attending one of the periodic "open houses" that are arranged at the DCIEM. Roy J. SHEPHARD, MD, PH D Professor of applied physiology Department of preventive medicine and biostatistics University of Toronto Toronto, Ont.

Dermoid cyst of the cecum To the editor: To date only three cases of dermoid cyst of the cecum have been reported in the literature. We report a new case of this rare entity.

A 53-year-old woman was admitted to hospital in July 1976 complaining of passing frank blood in the stools following intermittent episodes of melena. Her medical history was unremarkable apart from a hysterectomy and appendectomy performed in 1956. She also had had intermittent epigastric distress for more than 20 years. Rectal examination revealed blood but there were no other positive findings. Laboratory investigation gave the following values: hemoglobin, 9.2 g/dL; leukocyte count, 6.7 X 105/L; platelet count, 181 X 109/L; prothrombin time, 13 secodds; and partial thromboplastin time, 35 seconds. The appearance on sigmoidoscopic examination was normal to 18 cm and on colonoscopic examination normal to 100 cm although some difficulty was experienced in negotiating the cecum. Roentgenography of the gastrointestinal tract showed spasm at the duodenal bulb. In view of the history and findings a vagotomy and pyloroplasty were performed from which the patient made an uneventful recovery. Within the next 7 months the patient was readmitted to hospital on four separate occasions. On each of these occasions her complaint was the passage of melena stools but physical examination disclosed no abnormality. At various times she was subjected to gastroscopy, aortic angiography, colonoscopy and laparotomy when intraoperative endoscopy failed to reveal the source of the repeated hemorrhages. On one admission the hemoglobin concentration was only 8.5 g/dL and a blood transfusion was given. On the final admission, in February 1977, she was in shock from profuse rectal bleeding. After she had been resuscitated a hepatic flexure colostomy

was performed. One week later there was bleeding from the proximal opening of the colostomy. Colonoscopy of the proximal limb revealed several questionable hemorrhagic areas in the cecum but no definite bleeding site. A right hemicolectomy and an ileotransverse colostomy were performed subsequently. She made an uncomplicated recovery and has been free of symptoms since. Pathologic examination revealed an irregular polypoid mass 4 cm in diameter, 5 cm distal to the ileocecal valve. The cut surface showed an irregular cavity containing old blood coagulum. Histologic sections of the cecum taken through this mass showed marked infiltration of the wall by acute and chronic inflammatory cells. Several fissure tracks were present that extended to the serosal surface. On the serosal surface were fragments of a cyst composed of stratified squamous epithelium with keratinous differentiation. There was a considerable amount of blood within the cyst cavity. In some areas of the bowel wall there was a foreign body giant cell reaction apparently to the keratinous debris. Skin appendages were evident within the stratified squamous epithelium.

A review of the literature reveals only three similar cases. Gowdy,1 in 1956, reported the first case, in a 21year-old woman presenting with intestinal obstruction. In 1971 Kay2 reported a case of a 1-year-old girl who had two cecal cysts, one lined with epidermis accompanied by sebaceous glands and hair follicles, the other lined with gastric-type glands. A third case, reported in 1973,. was of a man aged 28 years who presented with a right lower quadrant mass, which, at laparotomy, was found to be a cecal cyst filled with sebaceous material and hair and lined by stratified squamous epithelium. All the authors agree that these cysts undoubtedly originated as a result of sequestration of ectopic tissue during embryologic development. A similar but distinctly different lesion is an epidermal cecal cyst. Pan, Rogers and Klass,4 in 1961, reported the first case of an epidermal cyst of the cecum and since that time two further cases have been reported.5'6 All these cysts were composed of stratified

.tIe I-Cases of epldermoldan4denpojd cysts of the cecunt Patients' age (yr), and sex 21, F 22, F 21,F 71,11 1,F 28, M right lower quadranL.

Case and reference nos. V 2'

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1372 CMA JOURNAL/DECEMBER 17, 1977/VOL. 117

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squamous epithelium without skin appendages. Epidermal cysts probably resuit from implantation of epidermal tissue during a surgical procedure, such as appendectomy. All reported cases of both types of lesion are summarized in Table I. J.F. MOSSEY, B Sc, MD

Department of surgery University of Alberta Edmonton, Alta.

LEN RIVERS, MD, FRCS[C] PETER PATrERSON, MD, ERc2P[CJ Departments of surgery and pathology Misericordia Hospital Edmonton, Alta.

References 1. GOWDY JM: Dermoid cyst of cecum. Gastroenterology 31: 447, 1956 2. KAY 5: Teratoid cyst of the cecum. Am I Dig Dis 16: 265, 1971 3. FINLAY-JONES LR, SINGH A: Dermoid cyst of the caecum. Med I Aust 2: 377, 1973 4. PAN A, ROGERS AG, KLAss AM: Epidermoid cyst of the cecum. Can Med Assoc 1 84:

1075, 1961 5. PEAR BL, WOLFF JN: Epidermal cyst of the

cecum. JAMA 207: 1516, 1969

6. CANDREVIOTIs N: Epidermoid cyst of cecum. JAMA 192: 425, 1965

Management of hypothermia To the editor: In a recent communication (Can Med Assoc J 117: 16, 1977) Dr. V. Wood reported the resuscitation of a patient with profound hypothermia (rectal temperature, 21 0C) and stated that only one other patient with accidental hypothermia has been reported to have survived a lower body temperature.' In fact, the lowest recorded core temperature of a survivor of hypothermia was 18 0C in an inebriated young woman as reported by Laufman.' Although mortality in hypothermia has been linked closely with underlying or associated disease states,3'4 the method of rewarming may also be a determinant.' Despite the lack of unanimity of opinion regarding indications for core rewarming, many authorities now advocate this mechanism for patients whose temperature is below 320C. In addition to the methods available for core rewarming mentioned by Sereda,6 including peritoneal dialysis, partial cardiopulmonary bypass and inhalation of heated oxygen, treatment with colonic infusions of warmed water was discussed in a recent report documenting the resuscitation of three patients with profound hypothermia (lowest temperature, 21.1 0C).7 As outlined by Dr. Wood, physiologic consequences of external rewarming make core rewarming techniques attractive, since many of these methods of reversing hypothermia can be rapidly instituted and require equipment available in most hospitals. Active external rewarming by water immersion, as advocated by Hunt,8 may interfere with adequate monitoring of the pa-

TOIL

tient, precipitate ventricular fibrillation due to the movement required and seriously hamper cardiopulmonary resuscitation if it becomes necessary, as is frequently the case. Physicians should be aware of these considerations when determining a therapeutic approach to the patient with hypothermia.

XIm.)

New topical corticosteroid

JAMES B. RUELER, MD Staff physician Ambulatory care medical services Veterans Administration Hospital Portland, Ore.

COMPOSITION

Each g of TOPICORT Emollient Cream contains 2.5 mg (0.25%) of desoximetasone. INDICATIONS For the relief of acute or chronic corticosteroidresponsive dermatoses.

CONTRAINDICATIONS

In untreated bacterial, fungal and moat viral lesions of the skin (including herpes simplex, vaccinia and varicella) and hypersensitivity to any of the components of the preparation.

WARNINGS

Systemic side-effects including adrenal suppression may occur with topical corticosteroid preparations, particularly when these preparations are used over large areas or for an extended period of time or with occlusive dressings. The safety of topical corticosteroid preparations durin g pregnancy and lactation has not been established. When md icated, they should not be used extensively, in large amounts or for prolonged periods of time on pregnant patients or nursing mothers. TOPICORT Emollient Cream 0.25% is not for ophthalmic use.

PRECAUTIONS

If local infection exists, suitable concomitant antimicrobial or antifungal therapy should be administered as primary therapy. If a favorable response does not occur promptly, application of the corticosteroid should be discontinued until the infection is adequately controlled. If local irritation or sensitization develops, TOPICORT Emollient Cream should be discontinued and appropriate therapy instituted. The use of occlusive dressings increases the percutaneous absorption of corticosteroids. For patients with extensive lesions it may be preferable to use a sequential approach, treating one portion of the body at a time. The patient should be kept under close observation if treated with large amounts of topical corticosteroid or with the occlusive technique over a prolonged period of time. Occlusive dressings should not be applied if there is an elevation of body temperature. Patients should be advised to inform subsequent physicians of the prior use of corticosteroids. Topical corticosteroids should be used with caution on lesions close to the eyes.

ADVERSE REACTIONS

TOPICORT Emollient Cream 0.25% is well tolerated; side-effects have been extremely rare. Similar to other topical corticosteroid preparations, it may cause burnin. sensation, dryness, itching, erythema, change in skin pigmentation, folliculitis, pyoderma, striae, telangiectasia and skin atrophy. The following reactions are reported when corticosteroid preparations are used extensively in intertriginous areas or under occlusive dressings: maceration of the skin, secondary infection, striae, miliaria, hypertrichosis, localized skin atrophy, adrenal suppression and posterior subcapsular cataracts.

OVERDOSAGE Symptoms

Toxic effects due to prolonged percutaneous absorption of large amounts of corticosteroids may include: reversible suppression of adrenal function, skin striae, ecchymoses, discoloration or atrophy, acneiform eruptions, hirsutism, infection. Prolonged systemic corticosteroid action may cause hypertension, peptic ulceration, hypokalemia, muscle weakness and wastage and subcapsular cataracts.

Treatment

Treatment should include symptomatic therapy and discontinuation of corticosteroid administration. In chronically affected patients, a gradual discontinuation may prevent the development of steroid withdrawal symptoms.

DOSAGE AND ADMINISTRATION

Apply a thin film of TOPICORT (desoximetasone) Emollient Cream 0.25% to the affected skin areas twice daily. Rub in gently.

SUPPLY

TOPICORT Emollient Cream 0.25% is supplied as a formulation containing 0.25% desoximetasone, in tubes of 20 g and 60 g.

Hoechst Pha,maceui.cai O,o,s,on. Canad,an Hoechst Lid. Moni.eaI EO,dHOECOS,R.O Tode..kccfHce.h.AG

1477/7107/E

References 1. WIcKSTROM P, RuIx E, LILJA GP, et al: Accidental hypothermia. Core rewarming with partial bypass. Am J Surg 131: 622, 1976 2. LAUFMAN H: Profound accidental hypothermia. JAMA 147: 1201, 1951 3. WEYMAN AE, GREENBAUM DM, GRACE WJ: Accidental hypothermia in an alcoholic populalion. Am J Med 57: 13, 1974 4. HUDSON LD, CONN RD: Accidental hypothermia. Associated diagnoses and prognosis in a common problem. JAMA 227: 37, 1974 5. GREGORY RT, DOOLITTLE WM: Accidental hypothermia. Part II: Clinical implications of experimental studies. Alaska Med 15: 48, 1973 6. SEREDA WM: Treatment of hypothermia (C). Can Med Assoc 1 112: 931, 1975 7. Bo.sir. E: Re-warming of three poisoned patients with profound accidental hypothermia. Ugeskr Laeger 139: 706, 1977 8. HUNT PK: Treatment of hypothermia (C). Can Med Assoc 1 112: 931, 1975

Primary Hemophilus influenzae pneumonitis in an adult To the editor: In children it is well recognized that Hemophilus influenzae commonly causes meningitis and, less frequently, epiglottitis and otitis media. In adults epiglottitis and, more commonly, acute exacerbations of chronic bronchitis are due to this organism. Acute primary bronchopneumonia in an adult without any predisposing disease, as described below, is a rare manifestation of infection with H. influenzae. A 44-year-old man, with a record of good health and no underlying pulmonary or cardiovascular disease, became acutely ill with cough, chills and vague right-sided chest pain. The cough, initially dry, rapidly became productive of sputum; the chest pain increased in severity, became sharp and midsternal and was made worse by coughing and movement. On admission the patient looked ill and was flushed and sweating. The pulse rate was 96 beats/mm, respiratory rate 32/mm and temperature 39.5 0C. Rales were heard at both lung bases. Findings on examination of all other systems were normal. A chest roentgenogram at the time of admission showed patchy infiltrates in the lower lobes and the right middle lobe, more extensive on the right than the left. There was no effusion in either pleural space. The leukocyte count was 12.0 X 109/L (37% polymorphs, 54% band cells and 7% lymphocytes). A diagnosis was made of bronchopneumonia. Sputum and blood

were sent for culture and sensitivity tests and the patient was given ampicillin, 1 g q6h intravenously. The sputum was copious and purulent; Gram's stain and culture demonstrated no recognizable pathogens. After 2 days' incubation the blood cultures revealed organisms subsequently shown to be H. influenzae sensitive to ampicillin. The organism was tested for production of penicillinase by means of a modified starch iodide reaction and gave a negative reaction. The patient's condition did not change during the ensuing 48-hour period but after the dosage of ampicillin was changed to 2 g q6h intravenously there was progressive clinical improvement. The fever settled after 5 days of therapy and there was roentgenologic resolution at the time of discharge when the leukocyte count had decreased to 7.9 X 109/L (51% polymorphs and 10% band cells). The patient was discharged with instructions to take ampicillin orally for 7 days. Standard medical texts have drawn attention to H. influenzae as a cause of pneumonitis secondary to an underlying respiratory problem such as pre-existing bacterial pneumonitis or viral influenza. The rarity of this organism as the etiologic agent in primary bacterial pneumonitis was confirmed by Marraro, McCleskey and Mitchell1 in a recent publication in which they reported pneumonitis in a mother and her child caused by penicillinase-producing H. influenzae biotype 3 isolated from a number of sites. This case and our own, the organism from which was not available for subsequent serotyping or biotyping, indicate the importance of H. influenzae as a causative agent of primary bacterial pneumonitis in adults. It would therefore appear pertinent to emphasize the need for the laboratory staff to report encapsulated strains of this organism isolated from sputum of patients with pneumonitis and perhaps from adults with pharyngitis; the frequent occurrence of H. influenzae, mainly nonencapsulated strains, in the upper respiratory tract of adults often leads laboratory staff to ignore a few such colonies in the belief that they are merely commensals. Further, although not constituting a problem in our particular case, the increasing prevalence of p-lactamase-producing H. influenzae underlines the need for the laboratory staff to test significant clinical isolates for the production of the enzyme. I.W. GEERE, MB, CH B, FRCP[C] M.K.B. SEGU, MD Regina General Hospital

Regina, Sask.

Reference I. MARRARO RV. MCCLESKEY FK, MrFCHELL IL:

Pneumonia due to Haemophilus in!luenzae (H. aegyptius) biotype 3. J Clin Microbiol 6: 172, 1977

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