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Uterine inertia
UTERINE INERTIA NORRIS Clinica
W.
VAUX,
M.D.
Professor of Obstetrics, Jefferson MedicaI College; Obstetrician and GynecoIogist-in-Chief, BuiIding of the PennsyIvania Hospital
Woman’s
PHILADELPHIA
T
HE most commonIy known definitions of “inertia uteri” are: (I) Iabor proIonged to such an extent as to be dangerous to both mother and chiId; (2) insuffIcient contractions of the uterus to overcome the norma resistance of the passage of the chiId through the parturient cana1, which may at times be produced by abnormaIities existing in the mother or in the fetus; (3) that condition in which the uterine contractions, by reason of their weakness or irreguIarity, are insuffIcient to diIate the cervical OS in the first stage of Iabor, or expe1 the fetus in the second stage. In the more recent literature on this subject, inertia uteri has assumed the phrase of “atonic uterus” or “atony of the uterus.” This modern conception of the inert uterus defined as “atony,” is not as specific or as comparabIe as the inertia uteri of the oIder authorities. The word inertia means sIuggish, persists in the state of rest, uniform motion unIess some force changes that state, which describes we11 the characteristics of uterine inertia. On the other hand, atonic is defined as Iack of tone or vigor, which does not symboIize as we11 the characteristics of the primary inert uterus, but couId we11 be utiIized in defining the secondary type. We shaI1 adhere to the oIder nomencIature of “ inertia uteri ” throughout this resume of the subject. Inertia uteri may therefore be divided into two distinct cIasses: primary or true inertia uteri, and secondary, or uterine exhaustion. Under these two main cIassifications we are abIe to pIace the etioIogica1 factors which produce one or the other of these conditions. Primary or true inertia uteri is that condition in which the uterine contractions have never been sufficient to throw the 358
uterus into contraction, either before the onset or from the beginning of labor. It is a most unusua1 type of inertia and probabIy one of the rarest varieties of proIongation of pregnancy or Iabor. Etiology. The primary inertia uteri arises from a variety of conditions such as: I. Defective intervention (paraIysis of nerve center which presides over uterine contractions) ; 2. Defective deveIopment of the uterine muscuIature; 3. AbnormaI shape of the uterus due to uterine abnormaIities; 4. AbnormaI positions of the uterus as seen in the anteflexions of penduIous abdomens, also in proIapsus uteri; 3. Overdistention of the uterus as in poIyhydramnios; 6. NeopIasms of the uterine waI1; 7. Adhesions between the embryona1 sac and the uterine waI1;’ 8. RapidIy succeeding pregnancies. As an etioIogica1 factor in this condition, FaIIs2 expIains the atypica1 types of Iabor producing habitua1 abortion due to overstimuIation of the pituitary secretions, hypersensitiveness of the peIvic sympathetic ganglia, or a decrease in the norma inhibiting activity of the thyroid. He further states that those cases that tend to go Ionger than the two-hundred and eighty days may be expIained on exactIy the opposite grounds; nameIy, a mild hyperthyroidism, weak pituitary hormone production, or reIativeIy insensitive peIvic sympathetic gangIia. According to this theory, primary inertia uteri may not necessariIy be due to abnormalities in the uterus, but may be secondary to faiIure of the hypophysis to produce sufficient hor-
NE:\\
5~m11.s V-or..
TXXV,
No.
2
Vaux---Uterine
mone; to failure of the sympathetic gangha to receive or transmit the proper impulse; or to an overactivity of the thyroid neutraIizing the stimulating effect of the pituitary secretion. Who knows but that this recent observation of Falls may not be the onIy cause of this reIativeIy rare primarv inertia lIteri. Time and further observation wiI1 bring to light more definite information on this particular factor. It is IogicaI to suppose that if overstimulation of the pituitary secretions wiII produce atypica1 types of labor, such as habitual abortion, the theory that the faiIure of the hypophysis t,o produce sufficient hormone and transmit the proper impuIse aIong with the overactivity of the thyroid, neutraIizing the effect of pituitary secretion, may be just as Iogical. The older authors cIaimed that primary inertia uteri impIies that the inertia is due to some inherent fault in the uterus and that it is certainiy not due to any recognizable cause outside of the uterus, which, in the light of the recent work of FaIIs, seems not to be entireIy so. It is proposed therefore, to use the term primary inertia uteri in a11 cases of weakness and ineffectiveness of uterine contractions, except those in which the uterus is in a state of exhaustion and has lost a11 power of contraction and retraction, a condition resulting from proIonged and powerfu1 action in the attempt to overcome abnormal resistance, and known as secondary inertia uteri. The primary inertia uteri is more commoniy seen in primiparae and next most frequently in eIderIy muItiparae; it occurs more frequentIy in very young and very eIderly women rather than in those of average age. Contributory Factors. Numerous contributory factors have been described and ha\,e been known to exist. As a contributory factor it is considered to be hereditary; common in eIderIy primiparae, and in elderly muItiparae who have many years interva1 between their pregnancies, in the obese, in delicate women, in invalids, in convalescents from the acute infectious
Inertia
American
Jwrnal
<,I Ptil-gc,v
359
diseases, and in those whose lack of nourishment may be attributed to hyperemesis gravidarum. Remediable Factors. Those occasionally pIaced among the causes of primary inertia uteri are, overdistention of the bladder, feca1 impaction of the rectum, abdomina1 tympanitis, and overloaded stomach, a11 of which have been known to impede or hamper the functiona actilrity of the uterine musculature. If we go more intimateIjinto defective intervention, the paraIysis of the nerve centers which preside over uterine contractions is well expIained under Falls’ recent work, to which I have already aIIuded. Improper development of the uterine muscuIature can be classed under congenital abnormaIities, which are easiI\ recognizabIe in the underdevelopment of the sex organs and the infantiIe uterus encountered in such individuaIs. Uterus dideIphus, uterus biceptus, uterus unicornis and hicornis, are uterine abnormaIities which IogicaIIy do not permit of proper uterine muscular function. AbnormaI positions of the uterus retard its functional activity to guide and expel the uterine contents by the norma mechanism of expuIsion. This frequently prohibits the presenting part from entering the birth cana in normal spontaneous relation, and resuIts in abnormalities of position and presentation as we11 as ineffective muscuIar contractions which fair to produce the diIatation of the Iower uterine segment and cervica1 OS. Likewise does this occur in term pregnancies where the uterus is in compIete proIapse. Overdistention of the uterus as in poIyhydramnios, where an excessive amount of fluid is present in multipIe pregnancies, and abnormalities of the fetus, causing an overstretching of the uterine muscuIature which interferes with the normal muscIe action of the uterus, producing ineffective contractions and resurting in proIonged Iabor. NeopIasms of the uterine waI1 such as muItipIe myoma uteri, so infiltrate the
360
American Journal of Surgery
Vaux-Uterine
muscIe waII that ineffective contractions rest&. Abnormalities which occasionaIIy arise between the firm adhesion of the embryona1 sac and the uterine waI1, as described by Edgar,l cause poor uterine muscIe action. The rapidIy succeeding pregnancies, where the increase of the connective tissue in the intermuscuIar interstices gives us the picture of a fibrous muscIe seen in the waI1 of the uterus, resuIts in poor and ineffIcient uterine contractions. Management. The management of primary inertia uteri caused by defective intervention of the nerve centers is, in most instances, operative intervention. Likewise the defective deveIopment of the uterine muscuIature, the abnorma1 shapes of the uterus, and the abnorma1 positions of the uterus, frequentIy require surgica1 intervention. Interference for the draining of the ffuid in poIyhydramnios cases is often sufficient to bring about and restore the muscIe tone. The neopIasms of the uterine waII occasionaIIy so infiltrate and interfere with function of the uterine contractions that rupture of the uterus is to be considered IogicaI when the tumor growths encroach upon and prohibit the presenting part from entering the birth cana1. In such cases operative intervention, with at times a Porro cesarean section, is considered the procedure of choice. If the diagnosis of adhesions between the sac and the uterine waI1 can be made previous to the onset of Iabor, operative intervention is considered just&abIe. In those individuaIs whose rapidIy succeeding pregnancies have produced fibrosis and interference with muscuIar contraction, it is wiser and safer to aIIow the uterus to rest itseIf during the course of Iabor, rather than embark upon too early operative intervention. Where the pituitary secretions and the overactivity of the thyroid are found to be the etioIogica1 factor, the administration of the proper substances may produce a prompt and compIete return of uterine muscuIar activity. In the active treatment of the contributory factors caution is considered of primary importance. ReasonabIe time shouId
Inertia be aIIowed for the first and second stages of Iabor. Intervention by operative procedures is justifiabIe when the feta1 and materna1 Iife is threatened. In the treatment of the remediabIe factors, the proper observation, care and treatment of the individua1 during Iabor wiI1 overcome the potentia1 abnormaIity and return the uterine muscuIature to proper functiona activity. Secondary inertia uteri occurs more frequentIy than primary and is more common in the primiparae whose soft parts are rigid, and is aIso found associated with any condition, either materna1 or feta1, which heightens the resistance of the passage of the chiId through the birth cana1. Among the common conditions causing obstructive inertia or atony of the uterus, we find that any obstruction of the birth cana which exhausts or threatens the muscuIar activity of vigorous uterine contractions, can be cIass&ed as. causative factors, as the secondary inertia uteri is characterized by exhaustion of the muscuIature, atony, or paresis of the structures. Primary and secondary inertia uteri are not cIoseIy reIated, yet the two forms do possess some factors in common. The secondary type of inertia wiI1 give threatening symptoms of exhaustion both in the first and second stages of Iabor, characterized by the faiIure of the contractions to cause progressive diIatation of the cervix, which manifest themseIves when the contractions occur at Ionger intervaIs and are of shorter duration. In the first stage of Iabor attention is caIIed to the Iong interva1 between the pains and the presence of nothing of moment, except the mere deIay or prolongation of Iabor. In individuaIs where the Iiquor amnii has Ieaked away sIowIy, the futiIe efforts of the uterine contractions wiI1 often Iead to beginning exhaustion. Dry Iabor which so often results from this too earIy and sIow escape of Iiquor amnii, is no Ionger feared, as in the past, but the danger of the tendency for the retraction of the Iower uterine segment to form a contraction ring, thus causing dystocia, is not to be overIooked.
Even the failure of dilatation and expuIsion of the presenting part may cause a further thinning out of the Iower uterine segment and threatening rupture of the uterus. Of a11 the etioIogica1 factors of secondary inertia ut.eri which cause uterine fatigue or exhaustion, the commonest are cephalopelvic disproportion, abnorma1 presentation and lie, maIpositions and fauIty positions, along with any obstructive Iesion of the bony peIvis, maternal soft parts, or feta1 structures. Secondary inertia uteri can aImost be prognosticated, if any of the mentioned etioIogica1 factors are determined before the onset of labor. It is for this reason aIone, that insistence is placed upon having thorough knowIedge of what is to be encountered during the course of the first stage of Iabor, so that treatment of the eventual exhaustion of the uterine muscuIature can be instituted immediateIy, when indicated. Serious and even fata postpartum hemorrhage from an exhausted uterine muscIe can in this way, by timeIy operative intervention, be avoided. AI1 treatment of secondary inertia uteri is based first, on the etioIogica1 factor, and second, on the proper conduct of the case to prevent the uterine exhaustion. Rest from the strain of vigorous contractions during the first and second stages of Iabor is the onIy treatment indicated, and is in most instances highIy satisfactory, if the obstruction is of moderate character. No patient, if the proper treatment is instituted at the onset, shouId be aIIowed to enter the realm of extreme fatigue and exhaustion. If such disproportion, malpresentation, or faulty- position is found to be present before the onset of labor, or during the course of Iabor, timeIy operative interference wiI1 prohibit this grave exhaustive reIaxation of the uterus. Operative deIivery before the uterine muscuIature threatens fatigue is justified, provided operative intervention at this time does not threaten more serious consequences for the individua1. The maIicious practice of the administration of pituitary extract hypodermicaIIy shouId
never be undertaken to overcome a disproportion, particuIarIy when the cer\is is not fuIIy diIated, the membranes unruptured, and the presenting part high in the pelvis, as this procedure increases the risk of maternal uterine rupture and permanent injury to the child. Secondary inertia uteri is a preventabIe condition, provided thorough and complete examination has been made and fuI1 knowIedge of the case is at hand. The primary inertia uteri is Iikewise a preventable condition if the findings of proper and sufficient examination are recorded and compIeteIy and accurateIy understood. CONCLUSIONS
Primary and secondary inertia uteri are essentialIy different and can be deferentiated when the etiological factor and cause of the condition are determined. The primary can we11 be associated with imperfect development of the structures and abnormaIities in construction of the parts, whiIe secondary inertia is more of an atonic condition brought about by the tiring and exhausting uterine muscuIature. Differentia1 diagnosis between the two is essentia1 in the proper handIing of this abnormality. REFERENCES I. 2.
3. 4. 5. 6.
Practice of Obstetrics, Ed. I, 5 and 6. FALLS, FREDERICK II. Curtis’ Obstetrics and Gynecology, vo1. 2, Chap. 35, p. 74. BLAND. PracticaI Obstetrics. FAIRBAIRN. Obstetrics and Gynaccologp. WILLIAMS. Obst.etrics, 6th Ed. L~co~wa, IV. Therapy of incoercible hemorrhages caused by atony in labor. Midicine, 16: 282-285 EDGAR.
(April)
1935.
of postpartum hemorrhage 7. SALACZ, P. Treatment due to atony. Jour. Obst. and Gynaec. hit. Emp., 42: 476-489
(June)
1935.
8. DEBIASI, E. and ROMUSSI, P. Intravenous
injection of pituglnndo1 in therapy of postpartum metrorrhagia from atony. C/in. Astet, 37: 2-m~7 (Jan.)
‘935. 9. STONE, E. L. De-vice for correction of postpartum atony. Am. Jour. Oh. and G~v~ec., 26: I 18-r rg (JuIy)
1933.
‘0. BOURNE, A. C. Inertia utei-i. Jour. Obst. and Gynec. &if. Emp., 40: 423-443 (,%Iay) 1933. II. GARBER, ILI. Diagnosis and treatment of IOOcases of inertia uteri. Ohio State Med. Jour., 28: 521-523 (July) 1932. F. Postpartum hemorrhage caused 12. TAUKERSI.EY, by uterine reIaxation, Jour. Med. Assn. Alabama,
2: ,g?.-rg5
(Nov.)
1932.
W.
VAUX,
M.D.
Professor of Obstetrics, Jefferson MedicaI College; Obstetrician and GynecoIogist-in-Chief, BuiIding of the PennsyIvania Hospital
Woman’s
PHILADELPHIA
T
HE most commonIy known definitions of “inertia uteri” are: (I) Iabor proIonged to such an extent as to be dangerous to both mother and chiId; (2) insuffIcient contractions of the uterus to overcome the norma resistance of the passage of the chiId through the parturient cana1, which may at times be produced by abnormaIities existing in the mother or in the fetus; (3) that condition in which the uterine contractions, by reason of their weakness or irreguIarity, are insuffIcient to diIate the cervical OS in the first stage of Iabor, or expe1 the fetus in the second stage. In the more recent literature on this subject, inertia uteri has assumed the phrase of “atonic uterus” or “atony of the uterus.” This modern conception of the inert uterus defined as “atony,” is not as specific or as comparabIe as the inertia uteri of the oIder authorities. The word inertia means sIuggish, persists in the state of rest, uniform motion unIess some force changes that state, which describes we11 the characteristics of uterine inertia. On the other hand, atonic is defined as Iack of tone or vigor, which does not symboIize as we11 the characteristics of the primary inert uterus, but couId we11 be utiIized in defining the secondary type. We shaI1 adhere to the oIder nomencIature of “ inertia uteri ” throughout this resume of the subject. Inertia uteri may therefore be divided into two distinct cIasses: primary or true inertia uteri, and secondary, or uterine exhaustion. Under these two main cIassifications we are abIe to pIace the etioIogica1 factors which produce one or the other of these conditions. Primary or true inertia uteri is that condition in which the uterine contractions have never been sufficient to throw the 358
uterus into contraction, either before the onset or from the beginning of labor. It is a most unusua1 type of inertia and probabIy one of the rarest varieties of proIongation of pregnancy or Iabor. Etiology. The primary inertia uteri arises from a variety of conditions such as: I. Defective intervention (paraIysis of nerve center which presides over uterine contractions) ; 2. Defective deveIopment of the uterine muscuIature; 3. AbnormaI shape of the uterus due to uterine abnormaIities; 4. AbnormaI positions of the uterus as seen in the anteflexions of penduIous abdomens, also in proIapsus uteri; 3. Overdistention of the uterus as in poIyhydramnios; 6. NeopIasms of the uterine waI1; 7. Adhesions between the embryona1 sac and the uterine waI1;’ 8. RapidIy succeeding pregnancies. As an etioIogica1 factor in this condition, FaIIs2 expIains the atypica1 types of Iabor producing habitua1 abortion due to overstimuIation of the pituitary secretions, hypersensitiveness of the peIvic sympathetic ganglia, or a decrease in the norma inhibiting activity of the thyroid. He further states that those cases that tend to go Ionger than the two-hundred and eighty days may be expIained on exactIy the opposite grounds; nameIy, a mild hyperthyroidism, weak pituitary hormone production, or reIativeIy insensitive peIvic sympathetic gangIia. According to this theory, primary inertia uteri may not necessariIy be due to abnormalities in the uterus, but may be secondary to faiIure of the hypophysis to produce sufficient hor-
NE:\\
5~m11.s V-or..
TXXV,
No.
2
Vaux---Uterine
mone; to failure of the sympathetic gangha to receive or transmit the proper impulse; or to an overactivity of the thyroid neutraIizing the stimulating effect of the pituitary secretion. Who knows but that this recent observation of Falls may not be the onIy cause of this reIativeIy rare primarv inertia lIteri. Time and further observation wiI1 bring to light more definite information on this particular factor. It is IogicaI to suppose that if overstimulation of the pituitary secretions wiII produce atypica1 types of labor, such as habitual abortion, the theory that the faiIure of the hypophysis t,o produce sufficient hormone and transmit the proper impuIse aIong with the overactivity of the thyroid, neutraIizing the effect of pituitary secretion, may be just as Iogical. The older authors cIaimed that primary inertia uteri impIies that the inertia is due to some inherent fault in the uterus and that it is certainiy not due to any recognizable cause outside of the uterus, which, in the light of the recent work of FaIIs, seems not to be entireIy so. It is proposed therefore, to use the term primary inertia uteri in a11 cases of weakness and ineffectiveness of uterine contractions, except those in which the uterus is in a state of exhaustion and has lost a11 power of contraction and retraction, a condition resulting from proIonged and powerfu1 action in the attempt to overcome abnormal resistance, and known as secondary inertia uteri. The primary inertia uteri is more commoniy seen in primiparae and next most frequently in eIderIy muItiparae; it occurs more frequentIy in very young and very eIderly women rather than in those of average age. Contributory Factors. Numerous contributory factors have been described and ha\,e been known to exist. As a contributory factor it is considered to be hereditary; common in eIderIy primiparae, and in elderly muItiparae who have many years interva1 between their pregnancies, in the obese, in delicate women, in invalids, in convalescents from the acute infectious
Inertia
American
Jwrnal
<,I Ptil-gc,v
359
diseases, and in those whose lack of nourishment may be attributed to hyperemesis gravidarum. Remediable Factors. Those occasionally pIaced among the causes of primary inertia uteri are, overdistention of the bladder, feca1 impaction of the rectum, abdomina1 tympanitis, and overloaded stomach, a11 of which have been known to impede or hamper the functiona actilrity of the uterine musculature. If we go more intimateIjinto defective intervention, the paraIysis of the nerve centers which preside over uterine contractions is well expIained under Falls’ recent work, to which I have already aIIuded. Improper development of the uterine muscuIature can be classed under congenital abnormaIities, which are easiI\ recognizabIe in the underdevelopment of the sex organs and the infantiIe uterus encountered in such individuaIs. Uterus dideIphus, uterus biceptus, uterus unicornis and hicornis, are uterine abnormaIities which IogicaIIy do not permit of proper uterine muscular function. AbnormaI positions of the uterus retard its functional activity to guide and expel the uterine contents by the norma mechanism of expuIsion. This frequently prohibits the presenting part from entering the birth cana in normal spontaneous relation, and resuIts in abnormalities of position and presentation as we11 as ineffective muscuIar contractions which fair to produce the diIatation of the Iower uterine segment and cervica1 OS. Likewise does this occur in term pregnancies where the uterus is in compIete proIapse. Overdistention of the uterus as in poIyhydramnios, where an excessive amount of fluid is present in multipIe pregnancies, and abnormalities of the fetus, causing an overstretching of the uterine muscuIature which interferes with the normal muscIe action of the uterus, producing ineffective contractions and resurting in proIonged Iabor. NeopIasms of the uterine waI1 such as muItipIe myoma uteri, so infiltrate the
360
American Journal of Surgery
Vaux-Uterine
muscIe waII that ineffective contractions rest&. Abnormalities which occasionaIIy arise between the firm adhesion of the embryona1 sac and the uterine waI1, as described by Edgar,l cause poor uterine muscIe action. The rapidIy succeeding pregnancies, where the increase of the connective tissue in the intermuscuIar interstices gives us the picture of a fibrous muscIe seen in the waI1 of the uterus, resuIts in poor and ineffIcient uterine contractions. Management. The management of primary inertia uteri caused by defective intervention of the nerve centers is, in most instances, operative intervention. Likewise the defective deveIopment of the uterine muscuIature, the abnorma1 shapes of the uterus, and the abnorma1 positions of the uterus, frequentIy require surgica1 intervention. Interference for the draining of the ffuid in poIyhydramnios cases is often sufficient to bring about and restore the muscIe tone. The neopIasms of the uterine waII occasionaIIy so infiltrate and interfere with function of the uterine contractions that rupture of the uterus is to be considered IogicaI when the tumor growths encroach upon and prohibit the presenting part from entering the birth cana1. In such cases operative intervention, with at times a Porro cesarean section, is considered the procedure of choice. If the diagnosis of adhesions between the sac and the uterine waI1 can be made previous to the onset of Iabor, operative intervention is considered just&abIe. In those individuaIs whose rapidIy succeeding pregnancies have produced fibrosis and interference with muscuIar contraction, it is wiser and safer to aIIow the uterus to rest itseIf during the course of Iabor, rather than embark upon too early operative intervention. Where the pituitary secretions and the overactivity of the thyroid are found to be the etioIogica1 factor, the administration of the proper substances may produce a prompt and compIete return of uterine muscuIar activity. In the active treatment of the contributory factors caution is considered of primary importance. ReasonabIe time shouId
Inertia be aIIowed for the first and second stages of Iabor. Intervention by operative procedures is justifiabIe when the feta1 and materna1 Iife is threatened. In the treatment of the remediabIe factors, the proper observation, care and treatment of the individua1 during Iabor wiI1 overcome the potentia1 abnormaIity and return the uterine muscuIature to proper functiona activity. Secondary inertia uteri occurs more frequentIy than primary and is more common in the primiparae whose soft parts are rigid, and is aIso found associated with any condition, either materna1 or feta1, which heightens the resistance of the passage of the chiId through the birth cana1. Among the common conditions causing obstructive inertia or atony of the uterus, we find that any obstruction of the birth cana which exhausts or threatens the muscuIar activity of vigorous uterine contractions, can be cIass&ed as. causative factors, as the secondary inertia uteri is characterized by exhaustion of the muscuIature, atony, or paresis of the structures. Primary and secondary inertia uteri are not cIoseIy reIated, yet the two forms do possess some factors in common. The secondary type of inertia wiI1 give threatening symptoms of exhaustion both in the first and second stages of Iabor, characterized by the faiIure of the contractions to cause progressive diIatation of the cervix, which manifest themseIves when the contractions occur at Ionger intervaIs and are of shorter duration. In the first stage of Iabor attention is caIIed to the Iong interva1 between the pains and the presence of nothing of moment, except the mere deIay or prolongation of Iabor. In individuaIs where the Iiquor amnii has Ieaked away sIowIy, the futiIe efforts of the uterine contractions wiI1 often Iead to beginning exhaustion. Dry Iabor which so often results from this too earIy and sIow escape of Iiquor amnii, is no Ionger feared, as in the past, but the danger of the tendency for the retraction of the Iower uterine segment to form a contraction ring, thus causing dystocia, is not to be overIooked.
Even the failure of dilatation and expuIsion of the presenting part may cause a further thinning out of the Iower uterine segment and threatening rupture of the uterus. Of a11 the etioIogica1 factors of secondary inertia ut.eri which cause uterine fatigue or exhaustion, the commonest are cephalopelvic disproportion, abnorma1 presentation and lie, maIpositions and fauIty positions, along with any obstructive Iesion of the bony peIvis, maternal soft parts, or feta1 structures. Secondary inertia uteri can aImost be prognosticated, if any of the mentioned etioIogica1 factors are determined before the onset of labor. It is for this reason aIone, that insistence is placed upon having thorough knowIedge of what is to be encountered during the course of the first stage of Iabor, so that treatment of the eventual exhaustion of the uterine muscuIature can be instituted immediateIy, when indicated. Serious and even fata postpartum hemorrhage from an exhausted uterine muscIe can in this way, by timeIy operative intervention, be avoided. AI1 treatment of secondary inertia uteri is based first, on the etioIogica1 factor, and second, on the proper conduct of the case to prevent the uterine exhaustion. Rest from the strain of vigorous contractions during the first and second stages of Iabor is the onIy treatment indicated, and is in most instances highIy satisfactory, if the obstruction is of moderate character. No patient, if the proper treatment is instituted at the onset, shouId be aIIowed to enter the realm of extreme fatigue and exhaustion. If such disproportion, malpresentation, or faulty- position is found to be present before the onset of labor, or during the course of Iabor, timeIy operative interference wiI1 prohibit this grave exhaustive reIaxation of the uterus. Operative deIivery before the uterine muscuIature threatens fatigue is justified, provided operative intervention at this time does not threaten more serious consequences for the individua1. The maIicious practice of the administration of pituitary extract hypodermicaIIy shouId
never be undertaken to overcome a disproportion, particuIarIy when the cer\is is not fuIIy diIated, the membranes unruptured, and the presenting part high in the pelvis, as this procedure increases the risk of maternal uterine rupture and permanent injury to the child. Secondary inertia uteri is a preventabIe condition, provided thorough and complete examination has been made and fuI1 knowIedge of the case is at hand. The primary inertia uteri is Iikewise a preventable condition if the findings of proper and sufficient examination are recorded and compIeteIy and accurateIy understood. CONCLUSIONS
Primary and secondary inertia uteri are essentialIy different and can be deferentiated when the etiological factor and cause of the condition are determined. The primary can we11 be associated with imperfect development of the structures and abnormaIities in construction of the parts, whiIe secondary inertia is more of an atonic condition brought about by the tiring and exhausting uterine muscuIature. Differentia1 diagnosis between the two is essentia1 in the proper handIing of this abnormality. REFERENCES I. 2.
3. 4. 5. 6.
Practice of Obstetrics, Ed. I, 5 and 6. FALLS, FREDERICK II. Curtis’ Obstetrics and Gynecology, vo1. 2, Chap. 35, p. 74. BLAND. PracticaI Obstetrics. FAIRBAIRN. Obstetrics and Gynaccologp. WILLIAMS. Obst.etrics, 6th Ed. L~co~wa, IV. Therapy of incoercible hemorrhages caused by atony in labor. Midicine, 16: 282-285 EDGAR.
(April)
1935.
of postpartum hemorrhage 7. SALACZ, P. Treatment due to atony. Jour. Obst. and Gynaec. hit. Emp., 42: 476-489
(June)
1935.
8. DEBIASI, E. and ROMUSSI, P. Intravenous
injection of pituglnndo1 in therapy of postpartum metrorrhagia from atony. C/in. Astet, 37: 2-m~7 (Jan.)
‘935. 9. STONE, E. L. De-vice for correction of postpartum atony. Am. Jour. Oh. and G~v~ec., 26: I 18-r rg (JuIy)
1933.
‘0. BOURNE, A. C. Inertia utei-i. Jour. Obst. and Gynec. &if. Emp., 40: 423-443 (,%Iay) 1933. II. GARBER, ILI. Diagnosis and treatment of IOOcases of inertia uteri. Ohio State Med. Jour., 28: 521-523 (July) 1932. F. Postpartum hemorrhage caused 12. TAUKERSI.EY, by uterine reIaxation, Jour. Med. Assn. Alabama,
2: ,g?.-rg5
(Nov.)
1932.