Using the internal inguinal ring as a landmark for the safe placement of secondary trocars at laparoscopy

Aim Avoidance of injury to the epigastric vessels is an important safety consideration in siting secondary ports at laparoscopy. We evaluated trans-illumination, direct visualization of vessels and using the internal inguinal ring, which has a constant relationship with the inferior epigastric vessels as an anatomical landmark to locate these vessels. Methods Ninety consecutive women undergoing laparoscopy were recruited for the study. The Ability to trans-illuminate the superficial and inferior epigastric vessels, to visualize inferior epigastric vessels and to locate the round ligament entering the internal inguinal ring were documented. The body mass index (BMI) was noted. The association of the body mass index (BMI) with these variables was calculated by simple regression analysis. Results Ability to visualize the internal inguinal ring was significantly higher than that of locating the superficial or inferior epigastric vessels by trans -illumination or by directvisualization. p Ability to visualize and to trans -lluminatethe inferior epigastric vessels decreased with increasing BMI (p Conclusion Locating the deep inguinal ring and using it as an anatomical landmark and placing the lateral trocars lateral to a saggital line originating from the internal ring is a reliable and useful method in preventing unintended injury to anterior abdominal wall vessels during secondary trocar placement


INTRODUCTION
The course of labour is the first challenge one ever undertakes.The uterine contractions during labour exposes the fetus to a possible risk of hypoxic brain injury due to repeated cord compression or reduction of utero-placental perfusion 1 .Intrapartum fetal surveillance evolved with the principal aim of preventing adverse perinatal outcomes arising from fetal metabolic acidosis / cerebral hypoxia related to labour.However, the severity of an asphyxial injury is influenced by many factors (e.g.tissue perfusion, tissue substrate availability, fetal condition prior to the insult, duration of the insult and the severity of the insult).Therefore, the relationship between metabolic acidosis and cerebral injury is complex.Furthermore, it is clear that very often damage is actually sustained during pregnancy, prior to labour, rather than arising de novo during labour and delivery 2 .In spite of this, intrapartum fetal surveillance for early detection of fetal hypoxia has become a key component of modern maternity care.Intrapartum fetal surveillance was traditionally carried out by intermittent auscultation (IA) of the fetal heart rate (FHR).This approach would be adequate to monitor a fetus at low risk of compromise, but may be inadequate for high-risk pregnancies.Therefore, the use of intrapartum electronic fetal monitoring (EFM) with cardiotocography (CTG), has steadily increased over the last three decades in an attempt to reduce the incidence of intrapartum fetal morbidity and mortality.

Leading articLe
www.slcog.lk/sljogbeen suggested that the only clinically significant benefit from the use of routine continuous EFM in comparison to IA was in the reduction of neonatal seizures but with no statistically significant improvement in long-term outcomes such as cerebral palsy, although it increased the caesarean section and operative vaginal delivery rates 3 .Therefore, the use of continuous CTG for low risk pregnancies is not recommended 4 .It is also widely appreciated that there are still shortcomings in interpretation of CTG which is evident by the reviews of cases with poor perinatal outcomes 5 .
In order to improve the interpretation of CTG, it is important to understand the control of the fetal heart rate by the sinoatrial node, sympathetic and para-sympathetic autonomic nervous systems, baroreceptors, chemoreceptors, catecholamines and cardio-regulatory center.In addition to that, the physiology of fetal oxygenation and how the fetus reacts to hypoxia, the types of intra partum hypoxia (gradual, subacute, acute, chronic), the pathophysiological basis for CTG abnormalities, and the principles of EFM should also be clearly understood for decision making on intrapartum CTG 6,7 .Because of the inherent limitations of the CTG, especially its poor specificity, newer techniques such as analysis of the ST segment of the fetal electrocardiograph (STAN), the calculation of the Fetal Physiological Score (FPS), and computer assisted interpretation of CTG are being studied 8 .

CARDIOTOCOGRAPHy
An Intrapartum CTG provides information about the fetal condition.A normal trace indicates a well-oxygenated fetus but an abnormal trace has poor specificity with upto 60% false positive rates being reported 9 .It has been suggested that FHR accelerations are a sign of a neurologically responsive fetus that does not have hypoxia/acidosis.However, the absence of accelerations in an otherwise normal CTG is of uncertain significance but it is unlikely to indicate hypoxia/acidosis 10 .
A mistake which could occur with intrapartum CTG is the recording of maternal heart rate, especially in the second stage of labour.A change in the pattern, sudden change in baseline rate and accelerations coinciding with contractions may help in the differentiation from FHR.

TACHySySTOLE AND UTERINE HyPERTONUS
More than five uterine contractions in 10 minutes without FHR abnormalities is defined as tachysystole.Contractions lasting >2 minutes in duration or contractions occurring within 60 seconds of each other, without FHR abnormalities is referred to as uterine hypertonus 2 .The management of these conditions includes reduction or cessation of oxytocin infusion and consideration of tocolysis.

UTERINE HyPERSTIMULATION
Tachysystole or uterine hypertonus in the presence of FHR abnormalities is defined as uterine hyperstimulation 2 .If conservative measures such as cessation of oxytocin and tocolysis fail, urgent delivery needs to be considered.Commonly used protocols for acute tocolysis include terbutaline 250mcg iv or subcutaneous, salbutamol 100mcg iv, and glyceryl tri nitrate spray 400mcg sublingual.

REDUCED VARIABILITy
A bandwidth amplitude < 5 bpm for > 50 minutes in baseline segments, or for more than 3 minutes during decelerations indicates reduced variability.It can occur due to central nervous system hypoxia/ acidosis, but it can also be seen with any condition which causes central nervous system (CNS) depression namely; deep fetal sleep, previous cerebral injury, infection, administration of CNS depressants or parasympathetic blockers, prematurity, and fetal abnormalities 10 .
Although its pathophysiology is poorly understood, it is thought to be due to a hyperactive fetal autonomic nervous system.It may be seen in fetal hypoxia associated with decelerations (10).

FETAL TACHyCARDIA
A baseline FHR > 160 bpm lasting > 10 minutes is considered as fetal tachycardia but is not associated with hypoxia in the presence of accelerations or with normal variability and absent decelerations 10 .Maternal fever and tachycardia, sympathomimetic medications (eg.terbutaline and salbutamol) chorioamnionitis, fetal tachyarrhythmias, a high inherent rate due to prematurity are some of the known causes of fetal tachycardia apart from fetal hypoxia.

VARIABLE DECELERATIONS
Variable decelerations represent a baroreceptor-mediated response to increased arterial pressure, as occurs with umbilical cord compression.They are variable in shape, depth, duration and timing with the contractions and exhibit a good variability within the deceleration.They typically have a rapid onset (onset to nadir < 30 seconds) and a rapid recovery to baseline.Variable decelerations constitute the majority of decelerations during labour.They are seldom associated with an important degree of fetal hypoxia/acidosis.Increases in FHR immediately before and after a variable deceleration have been referred to as "shoulders."These increases can be visually similar to accelerations, and this led to speculations that they had a similar predictive value.However, there is inadequate evidence to support the notion that "shoulders" have the same predictive value as accelerations 12 .
Variable decelerations were formerly categorized as 'typical' if they were considered to be normal and not indicating fetal hypoxia and 'atypical' if they were considered to be abnormal and indicating probable fetal hypoxia.Although the terms 'typical' and 'atypical' are not currently used, the non-reassuring features in variable decelerations which require appropriate action, as they indicate the likelihood of fetal hypoxia, have been clearly described 2,6,11 .These nonreassuring features which are also referred to as 'complicated variable decelerations' include a persistently large amplitude (> 60 bpm in depth) and / or long duration (> 60 seconds duration), a slow return to the baseline after the contraction, smooth (with no baseline variability) postdeceleration shoulders ("overshoots") often associated with a rising baseline or a baseline tachycardia and a reduced baseline variability 6 .

LATE DECELERATIONS
Late decelerations are caused by contractions in the presence of fetal hypoxia.These are uniform and repetitive.Late decelerations start after the start of the contraction and the nadir of the deceleration is more than 30 seconds after the peak of the contraction.They return to the baseline after the contraction has finished.Late decelerations of any depth are significant and should be immediately attended to.In fact shallow decelerations (with decreases of < 10 bpm ) with reduced baseline variability are particularly dangerous and indicate significant fetal hypoxia.These can even be detected with careful IA of FHR immediately after uterine contractions, but not in between uterine contractions when the FHR has returned to its normal baseline

PROLONGED DECELERATIONS
Decelerations lasting > 3 minutes are defined as prolonged decelerations.They may indicate chemoreceptor-mediated hypoxaemia.Decelerations exceeding 5 minutes, with FHR less than 80 bpm and reduced variability within the deceleration are frequently associated with acute fetal hypoxia/acidosis and require urgent intervention 10 .

SINUSOIDAL PATTERN
This is an oscillating pattern resembling a sine wave (very smooth with a regular cycle rate).It has a relatively fixed period of 3-5 cycles per minute and typically an amplitude of 5-15 beats.Its pathophysiology is poorly understood but it may be seen with severe fetal anemia (fetal-maternal haemorrhage, twinto-twin transfusion syndrome, anti-D alloimmunization and vasa previa) It has also been described in cases of acute fetal hypoxia, infection, cardiac malformations, hydrocephalus, and gastroschisis 10 .
There is agreement about baseline FHR and fetal tachycardia, with FIGO describing a time frame too .Although NICE Guidelines describe FHR of 160-180 bpm as non-reassuring and FHR > 180 bpm as pathological, FIGO Guidelines do not sub categorize fetal tachycardia in this manner.A fetal tachycardia (FHR > 160 bpm) may be secondary to fetal compensatory response to evolving hypoxia.A mere increase in  There is no significant difference in the definitions of normal baseline variability and reduced variability, between the different guidelines.However, the NICE Guidelines further categorize reduced baseline variability being non-reassuring or abnormal according to the duration, which would be more useful in clinical decision making.

STEP 1-THE NORMAL AND THE ABNORMAL INITIAL CTG
If the CTG is normal the fetus is very likely to be neurologically intact, normoxic, without acidaemia or acidosis, at low risk of intrapartum asphyxia, and is able to react and defend itself against intrapartum hypoxia.Surveillance may continue depending on the situation or the woman may be monitored by IA 13 .

STEP 2-RECOGNITION OF THE COMPENSATED AND THE DECOMPENSATING FETUS
An intact fetus with a previously normal CTG will exhibit predictable patterns of FHR responses if exposed to hypoxic ischaemic insults during labour.Based on the intensity and duration of hypoxic stress during labour, three types of intrapartum hypoxia had been described, namely: gradually evolving hypoxia; subacute hypoxia; and acute hypoxia.The management should be tailed according to the type of hypoxia to optimize fetal outcome 7 .

GRADUALLy EVOLVING HyPOxIA
The hypoxic stress evolves over time (hours) giving the fetus time to use its compensatory mechanisms effectively in order to prevent hypoxic damage.The first feature on CTG is the presence of decelerations with contractions.If the hypoxic insult continues, the decelerations will be followed by ABCDE.

End stage
The accelerations disappear in order to conserve oxygen and energy substrates in the fetus.The catecholamine release increases the FHR and cardiac output to maintain perfusion to the vital organs.Therefore, a sustained FHR tachycardia in association with uterine contractions is a sensitive marker of a compensatory Leading articLe www.slcog.lk/sljogincrease in fetal cardiac output.If the hypoxic insult continues, depending on the fetal reserve and the intensity and duration of hypoxia, fetal decompensation may ensue.When the perfusion to the brain is compromised, loss in the baseline variability would be observed in the CTG trace.Finally, myocardial hypoxia and acidosis may lead to a terminal bradycardia resulting in the 'step-ladder pattern to death' 7 .
The management should be tailored according to the level of hypoxia.In the presence of a stable baseline in between decelerations and normal baseline variability, labour can be continued with continuous CTG monitoring.If raised baseline and or abnormal variable or late decelerations appear on the CTG, care should be taken to improve fetal environment (intrauterine resuscitation) which may include stopping or reducing oxytocin, iv fluids and placing patient in the left lateral position.If baseline variability is reduced despite conservative measures, immediate delivery should be considered 7 .

ACUTE HyPOxIA
This is characterized by a sudden drop in the baseline heart rate, which is also known as a 'single prolonged deceleration'.This could be either suspicious (lasting for < 3 minutes and returning to the normal baseline with good variability) or abnormal (lasting for > 3 minutes ) First, it is essential to exclude three major intrapartum accidents (placental abruption, umbilical cord prolapse and uterine rupture) and two iatrogenic causes (hyper-stimulation due to oxytocin or prostaglandins and maternal hypotension usually secondary to supine hypotension or epidural analgesia).In case of intrapartum accidents, delivery should be expedited via the safest and quickest way to save the fetus.
If acute hypoxia is considered to be due to an oxytocin infusion, 'intrauterine resuscitation' should be initiated immediately.In the presence of normal variability prior to deceleration and within the first three minutes of deceleration and the three accidents mentioned above are absent, unto 90% of the prolonged decelerations have been reported to recover by 6 minutes and 95% by 9 minutes 14 .
In case of acute hypoxia occurring in the absence of intrapartum accidents or iatrogenic causes, the '3, 6, 9, 12 and 15-minute' rule , which includes the following ,should be applied: if a normal baseline variability has been noted before the onset of deceleration and within the first 3 min of the deceleration , appropriate intrauterine resuscitation by 6 min, moving the patient to a theatre by 9 min, and if the CTG shows no signs of recovery, commencing delivery by 12 min with the aim of delivering the baby by 15 min 15 .
Reduced baseline variability before or within the first 3 min of the deceleration, repetitive late decelerations before the onset of the prolonged deceleration or a drop in the heart rate to >60 bpm are associated with a poor outcome.In these circumstances, the '3, 6, 9, 12 and 15minute' rule should not be applied, and immediate delivery should be undertaken 7 .

SUBACUTE HyPOxIA
This is characterized by complicated variable decelerations, with the amplitude of the deceleration > 60 bpm and lasting for > 90 seconds.When the FHR returns to its baseline in subacute hypoxia, it spends less than 30 seconds at the baseline level before the onset of the next deceleration 7,16 .Therefore, the time available at the baseline to wash off the acid and carbon dioxide and to obtain fresh oxygenated blood from the placenta becomes progressively shorter.Therefore, a rapidly cumulative build up of CO2 takes place which results in an initial respiratory acidosis and a subsequent metabolic acidosis.The baseline FHR may remain within the normal range (110-160 bpm) as the fetus is unable to raise its baseline heart rate because of the short duration of time spent at the baseline in between two decelerations.Subacute hypoxia is associated with a rapid decline Leading articLe www.slcog.lk/sljog in pH, usually at the rate of 0.01 every 2-4 minutes, in contrast to the gradually evolving hypoxia 16 .
Once subacute hypoxia is established, there is likely to be insufficient time to obtain, analyze and react to a fetal blood sample result without the risk of severe acidaemia.Therefore, in clinical practice, it is crucial to recognize this pattern 16 .
The management involves in utero resuscitation and discouraging active maternal pushing for the next few contractions to ensure oxygenation of placental venous sinuses.Immediate delivery should be considered if changes are not reversed with conservative measures 7 .

CHRONIC HyPOxIA
In this situation, the fetus has been exposed to a prolonged period of hypoxia with or without resultant neurological injury during the antenatal period before the onset of labour.This happens usually secondary to chronic utero-placental insufficiency.The fetus adapts several compensatory mechanisms for survival including reduction in growth, movements and diversion of oxygenated blood and nutrients from non-vital organs to supply the vital organs 7 .
The affected fetus may be identified by the features observed on the CTG; increase in the baseline rate with reduced variability and the presence of shallow decelerations.Even though some degree of cerebral damage may have already taken place, the presence of this CTG pattern requires immediate delivery.This is because, there will be further reduction in oxygenation of the fetus with the onset of labour due to uterine contractions, intermittent umbilical cord compression and reduction in utero-placental circulation.This will eventually lead to hypoxic ischaemic encephalopathy, terminal bradycardia and fetal death 7 .

FETAL SCALP BLOOD SAMPLING (FBS)
This is a test to assess the acid-base status of the fetus.The units employing EFM are encouraged to have access to FBS facilities to aid in the management of labours where fetus shows equivocal CTG changes.FBS can be assessed for pH and lactate levels.The incidence of false positives from an abnormal CTG can be reduced with FBS.A reduction in the total caesarean section rate from 18% to 11% and caesarean section indicated by fetal distress from 7% to 3%, when fetal scalp blood sampling was allowed, has been reported 17 .
The most important question is the identification of the appropriate clinical situation for FBS.Delivery must be expedited and FBS should not be undertaken, if there is clear evidence of serious and/or sustained fetal compromise.Delivery also needs to be expedited if CTG abnormalities are of a degree requiring further assessment, but FBS is unavailable or contraindicated.

Using the internal inguinal ring as a landmark for the safe placement of secondary trocars at laparoscopy
Jayasundara DMCS a , Senanayake HM b , Samarasinghe SHMEC c

INTRODUCTION
With evolution of technology and instruments, laparoscopy has achieved a preeminent role in gynaecologic surgery.
Vascular injuries are one of its dreaded complications.While avoidance of injuries to major vessels such as the aorta, inferior vena cava and ileac vessels has received a great deal of attention, avoidance of injury to the vessels situated in the anterior abdominal wall has received less attention.
Abdominal wall vessels injuries occurs in 0.2-2% of all procedures 1, 2 , almost exclusively during placement of secondary ports.Both the superficial epigastric and inferior epigastric vessels are at risk 3 and injuries to these vessels could be potentially lethal.In a large multicenter observational study, Jansen et al. found injury to the inferior epigastric vessels to be the most common complication encountered and to account for one of the two fatalities reported in their series 4 .In addition, significant morbidity and litigation results from damage to abdominal wall vessels as well 5 .In a study done on entry-related laparoscopic injuries in Finland, it was foundthat 10% of all entry related injuries occurreddue to small vessel injuries with one case needing laparotomy to achieve hemostasis 6 .Injury to epigastric vessels could also create a nuisance, with blood trickling down to the operative field 7 .
In most patients it is possible to avoid these injuries by identifying the vessels by direct laparoscopic visualization and by trans-illumination 8 .Standard teaching dictates that the inferior epigastric vessels should be identified either by transillumination or direct visualization 9 .Trans -illuminationcan often identify the superficial vessels but except in the extremely thin individuals,transillumination of inferior epigastric vessels are difficult 8 .Direct visualization of the inferior epigastric vessels by laparoscope is also not possible in all patients, especially in the obese 7 It has been suggested that other landmarks may have to be considered prior to insertion of secondary trocars for the above reasons 8 .Inferior epigastric vessels arise from the external iliac vessels just before they enter the femoral canal 10 .They then run on the medial margin of the internal inguinal ring to run along the under surface of the lateral third of the rectus abdominis muscle 10 .Its course can be surface marked on the anterior abdominal wall in thin individuals from a point midway between the pubic symphysis and anterior superior iliac spine 10 .As it runs superiorly its distance from the midline reduces.The distance from the midline to the inferior epigastric vessels at the level of the pubis is 7.5 cm while at the level of the umbilicus it is 4.6cm 1 .Since its relationship to the medial margin of the internal ring is consistent, entry of the round ligament provides a convenient pointer to the internal inguinal ring.At laparoscopy, displacement of the uterus in the opposite direction using Sri Lanka Journal of Obstetrics and Gynaecology OCTOBER 2016 the uterine manipulator will make this identification easier.
Therefore, if the lateral trocars are placed lateral to a vertical line originating and extending cephalad from the internal inguinal ring, injury to the inferior epigastric vessels could be avoided.
The objective of this study was to determine the effectiveness of trans -illumination, direct visualization and using the internal inguinal ring as an anatomical landmark to locate the epigastric vessels to safely place secondary ports.We also compared the value of each of these methods with variation of body mass index (BMI).

METHOD
A prospective descriptive study was conducted at the Professorial Gynaecology unit of the Teaching Hospital, Peradeniya, Sri Lanka.Ethical clearance was obtained from the Ethics Review Committee of the Faculty of Medicine of the University of Peradeniya.Informed written consent was obtained from all the participants in the study.Ninety consecutive women undergoing laparoscopy for gynaecologic indications were included in the study.The body weight in kilograms and the height in centimeters,was recorded prior to surgery.The Veress needle was inserted trans-umbilically to create the pneumo-peritoneum in all patients and the abdominal cavity insufflated with carbondioxide gasto a filling pressure of 20 mmHg.A 10mm trocar was inserted via the umbilicus and the laparoscope introducedthrough this trocar.
The ability to identify superficial and inferior epigastric vessels by transillumination and the ability to directly visualize the inferior epigastric vessels by laparoscopy were recorded.Transilumination was done by switching off the theatre lights and visualizing the vessels through the skin while holding the laparoscope intra abdominally with the laparoscope light on, And direct visualization was done using the laparoscope to visualize the inferior epigastric vessels running underneath the peritoneum in the anterior abdominal wall.The ability to locate the round ligament entering the deep ring and visualization of the origin of the inferior epigastric vessels intraabdominally by laparoscopic inspection was also recorded.
To differentiate between superficial and deep vessels the assistant applied firm perpendicular pressure over the vessel located via trans-illumination.Laparoscopically it was determined whether this coincided with the direction of the inferior epigastric vessels 8 .If the inferior epigastricvessels were visualized directly it was also inspected for 5 to 8 cm above the pubic symphysis since this area has been shown to be ideal for placement of the trocar 11 .This was done on both sides of the abdomen.The rest of the surgical procedure was done according to the surgery being carried out.
Proportions of cases with positive resultswere compared usingthe chisquare test.A p value of <0.05 was considered to be significant.The relationship of the effectiveness of trans -illumination, direct visualization and the use of the internal inguinal ring as an anatomical landmark to locate the epigastric vessels with changes in BMI was evaluated using simpleregression analysis.The statistical package Minitab (Version 15) was used.

RESULTS
A total of 90 women with a mean age of 31.8 years (range21-44years, SD; 4.95) were enrolled.The mean BMI was 23.9kg/ m 2 (range 15.6-43kg/m 2 , SD; 4.93) with 55 having a BMI <25kg/m 2 and 35 having a BMI >25kg/m 2 Internal inguinal ring was successfully visualized in 84 (94%) patients, whereas the ability to trans-illuminate superficial epigastric vessels was successful in 50% of the cases and the ability to transilluminate inferior epigastric vessels was successful only in 30% of cases.Inferior epigastric vessels were directly visualized in 56% of cases of which 38% of cases it was also visualized 5cm-8cm above the pubic symphysis which is the area commonly used to insert the lateral trocars.(Table 1) Ability to visualize the internal inguinal ring was significantly higher than the ability to visualize superficial or inferior epigastric vessels either by trans-illumination or directly from the laparoscope (p< 0.001).(Table2).Ability to trans -illuminate the superficial epigastric and inferior epigastric as well as ability to visualize the inferior epigastric vessels directly from the laparoscope decreased with increasing BMI (p< 0.05) However there was no significant relationship between the BMI and the ability to visualize the round ligament entering the deep inguinal ring.(p=0.64).(Table 3).

DISCUSSION
Visualization of the internal inguinal ring was easier than direct visualization or trans-illumination of the superficial and inferior epigastric vessels.The fact that visualization of internal inguinal ring was unaffected by BMI increases its value as a landmark in introducing the lateral ports.
Superficial epigastric vessels were more amenable to trans-illumination than inferior epigastric vessels and there was a strong inverse relationship between the BMI and the ability to trans-illuminate the superficial and inferior epigastric vessels.This same relationship was observed when the inferior epigastric vessels were visualized directly using the laparoscope.These findings have been reported in previous studies as well 8 .
The above findings indicate that traditional methods of avoiding lateral abdominal wall vessel injuries during placement of lateral trocars at laparoscopy like transillumination and direct visualization are helpful when the patient is of normal BMI.These methods become less reliable when the patient becomes overweight

Right Left
Visualization of round ligament entering internal inguinal ring 84 76

Table 1 Success of Methods used for safe placement of the secondport (n= 90)
or obese.This disadvantage was not seen when using internal inguinal ring as an anatomical landmark to locate the origin of the inferior epigastric vessels and placing the lateral trocars lateral to a saggital line extending cephalad from the internal ring.The use of anatomical landmarks as a guide to placing lateral trocars has been described in other studies as well 8.11 .However none of these studies have suggested the use of round ligament entering the internal ring as an anatomical landmark for this purpose.Using midline trocars are also helpful in avoiding lateral abdominal wall vessel injuries but not all gynaecologists are comfortable doing surgeries with midline secondary trocars.
Our study population consisted only of women in the District of Kandy, Sri lanka and we were not able to assess the effect of difference in skin color on trans -illumination of anterior abdominal wall vessels.This could be verified only by conducting studies in women with different skin colours.
In conclusion, identifying the internal inguinal ring is easier than identifying abdominal wall vessels.Placing the secondary trocars lateral to a saggital line originating from the medial border of the internal inguinal ring and extending cephalad is a good method to safely insert the secondary trocars at laparoscopy.This method is not affected by the BMI of the woman.

1.
Signs and/or symptoms of increased intracranial pressure.

4.
No evidence of hydrocephalus, mass, structural, or vascular lesion on imaging.

5.
No localizing neurological signs except a unilateral/ bilateral VI nerve paresis.

Accidental self-insertion of an intrauterine contraceptive device into the bladder
Chandrasiri MD a , Wijeyarathna SN b , Abeygunasekera AM c Colombo South Teaching Hospital, Kalubowila, Sri Lanka.

CASE REPORT
A 20-year old mother of one child had an intrauterine contraceptive device (IUCD) inserted by a primary care medical doctor.Few days later her husband complained of discomfort during coitus and the woman removed the IUCD by herself.Following coitus, due to the fear of another pregnancy she self inserted the IUCD.Few days later she developed dysuria and suprapubic pain.As the symptoms were persisting even after two days, she sought medical advice.She did not have haematuria or difficulty in passing urine.A transvaginal ultrasound scan could not locate the device in the uterine cavity, but showed the IUCD freely floating inside the bladder.X-ray pelvis showed the IUCD in the region of the bladder.(Fig 1) A cystoscopy showed the floating IUCD in the bladder, with no features of perforation or migration.It was retrieved with ease by grasping forceps (Fig 2 ).

DISCUSSION
Foreign bodies in the bladder can be due to self-insertion, migration from adjacent organs (uterus) and by iatrogenic causes.Among commonly self inserted objects, cotton swabs, tampons, paper clips, grass leaves, and plastic beans are reported in literature and are mostly related to acts of sexual gratification.

Case RepoRt
www.slcog.lk/sljogreported and is well known. 2,3 ccidental primary placement of IUCD is rarely reported. 4Accidental self-insertion of an IUCD into the bladder via the urethra is unreported.Although the short female urethra could provide easy access to the bladder for foreign body placement, the extended limbs of the IUCD makes it less likely to be accidentally inserted to the bladder via the urethra.Short duration of few days makes migration unlikely in this patient.Discomfort to the male partner during coitus due to long trailing threads of IUCD is well known and the remedy is to cut the threads shorter.Women should be advised to seek medical assistance for problems related to the IUCD and should be discouraged to manipulate the IUCD by their own.

ESTABLISHING THE CAUSE OF A FETAL DEATH
A 27 year old woman who had not received any antenatal care for her 2 nd pregnancy, was admitted to the academic obstetric unit of the THMG on the morning of 3 rd December 1982 at 34 weeks gestation, with significant lower abdominal pain of sudden onset since the previous evening.She appeared to have a tender uterus extending almost up to the xyphisternum but with ill-defined lateral margins.A death in utero was diagnosed with a Pinnard fetal stethoscope.Identification of fetal parts was difficult but the fetal head was thought to be in the right upper quadrant of the abdomen.She had mild pallor but was haemodynamically stable.The cervix was not effaced, the os was closed and there was no bleeding.She had a two year old son who had been delivered normally but 10 days later she had probably undergone an evacuation of retained products following a secondary postpartum haemorrhage ( no details were available).management and awaiting the spontaneous onset of labour.The next morning as she had still not established labour, a plain X-ray of abdomen (antero-posterior view) was carried out which confirmed the death in utero with marked over riding of skull bones ( Spalding's sign ), and also showed that the fetus was lying transversely in the upper part of the abdomen with its head in the right hypochondrial region.As the initial diagnosis was held in doubt, an exploratory laparotomy was carried out.A macerated fetus of 34 weeks gestation was found in the peritoneal cavity, with its placenta attached to the fundus of the 'post partum' uterus which had a transverse fundal rupture of approximately eight centimeters in length.. Approximately 300 ml of altered blood and meconium was found in the peritoneal cavity.The uterine rupture was repaired in two layers and she was transfused with 500 ml of blood.She had an uncomplicated recovery.The spontaneous rupture of the uterus was presumed to be as a result of a weak scar on the fundus of the uterus, probably consequent to a uterine perforation during a probable evacuation of retained products after the previous normal delivery two years earlier.

ESTABLISHING THE UNDERLyING CAUSE OF SUSPECTED HYPEREMESIS GRAvIDARUM IN A yOUNG GIRL
On 30 th September 1983 a 14 year old girl who was virgo intacta, and denied any form of sexual contact, was admitted to the academic gynaecological unit of the THMG with episodes of vomiting following 17 weeks amenorrhoea, nine months after her menarche.She had an abdomino pelvic mass corresponding to a 16 weeks gravid uterus.Urinary human chorionic gonadotrophin (hCG) was > 700,000 iu/L.In the absence of liquor on aspiration of the mass, an attempted radiological amniogram, using a contrast medium, showed a radio opaque mass with irregular outlines but no vesicles.A haemorrhagic, necrotic tumour about 25 cm in diameter, filling the Pouch of Douglas, the right fallopian tube overlying it and the uterus and the normal left adenaxae on its left, was found on exploratory laparotomy.There was no ascites or secondary deposits.The tumour was almost completely dissected out.Histopathology confirmed a pure chorio carcinoma.Post operatively she was treated with intravenous Methotrexate and Cyclophosphamide in the academic gynaecology unit itself, and she is quite well up to date.Taking into account the clinical and histopathological features, the tumour was considered to be a primary non gestational choriocarcinoma arising from the right ovary.
Both the above cases have been reported earlier 1,2 but are briefly presented again to enable a comparison with the current methods of diagnosis with the aid of sonography and CTG.Spalding's sign is now observed by sonology and not by radiology and the absence of the fetal heart sounds is confirmed by a hand held Doppler fetal heart detector, CTG or sonology, and not by a Pinnard fetal stethoscope.
Only semi-quantitative assays of urinary hCG were available then, using stepwise increasing dilutions of urine and a 'Gravindex Test' which had a sensitivity of only 3500 iu/L.Amniograms are not carried out today to confirm trophoblastic tumors, because sonology is available.

LOCALISATION OF THE PLACENTA PRIOR TO AMNIOCENTESIS.
Prior to the sonology era, localizing the placenta prior to amniocentesis, to prevent inadvertent injury to the placenta during the insertion of the needle, was a challenge.The method adopted then was to: a) exclude a placenta praevia by the ability to palpate the fetal head directly through the vaginal fornices, b) identify the back of the fetus because the placenta would most likely be opposite to it, c) ensure that the bladder was empty, d) elevate the fetal head away from the pelvic inlet towards the umbilicus, in order to increase the volume of liquor in the 'forewaters' below the head, and e) to insert the amniocentesis needle in the midline immediately above the pubic symphysis 3 .

ESTABLISHING LUNG MATURITy OF A FETUS PRIOR TO ELECTIVE, EARLy PRETERM DELIVERy
Fetal lung maturity prior to elective preterm delivery could be predicted by using the foam stability test ('Shake or Bubble Test') 4 .This was a rapid and simpler method compared to the assessment of the Lecithin Sphingomyelin ratio, which required sophisticated and expensive biochemical techniques 5 .The amniotic fluid obtained by amniocentesis was serially diluted in normal saline, an equal volume of 95% ethanol added, shaken for 15 seconds, allowed to stand for 15 minutes, and examined for the presence of bubbles at the level of the meniscus.Absence of bubbles indicated a negative test while the positive results were graded according to the dilution at which bubbles persisted.Although antenatal corticosteroid therapy for impending preterm birth was being practiced , because surfactant therapy was not available in the THMG then, the foam stability test was useful in high risk women who required elective, early preterm delivery (between 28 -31 weeks gestation) and were unwilling to be transferred to Colombo for delivery.
Paradigm changes have occurred in the diagnosis of diseases, including obstetric and gynaecological problems, over the last four decades.Technological advances have contributed a great deal to these changes.A brief glimpse of the past has been provided.This may perhaps amuse the younger obstetricians and make them chuckle, while bringing nostalgic memories to those who are more senior.
For low-risk women in labour, it has a Consultant Obstetrician and Gynaecologist, District Base Hospital, Rikillagaskada, Sri Lanka b J.M.S.W Jayasundara, Registrar in Obstetrics and Gynaecology, Castle Street Hospital for Women, Colombo 8, Sri Lanka Correspondence: Dr. C. G. A. Gunasena MD MRCOG E mail -asankagunasena@gmail.comCompeting interests: The authors report no conflict of interest

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baseline value < 110 bpm lasting > 10 minutes is considered as fetal bradycardia.However a baseline FHR between 100 and 109 bpm with normal baseline variability and no variable or late decelerations should not prompt any further action 11 .The causes of fetal bradycardia include low inherent rate, medications (e.g.local anesthetics), maternal hypothermia, maternal hypotension, fetal heart conduction defects, prolonged umbilical cord compression, and sustained hypoxia 10 .

Fig 1 xFig 2
Fig 1 x ray showing the IUCD in the pelvis

Table 1 : Antenatal risk factors which would justify continuous intrapartum cardiotocography -adapted from RANZCOG Guidelines 2014 (2)
Hyperglycaemia in pregnancy requiring medication, or if it is poorly controlled, or if associated with macrosomia Current or previous conditions which constitute a risk of fetal compromise e.g.cholestasis, isoimmunisation, substance abuse Significantly reduced fetal movements preceding labour Morbid obesity BMI ≥ 40 Maternal age ≥ 40