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The alar base composite graft in cleft lip noses
ABSTRACTS
importance of monitoring the blood levels when using this valuable drug. In this study more frequent administration and larger dosage requirements to maintain an effective blood concentration (20 to 30 #g/ml) made individualization of the dosage regimen necessary. Drug toxicity was not observed.--William K. Sieber Cimetidine Inhibits Burn Edema Formation. T. Yoshioka, IV.
W. Monafo, V. H. Ayvazian, et al. Am J Surg 136:681-685, (December), 1978. Based on the assumption that burn wound edema may be caused by histamine-mediated increase in extravascular water-flux and experimental evidence that H~ inhibitors could not be used to prevent edema formation after thermal injury, the investigators studied the effects of large doses of cimetidine (3-6 times the usual clinical dose). A series of rats pretreated with 0.2 mg/g body weight of Cimetidine with an additional 0.1 mg/g given at 4 and 8 hr were investigated following induction of a full thickness 20% body surface area burn and compared to control group similarly burned but not treated with Cimetidine. There was a marked inhibition of burn wound edema formation, potassium ettlux, and sodium influx in the group treated with Cimetidine. Differences were statistically significant to 72-hr post-burn. In a second set of experiments, treatment with cimetidine was delayed so that treatment was begun at 1,4, and 14 hr post-burn. Intragroup differences decreased as the interval between injury and treatment increased. There was no detectable effect of cimetidine when it was given beginning 14 hr after burn injury. In a third set of experiments, a rough dose response curve was constructed. At 1/4 the original dose, potassium efltux was still significantly inhibited although it was less than that originally observed. The authors could not differentiate whether or not the blunting of ion fluxes was secondary to the minimization of burn wound edema or some direct protective effect of Cimetidine on the cellular membrane function. They infer that this technique may be worthy of study in man since man is highly histamine sensitive and since the drug may be effective in lower doses (i.e., clinical range) when given by continuous administration over the first 24-36 hr.--Carey P. Page
High Voltage Eleetrie Injury. C. Wilkinson and M. Wood. Am J Surg 136:693-696, (December), 1978. This article from the Maricopa County General Hospital in Phoenix, Arizona, summarizes the clinical course of 28 patients with electrical injury due to an electrical potential of more than 1,000 volts treated between 1973 and 1977. The article is of note because of the excellent summary of pathophysiology of electrical injury, the establishment of general guidelines for treatment based on this pathophysiology, and the presentation of an excellent bibliography. The authors point out that it is the conversion of electrical energy into heat which produced the electrical injury, the degree of injury being directly proportional to the resistance of the tissue to electrical flow and inversely proportionally to the sensitivity of the tissue to the injury. One pathophysiologic sequelae of high voltage electrical injury is the coagulation of multiple small vessels resulting in tissue death of the organ system involved. Specifically, it may cause delayed rupture of large blood vessels, death of peripheral nerves, death of
489
affected muscles, and transmural necrosis of the intestines. Direct central nervous damage is usually transient, but the resulting convulsions may result in musculoskeletal injuries both from the force of the convulsions and from the fall which often follows. Suppression of the respiratory center may result in respiratory arrest. Tendons may be melted by the high voltage injury. Cardiac injuries may result either from ventricular fibrillation or myocardial or conduction system abnormalities from microvascular injuries. Not uncommonly the extent of injury from high voltage electrical burns is underestimated. This results in inadequate fluid resuscitation with concommitant decrease in urinary output, diminished ability of the kidney to handle the filtered myoglobin and hemoglobin load which results from hemolysis and myonecrosis. Renal failure may ensue in a clinical situation similar to the crush syndrome. The treatment of high voltage injuries is primarily aimed at removal of the patient from the source of injury, establishing cardiopulmonary resuscitation, initiating vigorous fluid replacement, insuring an adequate urinary output along with urinary alkalinization, and maintenance of local tissue perfusion by both local and systemic means. Escharotomy and fasciotomy are performed early-on to insure optimal perfusion of injured extremities. The burn surface wound is managed according to usual guidelines. Because of severe peripheral tendon and nerve injuries along with extensive local tissue destruction, amputation is more frequently used in the treatment of electrical burns than in thermal burns. The authors point out the difficulty in balancing the preservation of an extremity with the risk of death from sepsis in an effort to save an extremity which may be useless. Of four mortalities among the 28 patients reported in this series, one resulted from severe central nervous system injury, one from respiratory insufficiency, and two from multisystem failure and sepsis.--Carey P. Page
HEAD AND NECK Antrochoaflal Polyps. R. Towbin, J. S. Dunbar, and K. Bove. Am J Roentgenol 132:27-31, (January), 1979. Five children with antrochoanal polyps, a solitary benign tumor arising from the maxillary antrum of a nonatropic patient, presented with either nasal obstruction, epitaxis or maxillary sinus opacification. A review revealed about 71% of patients with this lesion to be in the 10-39 yr age group with an 1.3:1 male-to-female ratio. The radiologic features include an opacified maxillary antrum which appears expanded and a nasopharyngeal mass. The differential diagnosis includes normal or hypertrophied inferior turbinates, chronic hypertrophic polypoid rhinosinusitis, juvenile nasopharyngeal angiofibroma, mucus retention cyst, mococele, and malignant tumors of the nasopharynx. In children the latter include lymphoma, rhabdomyosarcoma, lymphoepithelioma, olfactory neruoblastoma, and chordoma. The CaldwelI-Luc operation yields the best results since removal by snare and avulsion carries about a 20% recurrence r a t e . Randall HI. Powell The Aler Base Composite Graft in Cleft Lip Noses. D. O.
Maisels. Br J Plast Surg 31:220-221, (July), 1978. The technique of the transfer of a free composite graft from the alar base to the opposite nostril is described. It is
ABSTRACTS
490
wedge-shaped and would be valuable in cleft lip noses and deficiencies due to injury.--A. Jolleys
Autogenous Septal Cartilage Graft in the Correction of Cleft Lip Nasal Deformity. Yoshihiko Nishimura and Yoichi
Ogino. Br J Plast Surg 31:222-226, (July), 1978. The use of cartilaginous struts to support the tip of the nose in cleft lip nasal deformity is discussed. It is suggested that a quadrilateral piece can be taken from the nasal septum, particularly when a submucous resection is frequently needed in these cases. Unfortunately, such a procedure is inappropriate in children, or when the septum is extremely deformed.--A. Jolleys
A Simplified Technique for Correction of the Cleft Lip Nasal Deformity. S. Ariyan and T. J. Krizek. Ann Plast Surg
1:568-574, (November), 1978. The deformity of the cleft lip nose is characterized by four components; collapse of alar cartilage; shortened distance from the nasion to the alar corner; widened nostril floor, or sill; and shortened nasal orifice. The author's technique seeks to overcome and correct all of these component deformities. The technique consists of freeing the malpositioned alar corner, where it is attached to the nasolabial fold. In addition, the skin of the lower portion of the nose is completely mobilized from the underlying cartilaginous skeleton and the malrotated ala is repositioned by an attachment to the contralateral upper lateral cartilage. The alar rim is inset into a normal location on the nasolabial fold to complete the procedure. The clinical pre- and postoperative photos demonstrate very satisfactory results with this technique. It is advised as an additional technique to the armamentarium of those surgeons performing this type of surgery.--A. B. Sokol
Anatomical Findings in Median Cleft of Upper Lip. D. R.
Wiemer, S. A. Hardy, and M. Spira. Plast Reconstr Surg 62:866-869, (December), 1978. Median clefts of the lip are quite rare and are divided into two groups. The first are generally incompatable with life, associated with an agenesis of the frontonasal process and associated with cerebral anomalies. Second, are less severe median clefts not associated with cerebral anomalies. The latter clefts may or may not have hypertelorism, while the former are generally associated with hypotelorism. The authors report on the surgical repair of two median clefts of the lip not associated with cerebral anomalies. In general, they were repaired with a straight line repair. Both children have had excellent results as indicated by pre- and postoperative photographs. Median clefts of the lips associated with cerebral anomalies, are generally unrepaired because of the rather bleak outlook for survival. The operative findings are set forth along with the surgical techniques. A review of the embryology leading to the median clefts is given by the authors. Essentially, the defect appears to be due to a failure of mesodermal migration into the fused frontonasal and maxillary processes.--A. B. Soko!
Angioma of the Mandible. C. Riberti and A. Bertani. Rass
Ital Chir Ped 19:352, 1977. A 6-yr-old boy was admitted because of a cavernous angioma of the left of mandible. At 24 me of age, the patient presented with a mass in the left parotid region that selective arteriography proved to be a hypertrophic angioma of the parotid gland. The patient was treated with local injection of triamcinolone acetonide and a complete ~gression of the angioma was obtained within 5 me. The total dosage injected was 90 mg. Two years later a swelling was noted on the left mandible that expanded mainly within the oral cavity. After slight trauma the lesion rapidly increased. On admission a mass of a bluish discoloration and of the size of an apricot invading the alveolus was found. Radiographic examination revealed two large osteolytic defects of the anterior twothirds of the left mandible. Selective arteriography showed that the lesion was of a vascular nature and was fed by an artery branching from the internal maxillary artery. The left external carotid artery was ligated and the controlateral external carotid artery was temporarily occluded. Curettage of the bony cavity was then performed, the residual cavity was filled with gauze for 4 days. Difference between the two angiomata are discussed on the basis of the angiographic aspects. No histologic findings are reported.--C. A. Montagnani Surgical Correction of the Facial Deformities of Acromega-
ly. J. M. Converse and D. C. Baker. Ann Plast Surg 1:612616, (November), 1978. A case report of the facial reconstruction in a white, male, acromegalic patient along with clinical, diagramatic and dental occlusal photos is given for the readers edification. A review of the historical contributions to the condition of acromegaly is given including the origin of the term acromegaly from Greek, referring to large extremities. In addition, the pathology of acromegaly is reviewed. The plastic surgical treatment in this particular case, required four operative stages. The stages were: correction of the verticle height of the mandible, mandibular prognathism correction by bilateral sagittal osteotomy of the ramus, rhinoplasty and iliac bone graft, and, finally, various soft tissue corrections. The author points out that although there are 300 new cases of acromegaly discovered each year, the plastic surgical treatment reviewed in the literature has, prior to this article, numbered only one contribution.--A. B. Sokol The Role of Pressure Therapy in Management of Earlobe Keloids: Preliminary Report of a Controlled Study. B. Brent.
Ann Plast Surg 1:579-581, (November), 1978. Earlobe piercing results in keloid complications in a significant number of individuals. The etiology of this collagenous "tumor" remains obscure. Its treatment is controversial and ranges from excision, steriod injection, and irradiation. Recently, there has been reported success in treating burn scars with compression. To this end, the author has created a decorative, spring-pressure earring, which exerts constant light pressure and is applied 2 wk after the initial keloid excision. The author reports on seven patients in whom bilateral earlobe keloids resulted following ear piercing. The initial results have been excellent with the use of the pressure
importance of monitoring the blood levels when using this valuable drug. In this study more frequent administration and larger dosage requirements to maintain an effective blood concentration (20 to 30 #g/ml) made individualization of the dosage regimen necessary. Drug toxicity was not observed.--William K. Sieber Cimetidine Inhibits Burn Edema Formation. T. Yoshioka, IV.
W. Monafo, V. H. Ayvazian, et al. Am J Surg 136:681-685, (December), 1978. Based on the assumption that burn wound edema may be caused by histamine-mediated increase in extravascular water-flux and experimental evidence that H~ inhibitors could not be used to prevent edema formation after thermal injury, the investigators studied the effects of large doses of cimetidine (3-6 times the usual clinical dose). A series of rats pretreated with 0.2 mg/g body weight of Cimetidine with an additional 0.1 mg/g given at 4 and 8 hr were investigated following induction of a full thickness 20% body surface area burn and compared to control group similarly burned but not treated with Cimetidine. There was a marked inhibition of burn wound edema formation, potassium ettlux, and sodium influx in the group treated with Cimetidine. Differences were statistically significant to 72-hr post-burn. In a second set of experiments, treatment with cimetidine was delayed so that treatment was begun at 1,4, and 14 hr post-burn. Intragroup differences decreased as the interval between injury and treatment increased. There was no detectable effect of cimetidine when it was given beginning 14 hr after burn injury. In a third set of experiments, a rough dose response curve was constructed. At 1/4 the original dose, potassium efltux was still significantly inhibited although it was less than that originally observed. The authors could not differentiate whether or not the blunting of ion fluxes was secondary to the minimization of burn wound edema or some direct protective effect of Cimetidine on the cellular membrane function. They infer that this technique may be worthy of study in man since man is highly histamine sensitive and since the drug may be effective in lower doses (i.e., clinical range) when given by continuous administration over the first 24-36 hr.--Carey P. Page
High Voltage Eleetrie Injury. C. Wilkinson and M. Wood. Am J Surg 136:693-696, (December), 1978. This article from the Maricopa County General Hospital in Phoenix, Arizona, summarizes the clinical course of 28 patients with electrical injury due to an electrical potential of more than 1,000 volts treated between 1973 and 1977. The article is of note because of the excellent summary of pathophysiology of electrical injury, the establishment of general guidelines for treatment based on this pathophysiology, and the presentation of an excellent bibliography. The authors point out that it is the conversion of electrical energy into heat which produced the electrical injury, the degree of injury being directly proportional to the resistance of the tissue to electrical flow and inversely proportionally to the sensitivity of the tissue to the injury. One pathophysiologic sequelae of high voltage electrical injury is the coagulation of multiple small vessels resulting in tissue death of the organ system involved. Specifically, it may cause delayed rupture of large blood vessels, death of peripheral nerves, death of
489
affected muscles, and transmural necrosis of the intestines. Direct central nervous damage is usually transient, but the resulting convulsions may result in musculoskeletal injuries both from the force of the convulsions and from the fall which often follows. Suppression of the respiratory center may result in respiratory arrest. Tendons may be melted by the high voltage injury. Cardiac injuries may result either from ventricular fibrillation or myocardial or conduction system abnormalities from microvascular injuries. Not uncommonly the extent of injury from high voltage electrical burns is underestimated. This results in inadequate fluid resuscitation with concommitant decrease in urinary output, diminished ability of the kidney to handle the filtered myoglobin and hemoglobin load which results from hemolysis and myonecrosis. Renal failure may ensue in a clinical situation similar to the crush syndrome. The treatment of high voltage injuries is primarily aimed at removal of the patient from the source of injury, establishing cardiopulmonary resuscitation, initiating vigorous fluid replacement, insuring an adequate urinary output along with urinary alkalinization, and maintenance of local tissue perfusion by both local and systemic means. Escharotomy and fasciotomy are performed early-on to insure optimal perfusion of injured extremities. The burn surface wound is managed according to usual guidelines. Because of severe peripheral tendon and nerve injuries along with extensive local tissue destruction, amputation is more frequently used in the treatment of electrical burns than in thermal burns. The authors point out the difficulty in balancing the preservation of an extremity with the risk of death from sepsis in an effort to save an extremity which may be useless. Of four mortalities among the 28 patients reported in this series, one resulted from severe central nervous system injury, one from respiratory insufficiency, and two from multisystem failure and sepsis.--Carey P. Page
HEAD AND NECK Antrochoaflal Polyps. R. Towbin, J. S. Dunbar, and K. Bove. Am J Roentgenol 132:27-31, (January), 1979. Five children with antrochoanal polyps, a solitary benign tumor arising from the maxillary antrum of a nonatropic patient, presented with either nasal obstruction, epitaxis or maxillary sinus opacification. A review revealed about 71% of patients with this lesion to be in the 10-39 yr age group with an 1.3:1 male-to-female ratio. The radiologic features include an opacified maxillary antrum which appears expanded and a nasopharyngeal mass. The differential diagnosis includes normal or hypertrophied inferior turbinates, chronic hypertrophic polypoid rhinosinusitis, juvenile nasopharyngeal angiofibroma, mucus retention cyst, mococele, and malignant tumors of the nasopharynx. In children the latter include lymphoma, rhabdomyosarcoma, lymphoepithelioma, olfactory neruoblastoma, and chordoma. The CaldwelI-Luc operation yields the best results since removal by snare and avulsion carries about a 20% recurrence r a t e . Randall HI. Powell The Aler Base Composite Graft in Cleft Lip Noses. D. O.
Maisels. Br J Plast Surg 31:220-221, (July), 1978. The technique of the transfer of a free composite graft from the alar base to the opposite nostril is described. It is
ABSTRACTS
490
wedge-shaped and would be valuable in cleft lip noses and deficiencies due to injury.--A. Jolleys
Autogenous Septal Cartilage Graft in the Correction of Cleft Lip Nasal Deformity. Yoshihiko Nishimura and Yoichi
Ogino. Br J Plast Surg 31:222-226, (July), 1978. The use of cartilaginous struts to support the tip of the nose in cleft lip nasal deformity is discussed. It is suggested that a quadrilateral piece can be taken from the nasal septum, particularly when a submucous resection is frequently needed in these cases. Unfortunately, such a procedure is inappropriate in children, or when the septum is extremely deformed.--A. Jolleys
A Simplified Technique for Correction of the Cleft Lip Nasal Deformity. S. Ariyan and T. J. Krizek. Ann Plast Surg
1:568-574, (November), 1978. The deformity of the cleft lip nose is characterized by four components; collapse of alar cartilage; shortened distance from the nasion to the alar corner; widened nostril floor, or sill; and shortened nasal orifice. The author's technique seeks to overcome and correct all of these component deformities. The technique consists of freeing the malpositioned alar corner, where it is attached to the nasolabial fold. In addition, the skin of the lower portion of the nose is completely mobilized from the underlying cartilaginous skeleton and the malrotated ala is repositioned by an attachment to the contralateral upper lateral cartilage. The alar rim is inset into a normal location on the nasolabial fold to complete the procedure. The clinical pre- and postoperative photos demonstrate very satisfactory results with this technique. It is advised as an additional technique to the armamentarium of those surgeons performing this type of surgery.--A. B. Sokol
Anatomical Findings in Median Cleft of Upper Lip. D. R.
Wiemer, S. A. Hardy, and M. Spira. Plast Reconstr Surg 62:866-869, (December), 1978. Median clefts of the lip are quite rare and are divided into two groups. The first are generally incompatable with life, associated with an agenesis of the frontonasal process and associated with cerebral anomalies. Second, are less severe median clefts not associated with cerebral anomalies. The latter clefts may or may not have hypertelorism, while the former are generally associated with hypotelorism. The authors report on the surgical repair of two median clefts of the lip not associated with cerebral anomalies. In general, they were repaired with a straight line repair. Both children have had excellent results as indicated by pre- and postoperative photographs. Median clefts of the lips associated with cerebral anomalies, are generally unrepaired because of the rather bleak outlook for survival. The operative findings are set forth along with the surgical techniques. A review of the embryology leading to the median clefts is given by the authors. Essentially, the defect appears to be due to a failure of mesodermal migration into the fused frontonasal and maxillary processes.--A. B. Soko!
Angioma of the Mandible. C. Riberti and A. Bertani. Rass
Ital Chir Ped 19:352, 1977. A 6-yr-old boy was admitted because of a cavernous angioma of the left of mandible. At 24 me of age, the patient presented with a mass in the left parotid region that selective arteriography proved to be a hypertrophic angioma of the parotid gland. The patient was treated with local injection of triamcinolone acetonide and a complete ~gression of the angioma was obtained within 5 me. The total dosage injected was 90 mg. Two years later a swelling was noted on the left mandible that expanded mainly within the oral cavity. After slight trauma the lesion rapidly increased. On admission a mass of a bluish discoloration and of the size of an apricot invading the alveolus was found. Radiographic examination revealed two large osteolytic defects of the anterior twothirds of the left mandible. Selective arteriography showed that the lesion was of a vascular nature and was fed by an artery branching from the internal maxillary artery. The left external carotid artery was ligated and the controlateral external carotid artery was temporarily occluded. Curettage of the bony cavity was then performed, the residual cavity was filled with gauze for 4 days. Difference between the two angiomata are discussed on the basis of the angiographic aspects. No histologic findings are reported.--C. A. Montagnani Surgical Correction of the Facial Deformities of Acromega-
ly. J. M. Converse and D. C. Baker. Ann Plast Surg 1:612616, (November), 1978. A case report of the facial reconstruction in a white, male, acromegalic patient along with clinical, diagramatic and dental occlusal photos is given for the readers edification. A review of the historical contributions to the condition of acromegaly is given including the origin of the term acromegaly from Greek, referring to large extremities. In addition, the pathology of acromegaly is reviewed. The plastic surgical treatment in this particular case, required four operative stages. The stages were: correction of the verticle height of the mandible, mandibular prognathism correction by bilateral sagittal osteotomy of the ramus, rhinoplasty and iliac bone graft, and, finally, various soft tissue corrections. The author points out that although there are 300 new cases of acromegaly discovered each year, the plastic surgical treatment reviewed in the literature has, prior to this article, numbered only one contribution.--A. B. Sokol The Role of Pressure Therapy in Management of Earlobe Keloids: Preliminary Report of a Controlled Study. B. Brent.
Ann Plast Surg 1:579-581, (November), 1978. Earlobe piercing results in keloid complications in a significant number of individuals. The etiology of this collagenous "tumor" remains obscure. Its treatment is controversial and ranges from excision, steriod injection, and irradiation. Recently, there has been reported success in treating burn scars with compression. To this end, the author has created a decorative, spring-pressure earring, which exerts constant light pressure and is applied 2 wk after the initial keloid excision. The author reports on seven patients in whom bilateral earlobe keloids resulted following ear piercing. The initial results have been excellent with the use of the pressure