tion does not exceed 0.5 to I mg/d, this highly effective and safe drug should be available in Canada. RALPH D. WJLKINSON, MD, FRCP[C]
Dermatologist in chief Royal Victoria Hospital Montreal, PQ
References 1. STIJTrGEN G: Zur Lokalbehandlung von Keratosen mit Vitamin-A-Saure. Dermatologica 124: 65, 1962 2. PEDACE FJ, SmOUGHTON R: Topical retinoic acid in acne vulgaris. Br J Dermatol 84: 465, 1971 3. Rx Bull 4: Nov/Dec 1973 4. DELUcA HF, RoaERTs AB: Pathways of retinoic acid and retinol metabolism. Am I Clin NuIr 22: 945, 1969 S. OLSON IA: The metabolism of vitamin A. Pharmacol Rev 19: 559, 1967 6. GIROUD A: Vitamine A et t6ratog6n.se. Bull Schweiz Akad Med Wiss 20: 440, 1964
Unusual cause of small-bowel obstruction
the object were removed from the bowel. The postoperative course was uneventful, and on follow-up 6 weeks later he was asymptomatic. It is not generally appreciated that small-bowel obstruction may be caused by food material, particularly fruits.1'2 So-called bolus obstruction due to food can induce mucosal ulceration and even perforation.3 The patient described above denied any recollection of swallowing the device. It is conceivable that he had swallowed the object up to 6 months before, when his abdominal symptoms first appeared. It is unusual that the hooked ends locked themselves in an upright position, entrapping intervening bowel wall and ultimately becoming surrounded by vegetable fibres and fecal material, and thus obstructing the bowel.
To the editor: We report a case of small-bowel obstruction due to a plastic device ("Quik Lok"). These devices are used almost exclusively to seal the open ends of plastic bags so that air will not enter the bag. A 63-year-old white man was admitted to hospital with a 4-day history of severe, crampy, generalized abdominal pain. Over the previous 6 months he had had intermittent abdominal pain, which had become increasingly more frequent and severe. Physical examination revealed signs of bowel obstruction. Three-view abdominal radiographs showed complete mid-smallbowel obstruction. At laparotomy a 7-cm segment of ileum was resected. A plastic device ("Quick Lok") was deeply embedded in an upright position (Figs. 1 and 2) and covered by vegetable fibres and fecal material. It was only with great difficulty that the hooked ends of
We sincerely thank Drs. E. Varty and R. Ginsberg for permission to publish this case.
FIG 1 Device deeply embedded in mucosa of small intestine
FIG. 2-Following removal of device, destruction of bowel mucosa is noted.
ALAN MEDLINE, MD, FRcP[c] Doo SHIN, MD, FRcP[c] Toronto Western Hospital Toronto, Ont.
References 1. NORBERG PB: Food as a cause of intestinal obstruction. Am J Surg 104: 444. 1962 2. CONNELLY HJ, DEL CARMEN BV: Intestinal obstruction due to food. Am Surg 35: 820, 1969 3. MoRsoN BC. DAWSON MP: Gastrointestinal pathology, first ed, Oxford, Blackwell Sci Pubi, 1972, pp 240-41
608 CMA JOURNAL/OCTOBER 4, 1975/VOL. 113
Apresoline
the unique "ADD ON" antihypertensive
INDICATIONS: Various forms of hypertension: fixed essential hypertension, whether of benign or malignant character; hypertension associated with acute and chronic glomerulonephritis; nephrosclerosis; hypertensive toxemias of pregnancy, pre-eclampsia, and eclampsia. DOSAGE: Hypertension: Orally: In general after initiating therapy gradually increase dosage, adjusting according to individual response. As a single agent, initially 10mg, four times daily increasing slowly to a maximum practical dosage of 200mg daily. In combination with other hypotensive agents, lower dosages of APRESOLINE will be appropriate. Parenterally: When there is urgent need, therapy in the hospitalized patient may be initiated intravenously or intramuscularly. Usual dose is 20 to 40 mg, repeated as necessary. Certain patients, especially those with marked renal damage, may require a lower dose. Pressure may begin to fall within a few minutes after injection, with an average maximal decrease occurring in 10 to 80 minutes. Most patients can be transferred to oral APRESOLINE within 24 to 48 hours. Toxemia of Pregnancy: a) Early toxemia and hypertension of pregnancy: One 10-mg tablet orally 4 times daily, slowly increasing the dosage up to 400 mg per d8y, or until a therapeutic result is obtained. b) Late toxemia and pre-eclampsia: Give 20 to 40mg intramuscularly, or slowly by direct intravenous injection or infusion. Repeat as necessary. SIDE EFFECTS: Tachycardia, headache, palpitation, dizziness, weakness, nausea, vomiting, postural hypotension, numbness and tingling of the extremities, flushing, nasal congestion, lachrymation, conjunctival injection, dyspnea, anginal symptoms, rash, drug fever, reduction in hemoglobin and red cell count, giant urticaria, and a lupus-like syndrome (arthralgia) in some cases following administration for long periods. CAUTIONS: Use cautiously in the presence of advanced renal damage and recent coronary or cerebral ischemia. APRESOLINE may potentiate the narcotic effects of barbiturates and alcohol. Peripheral neuritis evidenced by paresthesias, numbness and tingling has been observed. Published evidence suggests an anti-pyridoxine effect and addition of pyridoxine to the regimen if symptoms develop. OVERDOSAGE: Symptoms: Hypotension and tachycardia. Treatment: Gastric lavage or, in the absence of coma, emetics. In the presence of hypotension, cautiously give norepinephrine (intravenously) or ephedrine to raise the blood pressure without increasing tachycardia. Avoid epinephrine. General supportive measures include intravenous fluids, external heat, and elevation of foot of bed. SUPPLIED: All forms contain hydralazine hydrochloride. Tablets of 10mg (yellow, scored); bottles of 100. Tablets of 25mg (blue, coated); bottles of 100 and 500. Tablets of 50mg (pink, coated); bottles of 100 and 500. Ampoules of 1 ml aqueous solution containing 20 mg; boxes of 10.
CIBA DORVAL, QUEBEC
C-5003
Dermatologist in chief Royal Victoria Hospital Montreal, PQ
References 1. STIJTrGEN G: Zur Lokalbehandlung von Keratosen mit Vitamin-A-Saure. Dermatologica 124: 65, 1962 2. PEDACE FJ, SmOUGHTON R: Topical retinoic acid in acne vulgaris. Br J Dermatol 84: 465, 1971 3. Rx Bull 4: Nov/Dec 1973 4. DELUcA HF, RoaERTs AB: Pathways of retinoic acid and retinol metabolism. Am I Clin NuIr 22: 945, 1969 S. OLSON IA: The metabolism of vitamin A. Pharmacol Rev 19: 559, 1967 6. GIROUD A: Vitamine A et t6ratog6n.se. Bull Schweiz Akad Med Wiss 20: 440, 1964
Unusual cause of small-bowel obstruction
the object were removed from the bowel. The postoperative course was uneventful, and on follow-up 6 weeks later he was asymptomatic. It is not generally appreciated that small-bowel obstruction may be caused by food material, particularly fruits.1'2 So-called bolus obstruction due to food can induce mucosal ulceration and even perforation.3 The patient described above denied any recollection of swallowing the device. It is conceivable that he had swallowed the object up to 6 months before, when his abdominal symptoms first appeared. It is unusual that the hooked ends locked themselves in an upright position, entrapping intervening bowel wall and ultimately becoming surrounded by vegetable fibres and fecal material, and thus obstructing the bowel.
To the editor: We report a case of small-bowel obstruction due to a plastic device ("Quik Lok"). These devices are used almost exclusively to seal the open ends of plastic bags so that air will not enter the bag. A 63-year-old white man was admitted to hospital with a 4-day history of severe, crampy, generalized abdominal pain. Over the previous 6 months he had had intermittent abdominal pain, which had become increasingly more frequent and severe. Physical examination revealed signs of bowel obstruction. Three-view abdominal radiographs showed complete mid-smallbowel obstruction. At laparotomy a 7-cm segment of ileum was resected. A plastic device ("Quick Lok") was deeply embedded in an upright position (Figs. 1 and 2) and covered by vegetable fibres and fecal material. It was only with great difficulty that the hooked ends of
We sincerely thank Drs. E. Varty and R. Ginsberg for permission to publish this case.
FIG 1 Device deeply embedded in mucosa of small intestine
FIG. 2-Following removal of device, destruction of bowel mucosa is noted.
ALAN MEDLINE, MD, FRcP[c] Doo SHIN, MD, FRcP[c] Toronto Western Hospital Toronto, Ont.
References 1. NORBERG PB: Food as a cause of intestinal obstruction. Am J Surg 104: 444. 1962 2. CONNELLY HJ, DEL CARMEN BV: Intestinal obstruction due to food. Am Surg 35: 820, 1969 3. MoRsoN BC. DAWSON MP: Gastrointestinal pathology, first ed, Oxford, Blackwell Sci Pubi, 1972, pp 240-41
608 CMA JOURNAL/OCTOBER 4, 1975/VOL. 113
Apresoline
the unique "ADD ON" antihypertensive
INDICATIONS: Various forms of hypertension: fixed essential hypertension, whether of benign or malignant character; hypertension associated with acute and chronic glomerulonephritis; nephrosclerosis; hypertensive toxemias of pregnancy, pre-eclampsia, and eclampsia. DOSAGE: Hypertension: Orally: In general after initiating therapy gradually increase dosage, adjusting according to individual response. As a single agent, initially 10mg, four times daily increasing slowly to a maximum practical dosage of 200mg daily. In combination with other hypotensive agents, lower dosages of APRESOLINE will be appropriate. Parenterally: When there is urgent need, therapy in the hospitalized patient may be initiated intravenously or intramuscularly. Usual dose is 20 to 40 mg, repeated as necessary. Certain patients, especially those with marked renal damage, may require a lower dose. Pressure may begin to fall within a few minutes after injection, with an average maximal decrease occurring in 10 to 80 minutes. Most patients can be transferred to oral APRESOLINE within 24 to 48 hours. Toxemia of Pregnancy: a) Early toxemia and hypertension of pregnancy: One 10-mg tablet orally 4 times daily, slowly increasing the dosage up to 400 mg per d8y, or until a therapeutic result is obtained. b) Late toxemia and pre-eclampsia: Give 20 to 40mg intramuscularly, or slowly by direct intravenous injection or infusion. Repeat as necessary. SIDE EFFECTS: Tachycardia, headache, palpitation, dizziness, weakness, nausea, vomiting, postural hypotension, numbness and tingling of the extremities, flushing, nasal congestion, lachrymation, conjunctival injection, dyspnea, anginal symptoms, rash, drug fever, reduction in hemoglobin and red cell count, giant urticaria, and a lupus-like syndrome (arthralgia) in some cases following administration for long periods. CAUTIONS: Use cautiously in the presence of advanced renal damage and recent coronary or cerebral ischemia. APRESOLINE may potentiate the narcotic effects of barbiturates and alcohol. Peripheral neuritis evidenced by paresthesias, numbness and tingling has been observed. Published evidence suggests an anti-pyridoxine effect and addition of pyridoxine to the regimen if symptoms develop. OVERDOSAGE: Symptoms: Hypotension and tachycardia. Treatment: Gastric lavage or, in the absence of coma, emetics. In the presence of hypotension, cautiously give norepinephrine (intravenously) or ephedrine to raise the blood pressure without increasing tachycardia. Avoid epinephrine. General supportive measures include intravenous fluids, external heat, and elevation of foot of bed. SUPPLIED: All forms contain hydralazine hydrochloride. Tablets of 10mg (yellow, scored); bottles of 100. Tablets of 25mg (blue, coated); bottles of 100 and 500. Tablets of 50mg (pink, coated); bottles of 100 and 500. Ampoules of 1 ml aqueous solution containing 20 mg; boxes of 10.
CIBA DORVAL, QUEBEC
C-5003
