OBSERVATIONS ON VITAMIN DEFICIENCIES*

I N AN EYE, EAR, NOSE, AND THROAT CLINIC OF A JAPANESE PRISON HOSPITAL

MAX EDWARD POHLMAN, M.D. Los Angeles, California

AND EDWARD FRANCIS RITTER, JR., M.D.f

Mattoon, Illinois

In view of the extensive reports on vita­min therapy in the literature, I thought it might be of interest to report observations on vitamin deficiencies seen in the eye, ear, nose, and throat clinic of a Japanese prison hospital, named Bilibid, for American pris­oners of war.

Bilibid, located in the heart of Manila, was originally a Philippine prison and was converted by the Japanese after the fall of Corregidor into a prison hospital.

Bilibid prison consisted of a five-acre com­pound surrounded completely by a 20-foot stone wall, topped with high-tension wires, with sentry-manned observation posts ap­proximately every 300 yards which made an escape virtually impossible. Inside the com­pound there were 15 80-foot long barracks with corrugated tin roofs and barred win­dows ; these became the hospital wards.

The prison hospital was under the super­vision of a captain in the Japanese medical corps who was later sentenced to 25 years' hard labor by the War Crimes Commission. From June, 1942, until October, 1944, Bili­bid Prison was staffed by the United States Navy Medical Corps. From October, 1944, until February, 1945, when the hospital was liberated, the United States Army Medical Corps was in command.

Bilibid was the best equipped and sup­plied medical center in the Philippine Islands due to the fact that the Japanese permitted the Americans to use hospital and medical equipment that had been captured in Manila

* Presented before the Kansas City Society of Ophthalmology, Otology, Rhinology, and Laryn­gology, March, 1951.

t Killed in action—China Sea—October, 1944.

and on Corregidor. The hospital had other advantages in that there was electricity, an ample supply of potable water, and it was relatively rain proof.

Bilibid not only functioned as a hospital but also acted as a clearing house for all of the prison camps in the Philippines. Sick men from working parties would be sent to the hospital for treatment and be replaced by men from convalescent groups. The hospital census would vary from approximately 800 to 1,500 bed patients. The total census of the camp, because of incoming and outgoing drafts of men, would be at times over 3,000.

The eye, ear, nose, and throat clinic was remarkably well equipped in contrast to other prison hospitals. Daily sick call was held and usual treatments were carried out. More than 1,000 men were refracted in the clinic and fitted with lenses through coopera­tion of the Philippine Red Cross.

XEROPHTHALMIA

The first serious eye complaint occurred in November, 1942, when 90 of the worst-looking human specimens imaginable were transferred from Cabanatuan (a prison camp in northern Luzon) to Bilibid for further treatment.

The men were all extremely emaciated, lousy, and suffering from deficiencies of all vitamins. Some of their pellagrous lesions resembled second-degree burns. However, they had been sent to Bilibid because of xerophthalmia with corneal ulceration. This was by no means the sum total of xerophthal-mic cases at Cabanatuan, but merely the worst cases.

These men were placed on the highest 228

OBSERVATIONS ON VITAMIN DEFICIENCIES 229

caloric diet possible but symptomatic treat­ment proved to be ineffective as our supply of vitamins A and D was extremely low. At least 10 percent of the cases terminated with collapsed eyeballs from corneal rupture and others were developing dense leukomas as a result of the corneal ulceration. Fortunately, at this time we received our first Red Cross food and medical supplies and it was re­markable to watch the dramatic response of the eyes to proper food and vitamin therapy.

No new cases of xerophthalmia were seen after the arrival of the Red Cross medical supplies, as it was now possible to issue a multiple vitamin capsule daily to every man in the camp.

OPTIC NEURITIS

There were no further serious eye com­plaints until October, 1943, when we began to see our first cases of optic neuritis. By February, 1944, optic neuritis had reached epidemic proportions; approximately 90 per­cent of the camp inmates had some degree of optic neuritis.

The chief symptoms were photophobia, excessive lacrimation, severe retro-orbital pain and bitemporal headache, eye fatigue, and later loss of vision. At times the loss of vision was dramatic, I have seen cases go from 20/20 vision to counting of fingers in 10 days.

Physical examination showed no increase in intraocular pressure (approximately 40 cases were tested with the tonometer). The cornea was clear except for those who had previously had xerophthalmia. The media were clear. The retinal findings were so typi­cal that we were able to classify them by grade.

CLASSIFICATION

Grade 1. There was a slight hyperemia of the retina but the disc margins were clear.

Grade 2. There was increased venous en­gorgement and hyperemia of the disc mar­gins.

Grade 3. Typical choked disc, the entire fundus resembled a beefsteak.

Grade 4. There would be numerous flame-shaped hemorrhages and, occasionally, fluffy exudative reactions especially around the macular area. The more advanced and older cases would show a typical secondary optic atrophy with marked excavation of the disc.

Medical technicians were trained to take visual fields and, in no time, they became exceedingly proficient and proud of their work. I would estimate that at least 2,000 visual fields were taken by our men.

At first the visual field would show a con­striction of the peripheral fields especially for the colors and an enlargement of the blindspot. Then small central and cecocentral scotomas would appear until eventually the blindspot and central scotoma would blend into one large scotoma.

TREATMENT

We felt that this eye complaint was due to malnutrition and a vitamin deficiency so we named it, how accurately I do not know, beri-beri optic neuritis. Since there was no way to improve the diet, our main treatment consisted of massive dosage of vitamins. Our course consisted of:

First week. 50 mg. vitamin B1; subcutane-ously daily; 200 mg. vitamin C, subcutane-ously daily; 100 mg. nicotinic acid by mouth; four vitamin-A and four vitamin-D capsules daily.

Second week. 20 mg. vitamin Bx sub-cutaneously daily; 100 mg. vitamin C, sub-cutaneously daily; 200 mg. nicotinic acid by mouth; four vitamin-A and four vitamin-D capsules.

Third week. 10 mg. vitamin Bj, subcu-taneously daily; 25 mg. vitamin C by mouth ; 300 mg. nicotinic acid; four vitamin-A and four vitamin-D capsules.

Fourth to seventh week inclusive. 5.0 mg. vitamin B : , daily orally; 25 mg. vitamin C orally; 200 mg. nicotinic acid; four vita­min-A and four vitamin-D capsules.

Following the intensive vitamin course, the visual fields would be retaken and the fundus reexamined. If there were no im-

230 MAX EDWARD POHLMAN AND

provement, or if the findings were worse, the vitamin course would be repeated.

In the acute cases, the patients would be atropinized for four weeks and would wear eyeshields made of cardboard with pinpoints for vision. Dilation of the pupils would usually relieve the complaint of severe bi­lateral temporal headache in the majority of the cases.

Efforts were made to eliminate tobacco as it was felt that it would further damage the inflamed optic nerve. However, despite our warnings of total blindness, we could not stop the men from smoking.

The intensive vitamin courses were not enough, however, the men also required a well-balanced diet that we were not able to furnish. I believe that vitamin therapy did prevent a great number of the men from de­veloping optic atrophy, as some cases actu­ally showed an improvement in the eye-grounds and visual fields after several courses of vitamins. The advanced cases of optic atrophy did not react at all.

DISCUSSION

At the time we were seeing optic neuritis in epidemic proportions, it was interesting to me that very few patients complained of any ear symptoms such as tinnitus, hear­ing loss, or vertigo. Theoretically, the eighth nerve should have been just as sensitive to malnutrition and vitamin deficiencies as the optic nerve.

With this in mind, approximately 25 cases of advanced optic atrophy were studied from an ear standpoint. Hearing tests were made with tuning forks supplemented with the

EDWARD FRANCIS RITTER, JR.

standard Navy whispered and spoken voice tests. Not one of these cases showed any appreciable hearing loss. Caloric tests with both hot and cold water on these individuals showed no remarkable change from the normal.

The same findings were obtained when 50 cases of acute, grade-4 optic neuritis were studied. Some of these individuals even suffered a dramatic loss in vision during the week they were being examined, yet showed no auditory changes.

Despite the extreme emotional and nervous strain of being imprisoned, with each day being a fight for survival, it is interesting that we did not see the acute labyrinthine reactions or Menierelike syndromes that one would expect in such an environment. Pos­sibly the low protein, low salt, rice diet may have been a factor. Other surveys in the camp revealed most of the men to have slow pulse rates with unusually low blood pres­sures.

A possible explanation for the greater resistance of the eighth nerve to malnutri­tion in contrast to that of the optic nerve was that noise at Bilibid was negligible. Maybe the number of nerve deafened would have equalled those with optic neuritis if the men had been imprisoned in a noisy place.

2200 West Third Street (5).

I would like to pay tribute to my colleague, Dr. Ritter, who was the ophthalmologist in our clinic and helped conduct this survey. Dr. Ritter lost his life when he and 1,800 other American prisoners of war were transported to Japan in an unmarked prison ship that was torpedoed by one of our sub­marines in the China Sea with five survivors.