ORIGINAL COMMUNICATIONS. SOME OBSERVATIONS ON BLOOD PRESSURE IN INTRA-CRANIAL COMPLICATIONS OF SUPPURATIVE DISEASES OF THE EAR AND ADNEXA.* By LESTER M. HUBBY, M.D.. Assistant Surgeon, Manhattan Eye, Ear and Throat Hospital. Systolic blood pressure and moderate intra-cranial pressure pursue like paths. Increase in intra-cranial pressure sufficient to compress the medulla has its immediate reflection in the blood-pressure curve. The brain, with its centers presiding over such vital processes as circulation and respiration, being ensconced in an inelastic box, would otherwise be at the mercy of every variation in pressure. Life would cease when the normal blood current, on account of increased intra-cranial pressure, was no longer able to reach and nourish these important nerve cells. Therefore, the heart must work harder and the blood pressure must increase under these conditions. Intrusion of a foreign body or growth, depressed fracture of the skull, intracranial hæmorrhage, oedema or collections of pus, pressure upon the veins of Galen by a tumor at the base of the brain or in the third ventricle and interference with the passage of the cerebro-spinal fluid at such points as the foramina of Monro, Magendie, or Key and Retzius, might thus cause increase in blood pressure. But there is another factor not so well understood at present. There is a limitable region in the cortex of dogs and cats, not co-extensive with the motor zone, but more anteriorly, irritation of which causes rise of blood pressure. This effect is produced by contraction of the splanchnic circulation (W. *Read at meeting of Riverside Practitioners' Society, New York City, November 12, 1907. Lewandowsky and E. Weber, Abt. Klinik, No. 15). Moreover, the dura is a very sensitive structure. Pressure causes headache, and the attempt to strip it from the skull in dogs, even under anæsthesia, causes pronounced irritative symptoms (H. Cushing, American Jour. Med. Sc., Vol. 125, p. 1023). Stimulation of all centripetal nerves, with the exception of the vaso-depressor, produces rise of blood pressure (“Clinical Study of Blood Pressure," T. C. Janeway, p. 21). This, perhaps, is an effort on the part of the organism to wash away the offending irritant. NOW, IN REGARD TO THE EFFECTS OF COMPRESSION. The nerves and nerve cells of the brain are practically incompressible. Therefore, aside from the slight reduction in size of the vessels of the brain by compression, the main safety-valve must be the escape of cerebro-spinal fluid. This is accomplished by a very free communication between the cerebro spinal space and the longitudinal sinus, and the action is valvular, not a mere filtration. This permits an escape of cerebrospinal fluid in increased intracranial pressure, thus restoring the equilibrium in pressures of moderate degree not occurring too suddenly. Theodore Kocher of Berne has divided intracranial compression into four stages (Hunerschütterüng, Hirndruck u. s. w., Nothnagel's Specielle Pathologie und Therapie, 1901, Bd. IX, Thiel 3, Abt. 2, p. 186). STAGE I. CIRCULATORY COMPENSATION. The escape of cerebro-spinal fluid and some narrowing of the venous channels prevents any pronounced degree of venous congestion of the brain. Symptoms lacking or insignificant. STAGE II. FAILURE OF CIRCULATORY COMPENSATION. Venous stasis of the brain, with decreased flow of blood through its capillaries. Symptoms of disturbed cerebral functions-headache, vertigo, restlessness, roaring in the ears, excitement or delirium, an unnatural sleep, etc. Distention and tortuosity of the veins radiating from the optic papilla, with beginning retinal oedema; slowing of the pulse, with or without a marked rise in blood pressure. STAGE III. ADVANCED COMPRESSION. Capillary anæmia. If pressure sufficient to extend to the bulb, vasomotor stimulation and rising blood pressure ensue. As the vasomotor center weakens respiration becomes irregular, the pupils alter rhythmically and other signs indicative of alterations between irritative and paralytic symptoms intervene. The slow vagus pulse appears and stupor ensues. STAGE IV. VASOMOTOR PARALYSIS. Falling blood pressure, irregular cardiac and respiratory efforts, deep coma and death. It has been found that if relief of intracranial pressure be deferred to the fourth. stage the vasomotor centers will often fail to recover. In my series of cases only one passed through the four stages of Kocher. I used Cook's modification of the Riva Rocci sphygmomanometer with its smaller armlet for Cases Nos. II, III, IV, VI and VII, and Janeway's instrument for the others. All the tests were made at the Manhattan Eye, Ear and Throat Hospital during last winter. Case I. E. J., aged 17; female. Acute mastoiditis following otitis media purulenta of three weeks' standing. Mixed bacterial infection; no streptococci. I did a simple mastoid operation, finding cells over aditus and those down to the tip of the mastoid necrosed, and the knee of the sigmoid sinus exposed about a quarter of an inch. Aditus full of granulations. During the next four days the findings were as follows: Blood-pressure findings negative. Acute mastoiditis following chronic otitis media purulenta of four years' standing. Temperature 103° on admission. Mixed bacterial infection; no streptococci. January 29. I did a radical mastoid operation; found a large periosteal abscess behind the ear over the antrum, dura above antrum covered with granulations, a large part of the sigmoid sinus covered with granulations and thickened, as well as a small part of the dura covering the cerebellum. Blood examinations: 99.4° 80 24 90 mm. Koerner flap made on February 5. Feb. 14.. 99.6° 116 Feb. 15.. 99.2° 92 28 100 mm. 2.30 P. M. 26 87 mm. 10.00 A. M. The blood pressure rose 20 mm. on the 9th, four days after operation. A possible explanation of this may be irritation of the dura by the retained secretions in the wound. Case IV. Irene R., age 10. Early in December, 1906, had acute mastoiditis, with subperiosteal abscess, following attack of acute otitis media purulenta. Simple mastoid operation. done at Bridgeport, Conn. The wound was not closed, so Dr. Daniel S. Dougherty performed a secondary mastoid operation at the Manhattan Eye, Ear and Throat Hospital early in January. She improved somewhat, but the wound refused to close, and late in January she began to have vertigo. The tendency to fall was toward the right generally-i. e., away from the affected ear. Blood examinations January 30: 20,888 23,555 Large mononuclear lymphocytes.. Small mononuclear lymphocytes.... Polynuclear leucocytes. 7.7% 11.5% 65.4% Mononuclear leucocytes 13.4% 1.5% Large mononuclear lymphocytes.... 2% 5% Transitorial leucocytes.. 86% 72% .1% 1% .4% 10% Transitional leucocytes. Eosinophiles...... -4% On admission January 31 the left eye fundus found mottled, congested and outline indistinct; the veins congested. A condition of retinitis or hyperæmia. Lateral active nystagmus. In the right eye the optic papilla indistinct and fundus congested. No oedema. Slight retinitis. February 1. Profuse foul discharge from ear. Some staggering on walking. Sways some on closure of eyes. Systolic blood pressure 147 mm. February 2, systolic blood pressure 132 mm. and vertigo decreased. February 3, systolic blood pressure 103 mm.; not so much discharge, though still foul, and no staggering in walking. February 4. Considerable discharge and systolic blood pressure 115 mm. February 5. Eyes examined again. Left disc slightly redder than the right. Veins somewhat congested. Retinas not quite clear and somewhat hyperæmic. No staggering in gait. Still coarse lateral nystagmus on extreme rotation to the left. Necrotic bone all over roof of epitympanum, exposing the dura, which was covered with granulations. Bone over external semi-circular canal and promontory normal. She improved steadily from now on, all the eye symptoms, etc., entirely disappearing. The systolic blood-pressure findings were as follows until the date of her discharge, February 16: Systolic blood Tempressure. perature. Feb. 10.... 108 Feb. II.... 112 Feb. 12.... 114 Feb. 13.... 112 Feb. 14.... 127 Respira Pulse. tion. 99.2° 98.8° 100 20 84 20 98.4° 96 20 98.6° 80 20 After walking. Feb. 15.... IOI Feb. 16.... 107 88 88 February 13, blood examination: Leucocytes... Large mononuclear lymphocytes. Transitional leucocytes. Eosinophiles.. Mast cells. Basophiles. 15,555 10% 22.4% 55.8% 9% .8% .8% .04% .8% This case was very interesting on account of the severity of the intracranial symptoms, such as double optic neuritis, vertigo, high blood pressure and nystagmus, when only a small area of the dura was exposed to necrosing bone. Case V. Irene K., age seven. Early in 1906 simple mastoid operation done for acute mastoiditis, followed immediately by weak, stiff neck, painful on movement. Wound refused to close. August, 1906, secondary mastoid performed. Tip of mastoid found necrosed, but neither sinus nor dura were exposed. She did not improve. March 23 temperature reached 104.2°; pulse 110: respiration 24. During the next five days the temperature reached 103° every afternoon. Thrombosis of lateral sinus suspected. March 15 the left ear began to ache and a swelling appeared on the remnants of the mastoid process. On the 22d a radical mastoid operation was then performed. The antrum was found filled with cholesteatomatous material, the dura above the antrum slightly exposed, the posterior pillar and the ossicles necrotic. Before operation the temperature was 100.2°, pule 114, respiration 24. March 23 became rather dull toward evening. March 24, delirious at 2 A. M., nauseated and vomited, fretful and irritable, pain on movement of head. Temperature 102°, pulse 136, respiration 24, systolic blood pressure 98 and diastolic blood pressure 80. March 25, more stuporous, head retracted, hyperæsthetic, unconscious latein day. Kernig's sign present. C. Lumbar puncture obtained 22 C. cloudy whitish fluid under pressure containing a pure culture of streptococci. Temperature 104.6°, pulse 168, respiration 40, systolic blood pressure 104, diastolic blood pressure 90. March 26, unconscious, head retracted, face flushed, pupils dilated, constant twitchings of arms. Temperature 104.6°, pulse 160, respiration 36, systolic blood pressure 106, diastolic blood pressure 90. March 27, dying. Temperature 105°, pulse 174, respiration 40, systolic blood pressure 92, diastolic blood pressure 80. The blood pressure was affected only slightly in this case, although there was a severe generalized cerebro-spinal meningitis. The findings in two other cases of meningitis not starting from the ear are as follows: Joseph B., age 14. Meningitis following removal of eye for suppurative condition. |