Female Sexual Dysfunction

What is normal sexual response? 

• Original landmark studies had a very linear model of “normal sexual response” 

  • Excitement → plateau → orgasm → resolution 

• More contemporary model is non-linear and encompasses a variety of sequences of the original four stages of as well as other stages 

  • Estrogen plays a significant role in female sexual response, including maintenance of genital tissue sensitivity, elasticity, secretions, pH, etc, as well as urinary continence, pelvic floor muscle tone, and joint mobility 

  • Approximately 43% of American women report experiencing sexual problems, with higher prevalence in women aged 45-64

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What are the different types of sexual dysfunction? 

Based on the DSM-V - 5 specific types of female sexual dysfunction:

• Female sexual interest and arousal disorder 

  • Lack of or significant decrease in at least three of the following: 

    • Interest in sexual activity 

    • Sexual or erotic thoughts or fantasies 

    • Initiation of sexual activity and responsiveness to a partner’s initiation 

    • Excitement or pleasure during all or almost all sexual activity

    • Interest or arousal in response to internal or external sexual erotic cues 

    • Genital or nongenital sensations during sexual activity in almost all or all sexuall encounters 

  • Symptoms have persisted for a minimum of 6 months and cause clinically significant distress in individuals 

• Female orgasmic disorder 

  • Marked delay in, marked infrequency of, or absence of orgasm, or markedly reduced intensity of orgamsic sensations in almost all or all occasions of sexual activity 

  • Symptoms have persisted for a minimum of 6 months and cause clinically significant distress in individuals  

• Genito-pelvic pain/penetration disorder 

  • The persistent or recurrent presence of one or more of the following symptoms:

    •  Difficulty having intercourse 

    • Marked vulvovaginal or pelvic pain during intercouruse or penetration attempts 

    • Marked fear or anxiety about vulvovaginal or pelvic pain anticipating, during, or resulting from vaginal penetration 

  • Symptoms have persisted for a minimum of 6 months and cause clinically significant distress in individuals  

• Substance/medication-induced sexual dysfunction 

  • Disturbance in sexual function that has a temporal relationship with substance/ medication initiation, dose increase, or discontinuation and causes clinically significant distress in the individual 

• Other specified or unspecified sexual dysfunction

  • Distressing symptoms characteristic of sexual dysfunction that do not meet the criteria of one of the defined categories. The major distinction between specified and unspecified is whether the clinician specifies reason that the symptoms do not meet criteria for other classes 

  • One specified reason: genitourinary syndrome due to menopause 

How should we evaluate for FSD? 

• Ask about it!

  • During routine visits, can ask questions about sexual function 

  • Ask broad, open-ended questions during routine history gathering 

  • “Many women experience concerns about sex. Are you experiencing any issues?” 

• Initial approach if patient answers yes, or if FSD is a complaint 

  • Comprehensive History 

    • Should ask detailed history about patient’s sexual and gender identity 

    • Nature, duration, and onset of symptoms - also if symptoms cause distress 

    • If patient is using medications 

    • Partner factors (ie. number of current partners, their gender, health problems, sexual function problems) 

    • Relationship quality - communication about sexual concerns with partner, past and current abuse or violence experience

    • Pain/injuries/Body image 

  • Physical Exam

    • Often, there are not specific physical exam findings 

    • However, use of mirror and pointing out female anatomy for education is sometimes helpful 

    • Can also identify if there are areas that are causing pain 

How do we treat FSD? 

• Psychological Interventions 

  • Relationship distress and partner sexual dysfunction can trigger sexual problems in other domains 

  • Options include sexual skills training, cognitive-behavioral therapy, mindfulness-based therapy, and couples therapy 

    • Sexual skills training: can include instructions in masturbation, other erotic stimulation, decrease feelings of guilt and shame with masturbation, as well as learning about anatomy (ie. clitoral stimulation)

    • Couples therapy: exercises to better communication with partner 

    • History of trauma - may need trauma-based psychotherapeutic approach  

  • Can consult or refer to mental health specialists with expertise in this area 

• Medical therapy

  • Estrogen

    • Low-dose vaginal estrogen therapy is the preferred hormonal treatment for FSD due to genitourinary syndrome of menopause  

    • Low-dose systemic estrogen can be an alternative 

    • Other alternatives include Ospemifene for management of dyspareunia due to genitourinary syndrome of menopause 

  • Androgen Therapy

    • Short-term use of transdermal testosterone can be considered for treatment of postmenopausal women with sexual interest andd arousal disorders 

    • Need to appropriately counsel that there are risks (ie. acne, increased hair growth, virilization - may be irreversible) and long-term side effects are not known 

    • Can try for 3-6 months after baseline testosterone is tested and after 3-6 weeks of initial use 

    • Should be discontinued if no effect after 6 months 

  • Flibanserin 

    • Addyi on the market 

    • Serotonin receptor agonist/antagonist and was approved in 2015 by the FDA to treat hypoactive sexual desire disorder in premenopausal women without depression 

    • However, systematic review and meta-analysis of existing studies showed that overall quality of evidence for efficacy and safety were low, and there was minimal to no improvement in hypoactive sexual desire disorder with use 

    • Black box warning against alcohol use - increased risk of syncope and hypotension 

  • Sildenafil (Viagra) 

    • Not efficacious

    • Hypothesized that it may increase pelvic blood flow to clitoris and vagina, but has not been proven to work 

  •  Bupropion 

    • If patient has antidepressant-induced female sexual dysfunction, supplementation with bupropion may improve symptoms 

•  Other 

  • For genito-pelvic pain and penetration disorders:

    • Education to help patient understand anatomy and etiology of their symptoms 

    • Vaginal dilators

    • Physical therapy (Pelvic PT) 

    • Intravaginal prasterone for treatment of postmenopausal women who have dyspareunia 

    • Lubricants and moisturizers 

      • Don’t cure the underlying cause, but may reduce or alleviate dyspareunia that is due to vaginal dryness 

        • Coconut oil is a good option, but do not use with condoms 

        • Tend to counsel more toward silicone-based lubricants because they do not dry out as quickly as water-based lubricants 

    • Vaginal lasers

      • Became a hot topic while we were senior residents and some people raved about them; latest evidence suggesting they’re not effective.

      • Vaginal CO2 fractional laser is inadequately studied for treatment of vulvovaginal atrophy 

      • Cost of treatment is rather high 

Endometriosis Part II: Treatment

How do we treat endometriosis? 

• Approach 

  • Should be based on severity of symptoms and make sure that other causes of pelvic pain are excluded 

  • Usually, medications are tried first because of the risks, recovery, and costs of surgery

  • Discussion of desire for fertility in the future can also help guide your management 

  • Review with patients that this is a chronic disease - it is not curable, but can be treated. Also, discuss that the road through treatment can be long, and that one mode of therapy that is effective for some, may not be effective for others 

• Medical 

  • NSAIDS 

    • Can be used to treat primary dysmenorrhea, and is first line for that 

    • However, no high-quality data reporting its efficacy in endometriosis; however it is low-cost and readily available; usually combined with combined hormonal therapy 

  • Estrogen-progestin contraceptives 

    • First line treatment for endometriosis because can be used long-term, well tolerated, and are relatively easy to use 

    • No formulation has demonstrated superiority

    • Both cyclic and continuous dose appear to be effective at reducing pain, but two systemic reviews reported that continuous COC regimens were more effective at reducing pain than cyclic (meaning you take the active pills in one pack → move on to the next pack, skip the placebos) 

    • This is because COCs suppress ovarian function while they are being taken and can reduce endometriosis disease activity and pain 

    • Obviously, there are risks and benefits of taking COCs, and there are many people that cannot take COCs because of the estrogen component (check out our past episode!)

  • Progestins 

    • If people can’t take estrogen, then they can use progestin only therapy 

    • Most commonly = norethindrone acetate 5 mg by mouth daily, but can be increased by 2.5 until l15 mg daily is the max

    • Depo Provera - 150 mg IM injection q12 weeks 

    • Progestins inhibit endometrial tissue growth. It also doesn’t carry the risk of VTE with COCs, and avoids risk of bone loss and menopausal symptoms associated with GnRH agonists

    • However, side effects include increased breakthrough bleeding, weight gain (Depo Provera), mood changes 

    • Alternatives: Etonogestrel implant - observational trial of 41 women showed it decreased intensity of endometriosis-related pain

    • LNG-IUD - limited evidence, but postop IUD can reduce recurrence of dysmenorrhea in women with surgically confirmed endo 

  • Gonadotropin-releasing hormone agonists 

    • I.e., leuprolide; others are things like buserelin, goserelin, etc 

    • Meta-analysis shows they are more effective than placebo, and just as effective as other medical therapies 

    • Common doses: Leuprolide 3.75 IM qmonth or 11.25 mg q3 month 

    • However, remember that it is a GnRH AGONIST 

      • Initially, can worsen symptoms for a little bit due to initial surge of LH and FSH before eventually suppressing the HPO axis (warn patients about 7-14 days of worsening symptoms) 

    • To counteract the hypoestrogenic effects (ie. menopausal symptoms, vasomotor symptoms), usually will do add-back therapy with 5 mg oral norethindrone 

  • GNRH Antagonist 

    • Also suppress HPO axis, but does so immediately, without initial LH and FSH surge like agonists 

    • Also induces a hypoestrogenic state and can cause vasomotor symptoms, as well as leads to decrease in bone density  

    • Easier to dose because they are oral rather than IM 

    • Ex: elagolix (Orilissa), dosed 150 daily up to 200 mg twice daily 

  • Danazol

    • Can be effective in reducing pain, but not common because it can cause androgenic side effects  

  • Aromatase inhibitors 

    • Usually reserved for severe, refractory endometriosis-related pain 

    • Often used in combination with progestins 

    • Off-label use of AI 

    • Limited data overall, but does seem to decrease pain compared to placebo 

    • Similarly, can cause hypoestrogenic side effects 

  • Neuropathic pain treatments 

    • Can be used if there is still pain from endometriosis (see other below)  

• Other 

  • Often, long-lasting pain from endometriosis can become chronic pain 

  • See our chronic pain episode → basically can lead to a cycle of lowered threshold of stimulus to cause pain, central sensitization 

  • May also need other therapy such as pelvic floor PT

  • May need neuropathic pain treatments (ie. gabapentin) to decrease sensitization. Remember to remind your patients that gabapentin does not take pain away immediately, and needs to be used consistently for several weeks 

• A note on opioids 

  • Patients with endometriosis and pelvic pain may receive opioids for pain relief when presenting for treatment urgently 

  • Opioids should be used sparingly or avoided for endometriosis and CPP because they only treat symptoms and do not address the issue 

  • Can lead to dependence and overuse 

• Surgical 

  • There are many, many surgeries out there for endometriosis, from simple ablation, to adhesiolysis, to nerve transections, to hysterectomies. We will cover a few 

  • Surgery offers the benefit of definitive diagnosis, but risks include damage to organs (especially if there is heavy burden of endometriosis as well as adhesions) like bladder and bowel

  • Most people will achieve initially pain relief after surgery - women who underwent operative laparoscopy were 3x more likely to report improvement in pain at 12 months than controls who had diagnostic laparoscopy (one study showed 73 vs 21%) 

  • However, nearly 20% of patient will undergo repeat surgery within 2 years because of recurrent symptoms, and risk of symptom recurrence is as high as 40% at 10 year follow up 

  • Risk factors for persistent or recurrent pain: incomplete excision, ovarian cyst drainage instead of cyst excision, and ovarian conservation

  • Endometriosis tends to get better with Menopause, and so longer latency to menopause gives more time for symptoms to recur 

  • Postoperative medical therapy: ASRM advises posteropative medical suppressive therapy for most women treated surgically 

    •  6-24 months of suppression can reduce symptom recurrence and thus potentially avoid need for multiple surgeries 

    • Best evidence comes from 2 systemic reviews: one using LNG-IUD, and another for postoperative use of COCs for prevention of relapse 

• Surgical techniques

  • Laparoscopy generally favored over laparotomy because less invasive and improves visualization, with better recovery and shorter hospital stay, elss pain 

  • Conservative 

    • Excision or ablation of endometriosis lesions with intent of preserving the uterus and as much ovarian tissue as possible 

    • First line option for most people who want surgery for endometriosis because it preserves fertility and hormone production

    • Remember: even in young patients who don’t want fertility, hormone production is necessary for bone and cardiac health!  

    • Less invasive and morbid than definitive surgery, and there is documented short term efficacy 

    • 2014 systematic review: decreased pain and increased live birth rate after conservative surgery 

    1. Disadvantages: 

       1. Rate of recurrent symptoms is higher compared to definitive surgery 

       2. Rate of reoperation increases with time, whereas it is relatively stable with definitive surgery 

  1. Hysterectomy without oophorectomy 

     1. For patients who have debilitating symptoms and whom have completed childbearing 

     2. Failed both medical therapy and at least one conservative treatment procedure 

     3. Also reasonable if other indications for a hyst (ie symptomatic fibroids, prolapse, etc) 

     4. Effective treatment for pain symptoms from endometriosis, with reoperative rates that are relatively low (19% in one study, compared to 58% in people undergoing conservative therapy) 

     5. Disadvantages 

        1. Longer, more morbid surgery with higher rates of complication 

  2. Hysterectomy with oophorectomy

     1. Those who would benefit are those with extensive adnexal disease and those for whom the risks of reoperation outweigh the risks of premature menopause 

     2. Likely increases the efficacy of definitive surgery but is accompanied by quality of life issues and potential adverse outcomes due to early menopause 

     3. Reason to do it: endometriosis is an estrogen-dependent disease, and tends to get better with menopause 

     4. Early menopause (<44 years) is associated with increase risks of overall mortality, cardiovascular disease, neurologic disease, osteoporosis 

Endometriosis Part I: Evaluation and Diagnosis

Be sure to check out our previous episode on chronic pelvic pain with Dr. Eva Reina to round out your CPP diagnosis skills!

What is endometriosis? 

• Gynecologic condition where endometrial glands and stroma occur outside of the uterine cavity that can respond to hormonal shifts of the menstrual cycle.

  • Most within pelvis, but can occur elsewhere: bowel, diaphragm, and even in the pleural cavity 

  • Benign, but can cause dysmenorrhea, dyspareunia, chronic pain, and infertility 

• Incidence

  • Occurs in 6-10% of reproductive age women, but is present in 38% of women with infertility and 71-87% of women with chronic pelvic pain! 

  • No data to suggest that endometriosis is increasing, but it is likely more recognized and being diagnosed more often now.

  • There is a familial association - first degree relatives of someone with endometriosis are at higher risk for also developing it, but the inheritance is likely polygenic-multifactorial 

• Risk factors

  • Nulliparity, prolonged exposure to endogenous estrogen (ie. early menarche, late menopause)

  • Shorter menstrual cycles, heavy periods, obstruction of menstrual outflow

  • Increased height, lower BMI, and high consumption of trans unsaturated fats

    • This does not mean that you’re going to get endometriosis if you’re tall or have a low BMI! And you’re not going to treat it by stopping eating trans fats.

    • Association doesn’t equate to causation.

• Etiology 

  • Endometriosis occurs when ectopic endometrial tissue implants, grows, and elicits inflammatory response 

  • Inflammatory response: COX-2 activity, overproduction of prostaglandins, and then chronic inflammation → triggers pain and causes infertility

    • Also why those with endometriosis will usually have flares that coincide with their menstrual cycle.

  • Nerve growth factor is also highly expressed in endometriotic lesions → increase density off nerve fibers → can explain increased sensitivity and pain 

    • Can also be explained by central sensitization (lowering threshold of pain) 

    • Go back go our CPP episode to remember what all these things are! 

  • Sampson’s Theory of Retrograde Menstruation - most popular/common theory where endometrial cells flow backwards through the fallopian tubes into the peritoneal cavity during menses

    • But, up to 90% of women HAVE retrograde menstruation, and not everyone has endometriosis 

    • Likely, there is a multifactorial cause of endometriosis, where ectopic endmoetrial tissue interacts with alterned immunity, imbalance of cell proliferation/apoptosis, aberrant signalling, and genetic factors 

    • There are certain genes that are statistically associated with endometriosis 

  • Chronic inflammation and endometriotic lesions can distort the pelvic anatomy through adhesions, endometriomas, and other substances lilke cytokines and prostaglandins that are “hostile” to normal ovarian function, fertilization, and implantation 

How do we evaluate for endometriosis? 

• History and physical

  • Usually patient will present during reproductive years with pelvic pain (ie. dysmenorrhea or dyspareunia), infertility, or ovarian mass 

  • However, there are many people with endometriosis who are asymptomatic! 

  • Diagnosis is more likely to be made in people with symptoms 

    • Remember the “PPUBS” framework 

      • Pain - can you describe your pain? 

      • Periods - menstrual history; is the pain surrounding menstruation or line up with other parts of their menstrual cycle? 

      • Urinary symptoms - there can be endometriotic lesions on the bladder → frequency, urgency, pain with voiding 

      • Bowel - symptoms include diarrhea, constipation, dyschezia, and bowel cramping 

      • Sexual dysfunction - peritoneal or deeply infiltrating endometriosis can present with dyspareunia 

  • Physical exam: can be variable depending on location and size of implants

    • You may feel nodules in the posterior fornix, uterosacral ligaments,, adnexal masses, and immobility or lateral displacement of the cervix or uterus 

    • However, exam can be completely normal 

• Rule out other causes for pelvic pain 

  • Labs - no pathognomonic lab for endometriosis 

    • CA125 can be elevated, but it’s not routinely ordered because other diseases can also elevate CA-125 levels 

    • It’s not specific and not helpful for endometriosis

  • Imaging 

    • Ultrasound is usually all you need - can see things like endometriomas, nodules, etc. 

    • Sometimes, can consider MRI

    • Imaging can help to rule out other causes of pelvic pain (ie. fibroids)  

• Definitive diagnosis vs. presumptive diagnosis 

  • Presumptive diagnosis

    • Endometriosis is a pathologic diagnosis - meaning you need histology of a lesion biopsied during surgery 

    • Sometimes, if surgery is not desired or not yet possible, presumptive diagnosis can be made based on combination of signs, symptoms, and imaging findings 

    • Clinical diagnosis is enough to start therapy that is low risk and easily tolerated

    • If patients improve, can actually hold off on surgery 

  • Definitive diagnosis 

    • Surgery - usually indicated for persistent pelvic pain that does not respond to medical therapy, evaluation of severe symptoms that limit function, andd treatment of anatomic abnormalities 

    • Usually laparoscopy - can get definitive diagnosis and treatment 

      • Peritoneal lesions can appear like reddish or bluish irregularly shaped islands, “powder burn” lesions, white opacifications, translucent blebs

      • Allen-Masters syndrome = scarred or puckered peritoneal surface 

      • Dense fibrous disease 

      • Endometriomas 

  • Pathologic Categorizations 

    • Superficial peritoneal lesions 

    • Ovarian lesion (endometrioma) 

    • Deeply infiltrating - solid endometriosis situated more than 5 mm deep to the peritoneum 

  • Surgical Staging - this is to report operative findings. They do NOT correlate with presence or severity of symptoms. However, there are studies that have shown inverse correlation with advanced stages and prognosis for fertility treatment 

    • Stage I - minimal disease; ie. isolated implants, no significant adhesions 

    • Stage II - mild endometriosis with superficial implants that are < 5 cm in aggregate and are scattered on peritoneum and ovaries. NO significant adhesions 

    • Stage III - Moderate disease with multiple implants, both superficial and deeply invasive, peritubal and periovarian adhesions may be evidence  

    • Stage IV - severe disease; multiple superficial and deep implants, including large ovarian endometriomas. Filmy and dense adhesions are usually present

Hysteroscopy: The Basics, feat. Andrey Dolinko, MD

Today we’re joined for a first part of a two-part talk on hysteroscopy with special guest, Dr. Andrey Dolinko! Andrey was our co-resident at Brown and is currently a second-year fellow in reproductive endocrinology and infertility at the University of Pennsylvania.

What is hysteroscopy?

• Ancient Greek hustérā, “the womb” & Skopéō - to see 

• History (Rudic-Biljic-Erski et al 2019)

  • First developed in mid-19th century

    • Pantaleoni performed hysteroscopy on a 60yo woman to diagnose an endometrial polyp and treated it with silver nitrate. Used cystoscope developed by Desormeaux that used series of concave mirrors and light source

  • Early 20th century

    • Carbon dioxide used as first distention medium in 1925

    • 1926 - two-channel hysteroscopy (introduction and suction of distention media)

    • 1927 - operative channel introduced

    • 1928 - irrigation system

    • 1930s - fixed optic systems and fluid delivery systems

  • Second half of 20th century

    • Fiberoptic cable added to hysteroscope in 1965 (cold xenon light)

    • Operative hysteroscopy and use of different distention media takes off in 1970s

    • Videoendoscopy started in 1982

    • 1996 - Bettocchi office hysteroscope

    • 1990s - resectoscopes, first monopolar and then bipolar

  • 21st century

    • Morcellators - i.e., MyoSure

How does hysteroscopy work?

• Contraindications

  • Pregnancy

  • Cervicitis

  • Active PID

  • Comorbidities that may be exacerbated by intravascular volume expansion

• Timing

  • Reproductive-aged women: proliferative phase CD5-12, ideally not during active bleeding

  • Exclude pregnancy!

  • Post-menopausal-aged women: any time
    

• Positioning

  • Dorsal lithotomy position

  • Avoid steep trendelenburg because risk of air embolism

    • Causes negative pressure in pelvic veins

• Patient prep

  • Vaginal prep w/4% chlorhexidine gluconate soap or providone-iodine

• Antibiotics

  • not indicated

• Anesthesia (ranges)

  • None

  • Can do PO/IM/IV NSAIDs, benzos

  • Paracervical blocks

  • Regional anesthesia

  • IV sedation

  • General LMA

  • GETA

• Vaginal instruments

  • Speculums and retractors

  • Tenaculum

  • Dilators

  • Curettes

• Hysteroscope

  • Hysteroscope components

    • Scope

      • Eyepiece

      • Barrell

      • Objective lens

        • 0 to 70 degrees (typically 0 or 30)

    • Inner sheath w/inflow

    • Outer sheath w/outflow for operative scopes

    • Light source

      • Most-commonly Xenon or LED these days

    • Camera-head and video monitor

  • Diagnostic

    • Flexible

    • Rigid

  • Operative

    • Rigid operative scope

    • Scopes to be used with hysteroscopic tissue removal systems

    • Resectoscopes

  • Distention media

    • Fluid choice

      • Historical

        • Gas - CO2

        • High-viscosity 32% Dextra (Hyscon)

      • Current

        • Low viscosity

          • Electrolyte-rich

            • Saline

            • LR (rarely)

          • Electrolyte-poor

            • 5% Mannitol

            • 3% Sorbitol

            • 1.5% Glycine

    • Fluid deficit

      • A reflection of potnetial systemic fluid absorption

        • Surgical disruption of endometrium and myometrium provides direct access to sinus/vessels

          • If intrauterine pressure greater than vascular pressure → intravasation -> a fluid bolus!

      • Where else may the fluid be going?

        • Out the tubes

        • Out the vagina

        • Onto the floor

  • Fluid management systems help to determine deficit

    • Simple

      • Gravity

      • Pressure bag

    • Automated systems

      • Can set fluid deficits for automatic calculation

      • Uterine pressure setting

Laparoscopy IV: Pneumoperitoneum

We’re back today with Dr. Ruhotina and the next piece in our laparoscopy series. Today we’re talking all about gas and pneumoperitoneum. As before, Dr. Ruhotina made some awesome notes — take a look below!

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Pneumoperitoneum Physiology 

-        Laparoscopic surgery involves insufflation of a gas (usually carbon dioxide) into the peritoneal cavity producing a pneumoperitoneum

-        Causes an increase in intra-abdominal pressure (IAP)

-        Insufflated at a rate of 4-6 L/Min to a pressure of 10-20mmHg

-        The pressure is maintained by a constant gas flow of 200-400 ml/min

Cardiovascular effects

-        Increased IAP affects venous return, systemic vascular resistance and myocardial function 

-        Increases in IAP result in compression of the vena cava decrease venous return decrease cardiac output 

-        Systemic vascular resistance is increase because of direct effects of IAP (+ increased circulating catecholamines)

o   The SVR change is usually greater than the reduction in cardiac output results in maintaining or even increasing systemic blood pressure

-        Increase SVR, systolic and diastolic pressures and tachycardia increased myocardial work load 

-        If IAP increases further decrease cardiac output further  decrease blood pressure 

Respiratory 

-        Supine position and general anesthesia decrease functional residual capacity 

-        Pneumoperitoneum + Trendelenburg cephalad shift of diaphragm further decrease FRC 

o   Can lead to atelectasis, ventilation-perfusion mismatch, potential hypoxemia, and hypercarbia 

Renal  Increased IAP increased renal vascular resistance and reduction in GFR decreased function and urine output 

GI Increased IAP can potential lead to regurgitation of gastric content with increased risk of pulmonary aspiration 

Neurological Rise in IAP increased intracranial pressure may result in decreased cerebral perfusion pressure 

Effects of gas absorption

-        CO2 most frequently used gas for insufflation colourless, nontoxic, nonflammable and has the greatest margin of safety in the event of a venous embolus since it is rapidly absorbed from the peritoneal cavity, additionally the  metabolic end products easily exhaled through the pulmonary alveoli. 

-        Alternatives to CO2: NO, Air, Helium, Argon

o   NO: Benefits: less acid-base disturbance, may be better for severe cardiopul disease, less post op pain, Risks: supports combustion, not flammable itself only when combustible gas present hydrogen or methane seen with bowel perforation

o   Argon/Helium(inert gases): avoids complications of hypercarbia or acidosis, although decreased solubility in blood therefore increased risk of extraperitoneal gas extravasation such as gas embolus, more expensive 

-        CO2 gas can be administered cold or heated, with or without humidification.

o   Compared with cold gas, heated gas led to only a minimal, clinically insignificant rise in core body temperature of 0.31° Celsius (95% CI 0.09-0.53), without any meaningful improvement in patient outcomes or ease of surgery extra cost of heating and/or humidifying gas used in laparoscopy cannot be justified, according to a Cochrane review of 22 randomized trials

-        Absorbed readily from peritoneum causing increase in PaCO2  increasing cardiac contractility and reduction in diastolic filling which can result in decreased myocardial oxygen supply to demand ratio and greater risk of myocardial ischemia 

-        Arrythmias  nodal rhythm, sinus bradycardia and asystole attributed to vagal stimulation that can be initiated by stretching the peritoneum 

o   Can see this effect more pronounced at the beginning of insufflation 

-        Subcutaneous emphysema, pneumomediastinum and pneumothorax

o   May occur because of incorrect positioning of the gas insufflation needle or trocars or by gas dissecting across weak tissue planes attributed to increased abdominal pressure

-        Venous gas embolism

o   Rare but fatal complication

o   May occur if carbon dioxide is insufflated directly into a blood vessel or by gas being drawn into an open vessel 

o   The physiological effect caused by CO2 are less than that with air because of its greater solubility 

o   However you can see hypotension, desaturation, and mill wheel murmur 

o   Treatment rapid deflation of the abdomen and resuscitation, place in left lateral position and the air aspirated from the central line 

Indicators on insufflator machines: 

Important readings of insufflator.

• Preset Insufflation pressure,

• Actual Pressure

• Gas flow rate and

• Volume of gas consumed

Preset Pressure

-        Pressure adjusted by surgeon before starting insufflation

-        The preset pressure ideally should be 12 mmhg- 15mmhg

-        Fifteen mmHg is used as the standard insufflation pressure. 

o   multiple reasons for the use of a 15 mmHg threshold most importantly it is a function of basic cardiovascular physiology

o   Elevated IAP exerts its effects primarily on the cardiovascular system and secondarily on the pulmonary and renal systems. It is well known that the cardiopulmonary, renal and abdominal affects are minimal and still reversible at an insufflation pressure of less then or equal to 15mmHg

o   Animal studies have shown that an intra-abdominal pressures of 20 mmHg has the following effects:

§  markedly impairs renal function, reducing GFR and RBF to 21% and 23% of their baseline values

§  Adverse cardiac and pulmonary effects for prolonged intra-abdominal pressures of 20mmHg lasting over three hours

§  Brief increases to a pressure of 20mm are tolerable

-        Whenever intra abdominal pressure decreases due to leak of gas outside, insufflator eject some gas inside to maintain the pressure equal to preset pressure and if intra-abdominal pressure increases due to external pressure, insufflator sucks some gas from abdominal cavity to again maintain the pressure to preset pressure.

Actual Pressure

-        Actual intra-abdominal pressure sensed by insufflator

-        With veress needle is attached there is some error in actual pressure reading because of resistance of flow of gas through small caliber of veress needle. Many microprocessor controlled good quality insufflator deliver pulsatile flow of gas when veress needle is connected, in which the low reading of actual pressure measures the true intra-abdominal pressure.

-        If there is any major gas leak actual pressure will be less and insufflator will try to maintain the pressure by ejecting gas through its full capacity.

Flow rate

-        Rate of flow of CO2 though the tubing of insufflator

-        Some information suggests that when you attach the veress needle the flow rate should be adjusted for 1 liter per minute. 

o   Experiment were performed on animals where direct I.V. CO2 were administered and it was found that risk of air embolism is less if rate is within 1 liter/minute.

o   At the time of access using veress needle technique sometime veress needle may be inadvertently enter inside a vessel but if the flow rate is 1 liter/minute there is less chance of serious complication

-        When initial pneumoperitoneum is achieved and canulla is inside abdominal cavity the insufflators flow rate may be set at maximum

Total Gas used

-        Fourth indicator of insufflator

-        Normal size human abdominal cavity need 1.5 liter CO2 to achieve intra-abdominal actual pressure of 12 mm Hg. In some big size abdominal cavity and in multipara patients sometime we need 3 liter of CO2 (rarely 5 to 6 liters) to get desired pressure of 12mm Hg. Whenever there is less or more amount of gas is used to inflate a normal abdominal cavity, surgeon should suspect some error in pneumoperitoneum technique. These errors may be leak or may be pre-peritoneal space creation or extravasations of gas.

Prior to starting your case: 

-        Turn the insufflator on and check the carbon dioxide (CO2) cylinder to make sure it contains sufficient gas to complete the procedure

o   Have extra CO2 container in room if needed

-        Check the insufflator to assure it is functioning properly

o   After  connecting sterile insufflation tubing  Turn the insufflator to high flow the actual pressure indicator should register 0 

o   Kink the tubing to shut off the flow of gas The pressure indicator should rapidly rise to 30mmHg and flow indicator should go to zero (Fig. 2.2). The pressure/flow shutoff mechanism is essential to the performance of safe laparoscopy. These simple checks verify that it is operating properly. 

Closed entry abdominal technique opening abdominal pressure

-        several prospective studies have demonstrated that the initial intra- abdominal pressure (IAP) 8 mmHg provides a reliable confirmation of appropriate Veress needle tip placement through the umbilicus or Palmer’s point [48–50]. 

o   In obese women IAP may be higher than in non-obese women, and can be up to 10 mmHg when the Veress needle is correctly inserted. 

TROUBLESHOOTING 

• Loss of working space → ACTUAL PRESSURE HIGHER THAN SET PRESSURE, FLOW RATE = 0

  • Check actual and set pressure of pneumoperitoneum

  • Check status of relaxation of the patient (look for intraabdominal muscle contractions or firmness of abdomen, this is different than anesthesia checking neuromuscular twitch as diaphragm relaxation is different than intraabdominal)

  • Check valve on for connection insufflator tubing

  • Check insufflator tubing along the entire path, make sure it is not kinked

  • Mechanical obstruction- kinking of tubing, someone standing on tubing, closed valve 

• Loss of working space→ ACTUAL PRESSURE LOWER THAN SET PRESSURE, FLOW RATE= HIGH indicates a leak 

  • Check insufflator tubing to make sure tubing is connected to insufflator and port

  • Check all ports and make sure the valves are closed

  • Check all ports for leaking co2 

  • Check for distention of bowel and bladder catheter as CO2 can escape into hollow organ (bladder or bowel)

• Loss of working space→ ACTUAL PRESSURE IS LOWER THAN SET PRESSURE, FLOW RATE=0 (no flow)

  • Ensure power is on 

  • Check tank gas level

• If screen blank

  • Most likely = disconnected power cords, disconnected cables, blown light source, disconnected light cable