The etiology of acute respiratory failure is unknown. Studies by Rowe and Randolph have suggested that the etiology of many respiratory diseases such as asthma, bronchitis, and emphysema are related to the repetitive ingestion of common foods through a basic congenital or acquired defect not necessarily mediated through known immunological pathways.1,2 Randolph has further shown that many other chronic clinical entities are caused by repetitive inhalation and ingestion of many chemicals. It is then logical to think that many patients with acute respiratory failure would have food and/or chemical sensitivities as causative factors in their inability to breathe. If sensitivities are the problem, knowledge of this might alter the final short- and long-term outcome of respiratory failure.


Eight patients ages eighteen to seventy-two admitted to the intensive care unit with acute respiratory failure (ARF) were studied and treated. The methods for determining whether food and/or chemical sensitivities were involved in ARF were the following: (1) careful history of food and chemical sensitivity; (2) blood cytotoxic test of Bryan and Bryan;3 (3) provocative intradermal testing of Rinkel, et al.,4 Lee, et al.,5 and Miller;6 (4) skin titration of Rinkel;7 and (5) total environmental control with withdrawal and direct food challenge of Randolph.2

All these patients were admitted to the intensive care unit with inability to breathe, requiring controlled ventilation by a volume respirator via a tracheostomy or endotracheal tube. Duration of total support by the respirator was from one week (eighteen-year-old) to ten weeks (seventy-two-year-old) with an average time for the group of six weeks. PaO2 was 50 mmHg or below with PaO2 of 60 mmHg or above. Tidal volumes were 200 cc or less, and all patients were clinically dying. Pulses were all above 130, with multiple arrhythmias including multifocal premature ventricular contractions (PVC's) and ventricular tachycardia. All patients initially required controlled ventilation by either respiratory center paralysis with narcotics or muscle paralysis by curare or succinyl choline. All required continuous positive pressure breathing (CPPB) of at least 5 cm of H2O to maintain a PaO2 of 70 mmHg with a PaO2 of 50 mmHg. All patients were on antibiotics including Keflin®, garamycin, carbanicillin, and/or kanamycin. Each patient received enough blood to keep the Hb above 12 and Hct above 35. Fifty grams of albumin were given daily to treat the protein depletion. Intravenous fluids of lactated ringers solution and/or 5% dextrose and/or 50% dextrose in protein hydrolysate were given. Total caloric intake was maintained at 1500 calories/24h or higher. All were given continuous intravenous vitamins including A, B, C, and D, and minerals including K, KHPO, MgSO, Ca, Na, and Cl. The dosage of vitamins was up to 3 gm/24hr of C and B complex, 15,000 units of A, and 1000 units of D. Twenty-five mgn of Aqua mephyton was given 2x/wk and B12 injections 2 cc weekly. Nothing was given by mouth (NPO) to all patients for at least one week. During this period of time, attempts were made to make the diagnosis of food and chemical sensitivities. All eight patients had a strongly positive history compatible with foods and/or chemical sensitivity.











TABLE 14.1


Age Sex Food Chemicals Time on Respirator


43 M 0 + 1 week

18 F + 0 1 week

61 F 0 + 9 weeks

66 M + + 9 weeks

72 M + + 10 weeks

56 M + + 4 weeks

56 M + + 7 weeks

63 M + + 7 weeks


All patients survived, though most of their courses were very stormy. All patients but one required a tracheostomy in order to handle the secretions with adequate endotracheal suction. Three required chest tubes due to pneumo- and hydrothorax. One had dizziness and hearing loss. Six required progressive exercise for one week to two months on an exercycle while still on the respirator in order to develop enough strength to breath spontaneously. With the proper internal and external environmental control, all patients were able to be off all medications two months after discharge.

Two patients had previous food tests prior to their respiratory failure but did not get their environment controlled fast enough to prevent the respiratory failure. One was a dispatcher for an auto repair garage and had obvious severe chemical sensitivities along with food susceptibility as shown by the cytotoxic test. The second patient had food injections and subsequently oral challenge. She went into acute respiratory failure after a meal of beef and potatoes which were her worst two sensitivities. The only patient with pure chemical sensitivity was a spray painter who had a three-year history of nasal problems of stuffiness and sinus headaches and was found to have no food sensitivities by cytotoxic studies and direct challenge. He went into fulminant pulmonary edema (non-cardiac type) after a routine day of spraying using his usual protective mask. The five remaining patients had a combination of food and chemical sensitivities as determined by history, cytotoxic tests, and oral challenge.

All patients but one were willing to institute arduous environmental control after discharge including rotating diets, using less chemically contaminated foods and eliminating as many environmental irritants as possible in the house. The one patient who did not completely eliminate his environmental problems as well as possible kept a gas cooking stove although he had electric heat. He suffered another acute respiratory episode one year after his initial failure. He did not have a respiratory arrest the second time but was in the intensive care unit for a week.. All other patients are off all medications at this time, except for the eighteen-year-old who is taking both pollen and food injections. All patients subjectively say they are breathing better than they have in years and objectively appear so as evidenced by pulmonary function tests. The only meaningful pulmonary function that was done at the time of failure and recovery was the arterial blood gases. PaO2痴 were 70 mmHg or above on room air in all patients at the time of discharge. This appears to be the only significant pulmonary function test since all were apneic on admission. Four patients have returned to work.


It was evident that all the patients studied were moribund upon arrival and were initially saved by the controlled ventilation. Not so evident is the fact that all patients went through a period of detoxification with relative environmental control. The majority of environmental inhalants had been eliminated since the patients were breathing tanked oxygen and compressed air. The internal environment was further controlled by the patients not being able to take anything by mouth. Since all patients initially had NaHCO3 to counteract the lactic acidosis induced by hypoxia, the allergic-endocrine reaction was also corrected. The intravenous vitamins and calories also aided in detoxification. It appears that the high caloric intravenous nutrition was of value in repleting the protein that was lost into the lungs. It is apparent that hyperalimentation was a significant aid in the patient's recovery, and this correlates well with Philpott痴 work with supernutrition in psychiatric patients.8 One interesting facet of this study was why the two corn sensitive patients tolerated the therapy so well. One explanation could be that the higher vitamin intake abated the allergic reaction. A second explanation would be that partial immune paralysis occurred after a severe allergic reaction large enough to produce ARF. This lasted for a few weeks, allowing the patient to tolerate the intravenous sugar. Or thirdly, the patients were only lightly sensitive to corn. In fact only one patient did have a severe susceptibility to corn. However, since it is not known if the response to these sensitivities is through the known immune system, it is not possible to say.

The most striking long-term finding in this study was the fact that these patients needed no medications or respirators at home, which is in contrast to previous studies in patients who survived acute respiratory failure. The fact that four patients returned to work is also worthy of note. Arterial blood gases were normal in all patients by the time discharge occurred, which is in contrast to the majority of conventionally treated patients with ARF. Since the number of patients is small in this series, it is possible that there was an abnormal coincidental number of good respondees. However, if it is doubtful that in eight patients so severely ill that one or two or even all patients would not have had abnormal blood gases upon discharge.

It appears that in certain patients with respiratory failure, food and chemical sensitivity plays an important role as a contributing or even as a causative factor of the respiratory failure. Attention to this aspect, couple with good nutrition, postrespiratory failure lessens the need for medication. One may even be able to look toward a brighter future in a once dismal entity.


  1. Rowe, A.H., and Rowe, A., Jr.: Food Allergy (Its Manifestations and Control and the Elimination Diets) A Compendium. Springfield, Thomas, 1972.
  2. Randolph, T.G.: Human Ecology and Susceptibility to the Chemical Environment. Springfield, Thomas, 1962.
  3. Bryan, W.T.K., and Bryan, M.P.: Allergy in otolaryngology. Otolaryngology. New York, Har-Row, 1972, vol. V.
  4. Rinkel, H.J., Lee, C., Brown, D.W., Willoughby, J.W., and Williams, J.M.: The diagnosis of food allergy. Arch Otolaryngol, 79:71, 1964.
  5. Lee, C.H., Williams, R.I., and Binkley, E.L., Jr.: Provocative inhalant testing and treatment. Arch Otolaryngol, 90:113, July, 1969.
  6. Miller, J.B.: Food Allergy: Provocative Testing and Injection Therapy. Springfield, Thomas, 1972.
  7. Rinkel, H.J.: Inhalant allergy, Part I: The whealing response of the skin to serial dilution testing. Ann Allergy, 7:625, 1949.
  8. Philpott, W.H.: Methods of relief of acute and chronic symptoms of deficiency-allergy-addiction maladaptive reactions to foods and chemicals. Seventh Advanced Seminar in Clinical Ecology, Ft. Lauderdale, Florida, Jan. 9, 1974.