proceedill8s of the Associaliou for Research ill Neroous and Melllal Disease, Vol. 13. Williams & Wilkins, Baltimore. 1934, p.558. 8. Fernandez. E.• and Cherniack, R.M.: The use and abuse of ventililtors. In HarriSOIl'S Principles of Intenral Medicine, Updatt 11, K.J. Isselbilcher, R.D, Adams, E. Braunwald, J.B. Martin, R.G. Petersdorf, i1nd J.D. Wilson. Eds. McGraw-Hill Book Co., New York, 1982, pp. 165-185 9. Greenblall, S.H.: Posttraumatic transient cerebral blindness. /.A.M.A. 225: 1073-1076, 1973. 10. Chilmlin, M., and Davidoff. L.M.: Homonymous hemianopia in multiple sclerosis. NeurO!ogli 4: 429, 1954. . 11. Boldt, H,A., Haerer, A.F., Tourtel!ote, W.W., Henderson, J.W., and Dejong, R.N.: Retrochiilsmal visuill field defects from multiple sclerosis. Arch. Neurtl!. 8: 115-125, 1963. Write [or reprillts 10: George T, FTilngieh. M.D., Department of Ophthalmology, American University of Beirut Medical Center. P.O. Box 113-6044, Beirut Lebanon. Journal of Clinical Neuro-ophthalmology |
