103
Vol. 67, No. 2
The Management of Traumatic Facial Nerve Injuries* MIRION P BOWERS, M.D., ChiefI, Division of Otolarvyigology, Martin Luther King, Jr General Hospital, Los Angeles, Califbrnia
Only a short time ago, there was no treatment for paralysis of the facial nerve. A severed nerve was doomed never to function again; and in other cases of facial nerve damage, one had to be satisfied with such pseudotreatments as galvanizaton of the facial musculature, salicylic acid and massage. The experiences at Walter Reed General Hospital with decompression and grafting of severed facial nerves seems to support surgical intervention in these injuries. Taverner' has shown statistically that these treatments are of no value except for keeping the patient quiet and the doctor satisfied. In cases of permanent disfigurement, the neurosurgeon was called to make a connection between the peripheral segment of the facial nerve and the central segment of another motor cranial nerve (eg. XI, XII) or the plastic surgeon was asked to restore some symmetry at rest. Cawthorne,2 3 Sullivan,4 and Kettel5 have demonstrated that the results following intratemporal surgery of damaged or severed nerves were significantly improved over unoperated patients with similar injuries. Jongkees6 operated on 124 cases of traumatic injury to the facial nerve and he reported satisfactory recovery in 73% of his cases. If the operation was performed within the first year, he reported 81% satisfactory recovery. He also reported 70% functional recovery following nerve grafting. Conley7 and Maxwell8 reported satisfactory results following repair of the facial nerve in the parotid gland and Dott9 and House'0"' reported satisfactory results following repair of the facial nerve in the internal auditory canal. The main advantage of recon0/ ('w nvu NVaional Mch'diwal .4As S(7(lloil Jiil *Read at I/hf' 78tli .4Annul Co of/h Is /973. Revisled fir piiIhlicaolol Dece'mher 1. /974. 28-A ugll
struction of the facial nerve itself over anastomosing the nerve with other motor cranial nerves is the recovery of facial expression. MECHANISM OF NERVE FUNCTION
The maintenance of nerve excitability has been shown to depend greatly on sodium (Na+) and potassium (K+) cations. Hodgkins,'2 Huxley'3 and Keynes'4 have demonstrated that sodium ions cannot pass through the cell membrane in their resting state. Potassium ions are concentrated within the cell membrane and sodium ions are concentrated outside the cell membrane. At the passage of an impulse, the membrane is first of all permeable to Na + ions enabling them to enter the interior of the cell. Then the permeability of the membrane undergoes a change and the K+ ions leave the cell. This change in permeability is the basis of all electrical impulses that have been observed in nerves. As long as the stimulus remains, the potassium ion concentration outside the membrane remains high. Another nerve impulse cannot be transmitted while the nerve is in this physiological state. A spicule of bone pressing on the nerve may result in continued stimulation which may explain the return of function in a nerve within 24 hours following decompression. PATHOPHYSIOLOGY OF NERVE INJURY
Injury to the facial nerve may result in either neuropraxia, axonotmesis, or neurotmesis. A nerve which develops only neuropraxia always undergoes complete recovery. The pathophysiology of paralysis of the facial nerve following trauma results in increased permeability of the nervous vasculature. This is followed by exudation of fluid into the Fallo-
104
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION
pian canal resulting in increased pressure in this enclosed canal. This causes compression of the nerve valsulature with ischemia, additional exudation and finally, complete obstruction of the blood supply. The compromised blood supply may result in Wallerian degeneration. In the severed nerve, the axons distal to the injury degenerate out to the motor end plate, while those in the proximal segment degenerate to the first node of Ranvier. Axonal regeneration is from the proximal segment to the motor end plate. Axonal regrowth may be blocked either by the presence of granulation tissue between the cut ends of the nerve or poor stabilization of the nerve stump with resultant movement and torsion. Treatment plans should be directed at romoving those factors which interfere with nerve healing. TYPES OF NERVE INJURY
Facial nerve injuries may be classified into two major groups depending on the degree of injury. Group I included injuries involving trauma to the nerve cells while the nerve fibers remain intact. Group I includes those injuries which result in severence of axons. An injury may involve both classes. Facial nerve injuries may be further divided into five major types depending on the location of the injury: Type I 0 Injury to the facial canal in the internal auditory canal. Type II * Injury to the facial nerve in its horizontal course through the middle ear. Type III 0 Injury to the facial nerve in its vertical course through the mastoid. Type IV 0 Injury to the facial nerve in its course through the parotid gland. Type V * A combination of the above injuries. FACIAL NERVE TESTING
For the purpose of this discussion, tests for facial nerve function will be divided into two major groups. Group I comprises those tests which attempt to determine the extent of injury and Group II those tests which attempt to locate the site of injury. Group 1. 1. Nerve Excitability Test. These are most commonly used to determine nerve function. However, these tests are not reliable until 1-3 days following the injury. This delay is the usual time required to elapse from the time a nerve is severed until the nerve looses its ability to conduct an electrical impulse. 2. Conduction-Latency Measurements. This test measures the rate of impulse transmission. 3. Strength (Intensity) Duration Curve. This test measures the intensity plus the duration of stimulus required to obtain a response. 4. Electromyogra-
MARCH, 1975
phy. a. Muscle fiber action potential disappears with nerve degeneraition and reappears with nerve regeneraition.. b. Fibrillation potential appears with nerve degeneraition aind disappeairs with nerve regeneration. These tests aire the best tests to determine nerve function; however, they do not become positive before 14-21 days following injury.
Group 11. 1. Shirmer Test. An abnormal Shirmer test places the injury proximal to the geniculate ganglion. 2. Acoustic Reflex. Absent acoustic reflex places the injury proximail to stapedius nerve (patient must have normal hearing to perform test). 3. Measurement of Taste, Anterior TwoThirds Tongue. If these tests are abnormal, the injury is proximal to exit of chord tympani. 4. Measurement of Submandibular Gland Flow. 5. Audiometry. 6. Vestibular Testing 7. Tomograms of Mastoid
MANAGEMENT
Surgical exploration should be performed on any facial nerve which develops abnormal excitability following trauma. The limitations for surgery are the general condition of the patient and the ability to locate the proximal and distal segments of the nerve. The duration of injury is probably not a limiting factor in the severed nerve. However, results are better if repair is performed shortly after injury. Surgical repair of facial nerves may be divided into three major categories: 1) decompression; 2) decompression and end-toend anastomosis; and 3) decompression and nerve grafting. Decompression alone should be performed in those facial nerve injuries which do not respond to hilger stimulation and on exploration the nerve is found to be intact. Decompression and end-to-end anastomosis should be performed in those injuries where the nerve is severed or badly damaged, if the nerve can be sutured without excessive tension. In those injuries where the injury results in a loss of segment, a nerve graft should be used. The greater auricular nerve is most commonly used for grafting. This nerve is accessible and does not interfere with motor function of other muscles and gives good results. If this nerve is not usable or subsequent flaps are needed in the area of the incision, the lateral femoral cutaneous nerve may be used. TECHNIQUE FOR SURGERY
The surgical approach for Types II-IV is through a post-auricular incision with a parotid extension. A simple mastoidectomy is performed, the posterior canal wall thinned and the facial recess entered through an A-P
Vol. 67, No. 2
Facial Nerve Injuries
approach. The entire tympanic portion of facial nerve is decompressed. If the nerve is not severed, this is all that is necessary and the incus need not be disturbed in this procedure. It is preferable to begin decompressing the facial nerve at a site away from the fracture. The distal segment of the nerve in the parotid gland is usually enmeshed in excessive scar tissue. The best procedure is to locate a peripheral branch such as the marginal mandibular or the buccal and follow it proximal to the main trunk. If it is a type II injury, and grafting is required, the incus and malleus must be removed. Type I injuries must be approached through a middle cranial fossa or translabyrinthine approach as described by House. TECHNIQUE FOR NERVE GRAFTING
After the proximal and distal segments of the nerve have been located, it is essential to cut the ends of the nerve with a sharp knife until normal nerve is identified. If an end-toend anastomosis can be performed, a DuckerHayes silastic sleeve is slipped over one end of the nerve and four 7-0 or 8-0 silk sutures are used to suture the nerve. The sutures should extend only through the nerve sheath making sure the axons are not disturbed. The dissecting microscope should be used for this procedure. The sleeve is then placed over the anastomotic site. If a graft is used, the same technique is used and two sleeves are used, one placed over each anastomotic site. Other temporal bone and otologic injuries should be repaired and the wound closed RESULTS OF SIXTEEN CASES
Sixteen patients who received temporal bone fractures and facial nerve injury in the Republic of Viet Nam underwent facial nerve decompression and autogenous nerve grafting at Walter Reed General Hospital. The results are reported as good, fair, poor and none. A good result is characterized by a near normal resting tone, facial symmetry, definite voluntary motion and the ability to close the eye. A fair result implies some voluntary motion with ability to close the eye and asymmetry with facial expression. A poor result implies definite resting asymmetry and inability to completely
105
close the eye.'5 The results of surgery in these 16 patients sustaining facial nerve injury are as follows: in five patients, good; in five patients. fair; in four patients, poor; and in two patients there was no improvement. The two patients with no response are less than one year, post surgery. The average time lapse between surgery and clinical evidence of recovery is eight to nine months and recovery continues for 12-24 months. EMG evidence of regeneration usually preceeds motion by two to three months. SUMMARY
A review of earlier surgical treatment of the facial nerve has been made. The results of 16 cases of traumatic facial nerve injury treated surgically were cited. The results of these cases and cases presented by other centers seems to show that surgical exploration and nerve grafting is beneficial in traumatic injury to the facial nerve. LITERATURE CITED
1. TAVERNER, T Cortisone Treatment of Bell's Palsy. Lancet, 2:1052-1054, 1954. 2. CAWTHRONE, T Peripheral Facial Paralysis from Aspects of its Pathology. Laryngoscope, 56:653-644, 1946. 3. CAWTHRONE, T Joint Summer Meeting with the Scottish Otol. Soc. held at Edenburgh: Facial Pain. Proc. of the Roy. Soc. of Med., 44:1033-1037, 1951. 4. SULLIVAN, J. A. and J. B. SMITH. The Otological Concept of Bell's Palsy and its Treatment. Ann. of Otol., Rhinol. and Laryng., 59:1148-1170, 1950. 5. KETTEL, K. Peripheral Facial Palsy. Munksgaard, Copenhagen, 1959. 6. JONGKEES, L. B. Surgery of the Facial Nerve. J. of Laryng. Otol., 82:575-584, 1968. 7. CONLEY, J. J. Facial Nerve Grafting in Treatment of Parotid Gland. Arch. Surg., 70:359-366, 1955. 8. MAXWELL, J. H. Diseases of the Parotid Glands. Chicago Med. Soc. Bull., 56:(50):972-976, 1954. 9. DOTT, N. M. Facial Paralysis-Restitution by Extrapetrous Nerve Graft. Proc. of the Royal Soc. of Med., 51:900-902, 1958. 10. HOUSE, W F Middle Cranial Fossa Approach to Petrous Pyramid. Arch. Otol., 78:460-469, 1963. 11. HOUSE, W F and J.A. CRABTREE. Surgical Exposure to Petrous Portion of the Seventh Nerve. Arch. Otol., 81:506-507, 1965. 12. HODGKIN, A. L. The Ionic Basis of Nervous Conduction. Science, 145:1148-1154, 1964. 13. HUXLEY, A. F Electrical Processes in Nerve Conduction. In: Ion Transport Across Membranes, edited by H. T Clarke and D. Nachmansohn. New York: Academic Press, 1954, p. 23-24. (Conticlded on page 148)
148
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION
and sleeve; 3) introduction of the laparoscope; 4) performance of "ancillary" procedures; and 5) anesthesia.
MARCH, 1975
problems secondary to the procedure. 1) Bleeding secondary to piercing an omental vessel, requiring laparotoiny to control bleeding. 2) Bleeding from the tube and mesosalpinx while attempting tubal cautery, requiring laparotomy to control the bleeding. 3) Preperitoneal space distention with two liters of
CO2.
4) Breakage of the cautery knife while attempting lysis of adhesions requiring laparotomy to locate the knife blade. 5) An abdominal wall hematoma.
This constitutes a morbidity rate of 2.1%. As the series grows we plan to continue the same strict controls and zero mortalities. In conclusion, I believe that the author has begun to prove that gynecologic laparoscopy can be performed safely in a small hospital environment. However, strict guidelines and controls must be followed in order to assure proper selection of patients and adequate experience of the operators. SUMMARY
Fig. 5. Adhesions-pelvic
In reviewing the literature, we find that the average mortality rate associated with laproscopy is approximately 0.2%. This usually stems from poor selection of patients, most of whom have pre-existing severe medical diseases; hemorrhage from biopsy sites other than pelvic organs, such as liver and spleen; air emboli; pneumothorax; and mediastinal emphysema secondary to displacement of the pneumoperitoneum needle; and cardiac arrest. We are gratified that our series had no mortalities. We did, however, encounter five
An historical review of laparoscopic techniques along with a detailed outline of the techniques used by the gynecological service of Lincoln Hospital, Durham, N.C. is presented. A review and analysis of 230 laparoscopic examinations during a two year period are discussed. LITERATURE CITED
1. KELLING, G. UJber Oesophagoskopie, Gastroskopie und Kolioskopie. Munch. Med. Wschr., 49:21, 1902. 2. JACOBAEUS, H.C. Ueber die Moglichkeit die Zystoskope bei Untersuchhung seroser Hohlung Anzuwenden. Munch. Med. Wschr., 57:2090, 1910. 3. BERNHEIM, B.M. Organoscopy: cystoscopy of the abdominal cavity. Ann. SURO., 53:764, 191 1. 4. RUDDOCK, J.C. Peritoneoscopy. West. J. Surg., 42:392, 1934. 5. COHEN, M.R. Laparoscopy, Culdoscopy and Gynecography. W B. Saunders, Co. Phila. 1: 1-68, 1970.
(Bowers, fiomn page 105) 15. KREKORIAN, E. A. Repair of Combat-injured Facial 14. KEYNES, R. D. The Ionic Movements During Nerves. Laryng., 81:1926-45, 1971. Nervous Activity. J. Physiol. (London), 114:119-150, 1 oc1
DETROIT PHYSICIANS RECEIVE POINDEXTER AUTOBIOGRAPHY Each of the approximately 300 Afro-American physicans and surgeons in metropolitan Detroit was recently presented a copy of My World of Reality the autobiography of Dr. Hildrus. A. Poindexter, by Parke. Davis & Co., a subsidiary of Warner-Lambert Co. Distribution was effected through the Detroit Medical Society for which Dr. Charles H. Wright was spokesman.
Vol. 67, No. 2
The Management of Traumatic Facial Nerve Injuries* MIRION P BOWERS, M.D., ChiefI, Division of Otolarvyigology, Martin Luther King, Jr General Hospital, Los Angeles, Califbrnia
Only a short time ago, there was no treatment for paralysis of the facial nerve. A severed nerve was doomed never to function again; and in other cases of facial nerve damage, one had to be satisfied with such pseudotreatments as galvanizaton of the facial musculature, salicylic acid and massage. The experiences at Walter Reed General Hospital with decompression and grafting of severed facial nerves seems to support surgical intervention in these injuries. Taverner' has shown statistically that these treatments are of no value except for keeping the patient quiet and the doctor satisfied. In cases of permanent disfigurement, the neurosurgeon was called to make a connection between the peripheral segment of the facial nerve and the central segment of another motor cranial nerve (eg. XI, XII) or the plastic surgeon was asked to restore some symmetry at rest. Cawthorne,2 3 Sullivan,4 and Kettel5 have demonstrated that the results following intratemporal surgery of damaged or severed nerves were significantly improved over unoperated patients with similar injuries. Jongkees6 operated on 124 cases of traumatic injury to the facial nerve and he reported satisfactory recovery in 73% of his cases. If the operation was performed within the first year, he reported 81% satisfactory recovery. He also reported 70% functional recovery following nerve grafting. Conley7 and Maxwell8 reported satisfactory results following repair of the facial nerve in the parotid gland and Dott9 and House'0"' reported satisfactory results following repair of the facial nerve in the internal auditory canal. The main advantage of recon0/ ('w nvu NVaional Mch'diwal .4As S(7(lloil Jiil *Read at I/hf' 78tli .4Annul Co of/h Is /973. Revisled fir piiIhlicaolol Dece'mher 1. /974. 28-A ugll
struction of the facial nerve itself over anastomosing the nerve with other motor cranial nerves is the recovery of facial expression. MECHANISM OF NERVE FUNCTION
The maintenance of nerve excitability has been shown to depend greatly on sodium (Na+) and potassium (K+) cations. Hodgkins,'2 Huxley'3 and Keynes'4 have demonstrated that sodium ions cannot pass through the cell membrane in their resting state. Potassium ions are concentrated within the cell membrane and sodium ions are concentrated outside the cell membrane. At the passage of an impulse, the membrane is first of all permeable to Na + ions enabling them to enter the interior of the cell. Then the permeability of the membrane undergoes a change and the K+ ions leave the cell. This change in permeability is the basis of all electrical impulses that have been observed in nerves. As long as the stimulus remains, the potassium ion concentration outside the membrane remains high. Another nerve impulse cannot be transmitted while the nerve is in this physiological state. A spicule of bone pressing on the nerve may result in continued stimulation which may explain the return of function in a nerve within 24 hours following decompression. PATHOPHYSIOLOGY OF NERVE INJURY
Injury to the facial nerve may result in either neuropraxia, axonotmesis, or neurotmesis. A nerve which develops only neuropraxia always undergoes complete recovery. The pathophysiology of paralysis of the facial nerve following trauma results in increased permeability of the nervous vasculature. This is followed by exudation of fluid into the Fallo-
104
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION
pian canal resulting in increased pressure in this enclosed canal. This causes compression of the nerve valsulature with ischemia, additional exudation and finally, complete obstruction of the blood supply. The compromised blood supply may result in Wallerian degeneration. In the severed nerve, the axons distal to the injury degenerate out to the motor end plate, while those in the proximal segment degenerate to the first node of Ranvier. Axonal regeneration is from the proximal segment to the motor end plate. Axonal regrowth may be blocked either by the presence of granulation tissue between the cut ends of the nerve or poor stabilization of the nerve stump with resultant movement and torsion. Treatment plans should be directed at romoving those factors which interfere with nerve healing. TYPES OF NERVE INJURY
Facial nerve injuries may be classified into two major groups depending on the degree of injury. Group I included injuries involving trauma to the nerve cells while the nerve fibers remain intact. Group I includes those injuries which result in severence of axons. An injury may involve both classes. Facial nerve injuries may be further divided into five major types depending on the location of the injury: Type I 0 Injury to the facial canal in the internal auditory canal. Type II * Injury to the facial nerve in its horizontal course through the middle ear. Type III 0 Injury to the facial nerve in its vertical course through the mastoid. Type IV 0 Injury to the facial nerve in its course through the parotid gland. Type V * A combination of the above injuries. FACIAL NERVE TESTING
For the purpose of this discussion, tests for facial nerve function will be divided into two major groups. Group I comprises those tests which attempt to determine the extent of injury and Group II those tests which attempt to locate the site of injury. Group 1. 1. Nerve Excitability Test. These are most commonly used to determine nerve function. However, these tests are not reliable until 1-3 days following the injury. This delay is the usual time required to elapse from the time a nerve is severed until the nerve looses its ability to conduct an electrical impulse. 2. Conduction-Latency Measurements. This test measures the rate of impulse transmission. 3. Strength (Intensity) Duration Curve. This test measures the intensity plus the duration of stimulus required to obtain a response. 4. Electromyogra-
MARCH, 1975
phy. a. Muscle fiber action potential disappears with nerve degeneraition and reappears with nerve regeneraition.. b. Fibrillation potential appears with nerve degeneraition aind disappeairs with nerve regeneration. These tests aire the best tests to determine nerve function; however, they do not become positive before 14-21 days following injury.
Group 11. 1. Shirmer Test. An abnormal Shirmer test places the injury proximal to the geniculate ganglion. 2. Acoustic Reflex. Absent acoustic reflex places the injury proximail to stapedius nerve (patient must have normal hearing to perform test). 3. Measurement of Taste, Anterior TwoThirds Tongue. If these tests are abnormal, the injury is proximal to exit of chord tympani. 4. Measurement of Submandibular Gland Flow. 5. Audiometry. 6. Vestibular Testing 7. Tomograms of Mastoid
MANAGEMENT
Surgical exploration should be performed on any facial nerve which develops abnormal excitability following trauma. The limitations for surgery are the general condition of the patient and the ability to locate the proximal and distal segments of the nerve. The duration of injury is probably not a limiting factor in the severed nerve. However, results are better if repair is performed shortly after injury. Surgical repair of facial nerves may be divided into three major categories: 1) decompression; 2) decompression and end-toend anastomosis; and 3) decompression and nerve grafting. Decompression alone should be performed in those facial nerve injuries which do not respond to hilger stimulation and on exploration the nerve is found to be intact. Decompression and end-to-end anastomosis should be performed in those injuries where the nerve is severed or badly damaged, if the nerve can be sutured without excessive tension. In those injuries where the injury results in a loss of segment, a nerve graft should be used. The greater auricular nerve is most commonly used for grafting. This nerve is accessible and does not interfere with motor function of other muscles and gives good results. If this nerve is not usable or subsequent flaps are needed in the area of the incision, the lateral femoral cutaneous nerve may be used. TECHNIQUE FOR SURGERY
The surgical approach for Types II-IV is through a post-auricular incision with a parotid extension. A simple mastoidectomy is performed, the posterior canal wall thinned and the facial recess entered through an A-P
Vol. 67, No. 2
Facial Nerve Injuries
approach. The entire tympanic portion of facial nerve is decompressed. If the nerve is not severed, this is all that is necessary and the incus need not be disturbed in this procedure. It is preferable to begin decompressing the facial nerve at a site away from the fracture. The distal segment of the nerve in the parotid gland is usually enmeshed in excessive scar tissue. The best procedure is to locate a peripheral branch such as the marginal mandibular or the buccal and follow it proximal to the main trunk. If it is a type II injury, and grafting is required, the incus and malleus must be removed. Type I injuries must be approached through a middle cranial fossa or translabyrinthine approach as described by House. TECHNIQUE FOR NERVE GRAFTING
After the proximal and distal segments of the nerve have been located, it is essential to cut the ends of the nerve with a sharp knife until normal nerve is identified. If an end-toend anastomosis can be performed, a DuckerHayes silastic sleeve is slipped over one end of the nerve and four 7-0 or 8-0 silk sutures are used to suture the nerve. The sutures should extend only through the nerve sheath making sure the axons are not disturbed. The dissecting microscope should be used for this procedure. The sleeve is then placed over the anastomotic site. If a graft is used, the same technique is used and two sleeves are used, one placed over each anastomotic site. Other temporal bone and otologic injuries should be repaired and the wound closed RESULTS OF SIXTEEN CASES
Sixteen patients who received temporal bone fractures and facial nerve injury in the Republic of Viet Nam underwent facial nerve decompression and autogenous nerve grafting at Walter Reed General Hospital. The results are reported as good, fair, poor and none. A good result is characterized by a near normal resting tone, facial symmetry, definite voluntary motion and the ability to close the eye. A fair result implies some voluntary motion with ability to close the eye and asymmetry with facial expression. A poor result implies definite resting asymmetry and inability to completely
105
close the eye.'5 The results of surgery in these 16 patients sustaining facial nerve injury are as follows: in five patients, good; in five patients. fair; in four patients, poor; and in two patients there was no improvement. The two patients with no response are less than one year, post surgery. The average time lapse between surgery and clinical evidence of recovery is eight to nine months and recovery continues for 12-24 months. EMG evidence of regeneration usually preceeds motion by two to three months. SUMMARY
A review of earlier surgical treatment of the facial nerve has been made. The results of 16 cases of traumatic facial nerve injury treated surgically were cited. The results of these cases and cases presented by other centers seems to show that surgical exploration and nerve grafting is beneficial in traumatic injury to the facial nerve. LITERATURE CITED
1. TAVERNER, T Cortisone Treatment of Bell's Palsy. Lancet, 2:1052-1054, 1954. 2. CAWTHRONE, T Peripheral Facial Paralysis from Aspects of its Pathology. Laryngoscope, 56:653-644, 1946. 3. CAWTHRONE, T Joint Summer Meeting with the Scottish Otol. Soc. held at Edenburgh: Facial Pain. Proc. of the Roy. Soc. of Med., 44:1033-1037, 1951. 4. SULLIVAN, J. A. and J. B. SMITH. The Otological Concept of Bell's Palsy and its Treatment. Ann. of Otol., Rhinol. and Laryng., 59:1148-1170, 1950. 5. KETTEL, K. Peripheral Facial Palsy. Munksgaard, Copenhagen, 1959. 6. JONGKEES, L. B. Surgery of the Facial Nerve. J. of Laryng. Otol., 82:575-584, 1968. 7. CONLEY, J. J. Facial Nerve Grafting in Treatment of Parotid Gland. Arch. Surg., 70:359-366, 1955. 8. MAXWELL, J. H. Diseases of the Parotid Glands. Chicago Med. Soc. Bull., 56:(50):972-976, 1954. 9. DOTT, N. M. Facial Paralysis-Restitution by Extrapetrous Nerve Graft. Proc. of the Royal Soc. of Med., 51:900-902, 1958. 10. HOUSE, W F Middle Cranial Fossa Approach to Petrous Pyramid. Arch. Otol., 78:460-469, 1963. 11. HOUSE, W F and J.A. CRABTREE. Surgical Exposure to Petrous Portion of the Seventh Nerve. Arch. Otol., 81:506-507, 1965. 12. HODGKIN, A. L. The Ionic Basis of Nervous Conduction. Science, 145:1148-1154, 1964. 13. HUXLEY, A. F Electrical Processes in Nerve Conduction. In: Ion Transport Across Membranes, edited by H. T Clarke and D. Nachmansohn. New York: Academic Press, 1954, p. 23-24. (Conticlded on page 148)
148
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION
and sleeve; 3) introduction of the laparoscope; 4) performance of "ancillary" procedures; and 5) anesthesia.
MARCH, 1975
problems secondary to the procedure. 1) Bleeding secondary to piercing an omental vessel, requiring laparotoiny to control bleeding. 2) Bleeding from the tube and mesosalpinx while attempting tubal cautery, requiring laparotomy to control the bleeding. 3) Preperitoneal space distention with two liters of
CO2.
4) Breakage of the cautery knife while attempting lysis of adhesions requiring laparotomy to locate the knife blade. 5) An abdominal wall hematoma.
This constitutes a morbidity rate of 2.1%. As the series grows we plan to continue the same strict controls and zero mortalities. In conclusion, I believe that the author has begun to prove that gynecologic laparoscopy can be performed safely in a small hospital environment. However, strict guidelines and controls must be followed in order to assure proper selection of patients and adequate experience of the operators. SUMMARY
Fig. 5. Adhesions-pelvic
In reviewing the literature, we find that the average mortality rate associated with laproscopy is approximately 0.2%. This usually stems from poor selection of patients, most of whom have pre-existing severe medical diseases; hemorrhage from biopsy sites other than pelvic organs, such as liver and spleen; air emboli; pneumothorax; and mediastinal emphysema secondary to displacement of the pneumoperitoneum needle; and cardiac arrest. We are gratified that our series had no mortalities. We did, however, encounter five
An historical review of laparoscopic techniques along with a detailed outline of the techniques used by the gynecological service of Lincoln Hospital, Durham, N.C. is presented. A review and analysis of 230 laparoscopic examinations during a two year period are discussed. LITERATURE CITED
1. KELLING, G. UJber Oesophagoskopie, Gastroskopie und Kolioskopie. Munch. Med. Wschr., 49:21, 1902. 2. JACOBAEUS, H.C. Ueber die Moglichkeit die Zystoskope bei Untersuchhung seroser Hohlung Anzuwenden. Munch. Med. Wschr., 57:2090, 1910. 3. BERNHEIM, B.M. Organoscopy: cystoscopy of the abdominal cavity. Ann. SURO., 53:764, 191 1. 4. RUDDOCK, J.C. Peritoneoscopy. West. J. Surg., 42:392, 1934. 5. COHEN, M.R. Laparoscopy, Culdoscopy and Gynecography. W B. Saunders, Co. Phila. 1: 1-68, 1970.
(Bowers, fiomn page 105) 15. KREKORIAN, E. A. Repair of Combat-injured Facial 14. KEYNES, R. D. The Ionic Movements During Nerves. Laryng., 81:1926-45, 1971. Nervous Activity. J. Physiol. (London), 114:119-150, 1 oc1
DETROIT PHYSICIANS RECEIVE POINDEXTER AUTOBIOGRAPHY Each of the approximately 300 Afro-American physicans and surgeons in metropolitan Detroit was recently presented a copy of My World of Reality the autobiography of Dr. Hildrus. A. Poindexter, by Parke. Davis & Co., a subsidiary of Warner-Lambert Co. Distribution was effected through the Detroit Medical Society for which Dr. Charles H. Wright was spokesman.
