Recognise and manage the complications of laparoscopic and hysteroscopic surgery

In one line

Most serious endoscopic injuries happen in the first 60 seconds (laparoscopic entry) or are made by a fluid and an electrolyte you chose before you started (hysteroscopic distension media); the consultant skill is anticipating the at-risk patient, recognising the injury the moment the physiology shifts, and converting or correcting without losing time.

This is the complications chapter for minimally invasive gynaecological surgery. It assumes you already know how to perform a laparoscopy and a hysteroscopy, and how to pick the route and the energy source for an operation — that groundwork sits in the companion surgical-procedures chapters on perioperative care and safe surgery, on surgical approach, route and energy, and on the intraoperative complications common to all gynaecological surgery (haemorrhage, ureteric and bladder injury). What follows is one level up: the failure modes that are specific to getting into the abdomen blind, to insufflating it with gas, and to distending the uterus with fluid.

Mechanism & pathophysiology

Two mechanisms underlie almost every complication of endoscopic surgery.

The first is that laparoscopy starts blind. Whatever the technique, the first instrument crosses the abdominal wall before you can see the structures on the other side of it. The anterior abdominal wall is thin — in a slim woman the aorta and the common iliac vessels lie only a few centimetres below the umbilicus, and the bowel is mobile and adherent in anyone who has had previous surgery or pelvic infection. So the catastrophic entry injuries are anatomically predictable: a Veress needle or trocar driven in the wrong axis spears the aorta, common iliac vessels or inferior vena cava (immediately life-threatening), or the anterior abdominal wall vessels — the inferior epigastric artery, lateral to the obliterated umbilical ligament — when a secondary port is placed without transilluminating, or it perforates bowel or bladder. The umbilicus is chosen because it is the one place the wall layers are fused and thinnest, but it is also fixed to the abdominal contents, so adhesions tether bowel directly under it in the previously operated patient. Every entry-safety manoeuvre — angle of the Veress needle, intra-abdominal pressure before the trocar, an alternative entry point — is an attempt to manage a blind step.

The second is that you are putting something into a body cavity that does not belong there. In laparoscopy that something is carbon dioxide under pressure; in operative hysteroscopy it is a column of fluid pushed into the uterus above venous pressure. CO2 is chosen because it is cheap, non-combustible (it does not support the diathermy spark the way oxygen would) and highly soluble, so small intravascular boluses dissolve and are exhaled — which is precisely why a gas embolism is usually survivable if recognised. But a pneumoperitoneum is not physiologically free: raised intra-abdominal pressure splints the diaphragm and compresses the IVC, and the Trendelenburg position needed for pelvic access loads the heart and the cerebral venous system. Hysteroscopic fluid does something subtler and more dangerous — it is absorbed through the open venous sinuses of the cut myometrium directly into the circulation, and what it does there depends entirely on what is dissolved in it. The tonicity and electrolyte content of the distension medium govern the whole hysteroscopy section: a hypotonic, electrolyte-free fluid absorbed in volume causes dilutional hyponatraemia; an isotonic, electrolyte-containing fluid absorbed in the same volume causes circulatory overload without the sodium catastrophe.

Assessment

The "assessment" in this topic is mostly risk assessment before the case and pattern-recognition during it — by the time you are taking a focused history the complication has usually declared itself.

• Stratify entry risk pre-operatively. Who is high-risk? The previously operated abdomen (especially midline laparotomy, previous caesarean with a low scar, previous peritonitis or extensive endometriosis), the very thin woman (in whom the great vessels are alarmingly close to the umbilicus and the wall offers no buffer), and the very obese woman (in whom the umbilicus migrates caudally relative to the aortic bifurcation and the wall is deep and hard to gauge). A known large pelvic-abdominal mass, gross ascites, or a gravid uterus changes the geography. This stratification is the assessment, because it dictates the entry technique — it is the difference between a routine sub-umbilical Veress and a planned Palmer's-point or open entry.
• Recognise entry injury intra-operatively. A drop of free blood welling up the Veress needle, or blood/bowel content aspirated through it, is a perforation until proven otherwise. After insufflation, the laparoscope's first job is to inspect the entry site and the bowel beneath it before any other manoeuvre — the under-umbilical loop of bowel, the great vessels, the omentum. Sudden cardiovascular collapse at insufflation is gas embolism until disproved.
• Recognise pneumoperitoneum physiology. Rising airway pressures and falling tidal volumes, hypercarbia on the capnograph (the absorbed CO2 the anaesthetist must blow off), subcutaneous surgical emphysema crackling up the chest wall and neck (extraperitoneal gas tracking — benign in itself but a marker that gas is going where it should not, and a warning of possible capnothorax/capnomediastinum), and the haemodynamic effects of a tense abdomen plus head-down tilt.
• Recognise fluid overload at hysteroscopy. This is monitored, not diagnosed late: the running fluid deficit (inflow minus outflow, measured continuously) is the single number that protects the patient. Clinically, overload declares as a rising filling pressure, bradycardia and hypertension then hypotension, falling oxygen saturation (pulmonary oedema), confusion and — with the hypotonic-media syndrome — nausea, visual disturbance and seizures from acute hyponatraemia and cerebral oedema. Send urgent serum sodium the moment the deficit climbs.
• Recognise uterine perforation. A sudden loss of distension and of the view, the hysteroscope advancing further than the measured uterine length, or seeing bowel/omentum/peritoneal fat through the scope. The critical first question is not that you perforated but with what and whether the energy was on.

Management

Organise the response immediate → ongoing → long-term — but recognise that each of the four headline complications has its own internal algorithm. Take them in turn, hardest first.

Laparoscopic entry injury

Vascular injury to a great vessel is the surgical emergency of this chapter. If the Veress needle or trocar is sitting in the aorta or a major vein, the instinct to pull it straight out is wrong as the first move: it is tamponading the hole. Call for help, convert immediately to laparotomy (do not waste minutes on a laparoscopic repair of a major retroperitoneal vessel), get large-bore access and activate massive transfusion, and have the assistant maintain pressure while you open. Vascular surgery help is summoned early. An anterior-abdominal-wall vessel (inferior epigastric) bleed is less dramatic but easily missed; it is controlled by direct pressure, a port-site suture passed full-thickness around the vessel (a Foley balloon can tamponade temporarily), or under-running.

Visceral (bowel) injury at entry is the one that kills slowly through missed recognition. The classic scenario is the Veress needle, or the primary trocar, passing through a loop of small bowel. The principles:

• A recognised, clean, small Veress-needle puncture of bowel — confirmed by aspirating bowel content — can sometimes be managed conservatively (leave it, observe, antibiotics) precisely because a needle hole is small; but you must be certain it is only a needle injury, and you inspect for a second injury (the needle passes through two walls of a loop).
• A trocar through bowel is a different problem — the defect is large. The key manoeuvre: do not remove the offending trocar. Leave it in the bowel to mark the injury and to splint the defect (it stops faeculent soiling and tells you exactly where the hole is), place a fresh entry elsewhere under vision, inspect, and then repair — primary closure for a clean small-bowel injury, with intra-operative general-surgical or colorectal help for large-bowel or complex injury, and a low threshold for converting to laparotomy. Wash out, cover with broad-spectrum antibiotics.
• The delayed presentation is the lethal one. A thermal bowel injury or an unrecognised perforation presents on day 3–5 with pain out of proportion, low-grade fever, ileus, tachycardia and rising inflammatory markers — not with an acute abdomen at first. A patient deteriorating after laparoscopy is assumed to have a bowel injury until imaging or relaparotomy excludes it; sending her home reassured is how this becomes a mortality and a medicolegal case.

The medicolegal weight here is real: entry injuries are a leading source of laparoscopy litigation, and the defensibility of the case rests on documented consent for the specific risk of visceral/vascular injury and conversion to laparotomy, an appropriate entry technique for that patient, and — above all — recognition and timely management. A bowel injury is a recognised complication of laparoscopy; failing to recognise and act on it is the negligence.

Preventing entry injury — technique matched to the patient

Prevention is where the consultant adds value, and it is mostly about choosing the entry to fit the abdomen.

The decision rules that matter: in a woman with a previous laparotomy the umbilicus is the one place you should not go blind — plan Palmer's point or an open entry from the start. In the very thin woman, lift the abdominal wall and keep the Veress as vertical as the body habitus allows, conscious that the aorta is centimetres away. In the obese woman the umbilicus has migrated caudal to the aortic bifurcation, so a vertical umbilical entry is actually safer than the flat angle you might assume, and the wall is deep. After two failed Veress attempts, stop repeating the same blind manoeuvre — switch to open or Palmer's. Always decompress the stomach (orogastric tube) before an upper-abdominal entry and empty the bladder before a sub-umbilical one.

The honest evidence position — developed below — is that no entry technique has been shown to prevent the rare major injuries; what the trials do show is that some techniques reduce failed entry. So technique is matched to the individual abdomen on anatomical logic, not on a claim that one method is universally "safest."

CO2 pneumoperitoneum complications

• Gas (CO2) embolism is rare but the reason CO2 entry demands vigilance. It occurs when gas is insufflated directly into a vessel (a misplaced Veress needle) or enters open venous sinuses. Recognition: a sudden, profound fall in end-tidal CO2 (gas-locked right ventricle stops pulmonary perfusion), hypotension, hypoxia, arrhythmia, and the classic "mill-wheel" murmur on auscultation. Management is immediate and sequential: stop insufflation and desufflate the abdomen at once; turn off any nitrous oxide and give 100% oxygen; place the patient head-down in the left lateral (Durant) position so the gas is trapped in the apex of the right ventricle away from the outflow tract; aspirate gas via a central venous line if one is in place; and support the circulation with fluids, vasopressors and CPR as needed. Because CO2 is highly soluble, the prognosis with prompt management is generally good.
• Subcutaneous (surgical) emphysema — extraperitoneal gas tracking into the soft tissues, palpable as crackling crepitus over the abdomen, chest and neck. In isolation it is benign and resolves; its importance is as a warning that gas may also have tracked to the mediastinum or pleura (capnomediastinum, capnothorax) and as a contributor to the absorbed-CO2 load.
• Hypercapnia and acidosis — absorbed CO2 raises arterial CO2; the anaesthetist compensates with minute ventilation, but a long case at high pressure in a patient with limited respiratory reserve can accumulate a respiratory acidosis. Keeping the intra-abdominal pressure as low as gives adequate working space (often 12–15 mmHg for the body of the case) limits both the absorbed CO2 and the cardiovascular load.
• Cardiovascular effects of the tense abdomen plus Trendelenburg — raised intra-abdominal pressure compresses the IVC and reduces venous return while increasing afterload; steep head-down tilt raises central venous and intracranial/intraocular pressure. The fit patient tolerates this; the patient with cardiac disease, raised ICP risk or severe respiratory disease may not, which is part of why the route decision is a whole-patient decision, not just a surgical-access one.

Port-site complications

These declare after the case. Incisional hernia through a port site is the reason for the rule that the rectus sheath at any non-midline port of 10 mm or more should be closed (a fascial-closure device or a J-needle under vision); 5 mm ports rarely herniate and are not routinely closed. The other is port-site metastasis in oncological laparoscopy — tumour seeding the trocar tracks — a recognised phenomenon that feeds the wider caution about minimally invasive surgery for some cancers and is one reason specimen retrieval bags and careful tissue handling matter when operating on a possible malignancy.

Hysteroscopic distension-media complications — fluid overload and the TURP-type syndrome

Fluid overload most reliably separates a safe operative hysteroscopist from an unsafe one, because the disaster is silent until it is severe and is entirely determined by choices made before the resectoscope is switched on. The logic runs from the medium up.

Step 1 — what fluid, and why. A resectoscope needs the uterine cavity distended and the blood and chips washed clear. The medium has to be compatible with the energy source:

• Monopolar resection cannot use an electrolyte-containing fluid (saline would disperse the current and stop the loop cutting), so it requires a hypotonic, electrolyte-free medium — historically glycine 1.5%, or sorbitol/mannitol solutions.
• Bipolar resection (and the modern default) returns the current locally and works in saline, so it uses isotonic normal saline (0.9%).

Step 2 — what the absorbed fluid does, and why tonicity is everything. Distension fluid is pushed above venous pressure into a cavity whose myometrial sinuses are cut wide open; it is absorbed straight into the circulation, faster the longer the procedure, the deeper the resection, and the higher the intrauterine pressure. Now the tonicity decides the syndrome:

• Hypotonic, electrolyte-free media (glycine, sorbitol/mannitol) with monopolar energy → dilutional HYPONATRAEMIA and the hypo-osmolar "TURP-type" syndrome. Water without sodium floods the extracellular space, the serum sodium falls, plasma osmolality drops, and water shifts into cells — most dangerously into the brain: cerebral oedema with nausea, headache, visual disturbance, confusion, seizures and, if uncorrected, brainstem herniation, plus pulmonary oedema and cardiovascular collapse. Glycine adds its own toxicities: its metabolism generates ammonia (encephalopathy) and glycine is a retinal neurotransmitter, so it causes transient visual disturbance and blindness that points to glycine specifically. The BSGE/ESGE arithmetic is straightforward: a fall in serum sodium of about 10 mmol/L corresponds to roughly 1000 mL of 1.5% glycine absorbed — which is exactly why 1000 mL is the hypotonic deficit limit.
• Isotonic saline (0.9%) with bipolar energy → circulatory fluid overload WITHOUT the hyponatraemia. Saline absorbed in volume still causes pulmonary oedema and right-heart strain, but it does not crash the sodium or osmolality, so the neurological catastrophe of the hypo-osmolar syndrome is avoided. This is the single biggest safety advantage of bipolar-in-saline and the reason it has become the default — but it is not a licence to ignore the deficit, because a litre or two of saline into a frail elderly heart is its own emergency.

Step 3 — monitor the deficit and stop at the limit. The fluid deficit (inflow minus outflow) is measured continuously, automatically where a fluid-management pump is available. The verified BSGE/ESGE and AAGL thresholds are:

On reaching the limit, stop the procedure — finish if you are seconds away, otherwise abandon and complete another day. Do not "just take the last fibroid out."

Step 4 — manage established overload. Stop infusing, complete or abandon, and call for help. Send urgent serum sodium and osmolality. For fluid overload with normal/near-normal sodium (the saline scenario): oxygen, sit the patient up, furosemide and fluid restriction, monitor in a high-care setting. For the hypotonic hyponatraemic syndrome: this is the dangerous one. Symptomatic acute hyponatraemia with seizures or coma is treated with hypertonic (3%) saline to raise the sodium just enough to stop the cerebral emergency, alongside oxygen and furosemide — but the critical safety rule is to correct slowly: rapid over-correction of hyponatraemia causes osmotic demyelination (central pontine myelinolysis), an irreversible neurological catastrophe. The standard ceiling is to raise serum sodium by no more than about 8–10 mmol/L in 24 hours (lower if the hyponatraemia is more chronic). Acute, procedure-induced hyponatraemia of a few hours' duration is more forgiving than chronic hyponatraemia, but the principle stands: enough to save the brain from oedema, slowly enough to save it from demyelination. Involve critical care and, if available, nephrology.

Prevention folds back into the choices: use bipolar-in-saline wherever the equipment allows, keep the intrauterine distension pressure at the lowest that gives a working view (around mean arterial pressure, not above), use an automated fluid-management system, limit operating time, and pre-treat large fibroids (GnRH agonists, where appropriate) to shorten resection. The safest fluid is the one you absorb least of.

Uterine perforation at hysteroscopy

The last endoscopic complication, and the one where the energy state changes everything.

• A perforation with the energy OFF (e.g. with the dilator, the hysteroscope sheath, or a cold instrument) is usually managed conservatively: stop, do not continue the procedure, give a uterotonic if bleeding, observe with serial observations for haemodynamic stability and signs of intra-abdominal bleeding. A fundal perforation in a stable woman rarely needs surgery.
• A perforation with the energy ON, or with a mechanical morcellator/resection loop — or a lateral perforation near the uterine vessels — is potentially a thermal or mechanical injury to bowel, bladder or the uterine/iliac vessels, and the uterine wall hole tells you nothing about the damage beyond it. This mandates diagnostic laparoscopy (or laparotomy) to inspect the bowel and pelvic structures, because an energy injury to bowel may look trivial from inside the uterus and present as peritonitis days later. The same delayed-thermal-injury logic as laparoscopic bowel injury applies. Threshold to look inside the abdomen is low whenever the energy was live at perforation.

Conversion thresholds — when laparoscopy becomes laparotomy

Converting is a decision, not a defeat, and a consultant states the triggers crisply: uncontrolled haemorrhage or a major vascular injury; a bowel injury that cannot be safely repaired laparoscopically (large defect, large-bowel injury, poor access); failure to progress / inability to achieve safe access because of dense adhesions or poor view; equipment failure; and patient instability (cardiorespiratory compromise from the pneumoperitoneum or from blood loss). The principle binding them is that conversion is appropriate the moment continuing laparoscopically increases risk to the patient — and the earlier, calmer decision is always the better one. Documenting why you converted is part of the defensible operation.

Guidelines compared

The bodies broadly agree, and the divergences are matters of emphasis and currency rather than contradiction.

Two real divergences worth stating: isotonic deficit limits are softer evidence than hypotonic ones (the 2500 mL figure is a good-practice point, not a hard physiological derivation like the 1000 mL/10 mmol glycine number), and the laparoscopic-entry guidance is consensus-and-anatomy-based rather than trial-proven, which the next section unpacks.

The evidence & the controversy

The defining feature of the entry-technique evidence is that the trials are too small to answer the question everyone actually asks. The Cochrane review of laparoscopic entry techniques (Ahmad et al., latest update 2019) pooled 57 randomised trials and nearly 10,000 women across 25 techniques, and its headline conclusion is deliberately deflating: there is no evidence that any single entry technique prevents the major vascular or visceral injuries that the whole debate is about. The reason is statistical, not nihilistic — these injuries are so rare (well under 1 in 1000) that no feasible trial is powered to detect a difference, and most trials excluded exactly the high-risk women (previous surgery, raised BMI) in whom the question matters most. What the review can show, on softer end-points, is that direct trocar entry reduces failed entry compared with the Veress needle (moderate-quality evidence), and that open entry reduces failed entry compared with closed entry without any signal of more visceral or vascular injury. So the evidence-honest viva answer is: "no technique is proven safer for major injury; I match the entry to the patient's anatomy on first principles, and I accept that previous surgery makes a blind umbilical entry the wrong default." A candidate who declares the open technique "proven safer" has over-read the data — the kit's warning about over-claiming a trial applies here.

The hysteroscopy evidence is firmer because it rests on physiology, not on a randomised trial of a rare event. The 1000 mL hypotonic limit is not an arbitrary number; it is derived from the measured relationship between glycine absorption and serum sodium (≈10 mmol/L fall per litre). The genuine practice shift of the last two decades — the closest thing this topic has to a "trial that changed management" — is the move from monopolar-in-glycine to bipolar-in-saline, which does not abolish fluid overload but removes the hyponatraemic, hypo-osmolar limb of it, and so removes the syndrome's neurological lethality. That is why the modern consultant default is bipolar-in-saline and why glycine-related blindness and TURP-syndrome deaths are now largely historical in well-resourced units — and a live risk wherever monopolar resection persists.

The topical controversy is the minimally invasive surgery pendulum. For two decades the assumption was that laparoscopic/robotic always beat open. Then the LACC trial in cervical cancer showed open radical hysterectomy gave better survival than minimally invasive surgery, and the wider lesson — that MIS is not automatically superior and carries its own specific harms (port-site metastasis, the entry injuries of this chapter, longer operating under pneumoperitoneum) — has tempered the enthusiasm. The defensible position is neither reflexive MIS nor reflexive open: it is that the route is chosen for the operation and the patient, weighing the recovery benefits of MIS against its specific complication profile and the surgeon's audited outcomes. Robotic surgery sharpens the same argument with a cost/access edge that is especially pointed in an SA public sector that cannot fund robots for benign gynaecology.

Landmark trials & key evidence

The arithmetic behind the hysteroscopy numbers: because a 10 mmol/L sodium fall corresponds to ~1000 mL of glycine absorbed, a woman who has absorbed her 1000 mL hypotonic limit has, on average, dropped her sodium to around 130 mmol/L from a normal 140 — already in the symptomatic range — which is precisely why the limit is set there and why "a bit over" is not a rounding error but the start of cerebral oedema. The isotonic limit is set higher (2500 mL) only because saline does not move the sodium, so the harm is pure volume and the heart tolerates more before failing.

Worked viva — how to structure the answer

A typical stem: "You are performing a hysteroscopic resection of a 4 cm submucosal fibroid in a 68-year-old woman with hypertension, using monopolar diathermy and 1.5% glycine. The scrub nurse tells you the fluid deficit has reached 800 mL." A high-scoring answer runs:

1. Recognise the danger from the medium, not just the number. "This is a hypotonic, electrolyte-free medium with monopolar energy, so my concern is dilutional hyponatraemia and the hypo-osmolar syndrome, not just volume. She is elderly and hypertensive, so her limit is the reduced one — 750 mL for hypotonic media — and at 800 mL I am already over it."
2. Stop. "I stop the procedure now — I do not attempt to finish the fibroid. I remove the resectoscope, account for the deficit, and inform the anaesthetist."
3. Assess and investigate. "I send an urgent serum sodium and osmolality, check her conscious level and for visual symptoms (glycine), examine for pulmonary oedema, and put her in a monitored setting."
4. Treat by the syndrome. "If she is hyponatraemic and symptomatic — seizures, confusion — I treat with hypertonic 3% saline to lift the sodium enough to relieve cerebral oedema, with furosemide and oxygen, but I correct slowly — no more than ~8–10 mmol/L in 24 hours — because over-rapid correction causes osmotic demyelination. I involve critical care."
5. Prevent the next one. "In future I would use a bipolar resectoscope in normal saline, which removes the hyponatraemic limb of this risk entirely, keep distension pressure low, pre-treat a fibroid this size to shorten the resection, and use automated deficit monitoring."
6. Note the SA reality. "Where only monopolar/glycine is available, these hypotonic limits are not historical — they are the live safety rule, and the manual deficit tally must be rigorous."

Exam traps & red flags

• Removing the trocar from a bowel injury. Leaving the offending trocar in situ to mark and splint the defect, then entering elsewhere under vision, is the taught move; pulling it out spills bowel content and loses the injury.
• Sending the post-laparoscopy patient home reassured. A bowel injury (especially thermal) presents on day 3–5 with pain out of proportion, not an immediate acute abdomen. Increasing pain, tachycardia, ileus or fever after laparoscopy is a bowel injury until excluded — the delayed diagnosis is the lethal and medicolegal one.
• Going blind through the umbilicus in a previously operated abdomen. Previous laparotomy tethers bowel under the umbilicus; plan Palmer's point or open entry from the start.
• Confusing the two distension-media syndromes. Hypotonic glycine/sorbitol with monopolar → hyponatraemia + hypo-osmolar TURP-type syndrome (the dangerous one, with cerebral oedema, and glycine's added ammonia/visual toxicity); isotonic saline with bipolar → volume overload without hyponatraemia. Quoting the saline limit for a glycine case (or vice versa) is a classic error.
• Forgetting that elderly/comorbid limits are halved-down. 750 mL hypotonic / 1500 mL isotonic — not the healthy-patient 1000/2500. The 68-year-old hits her limit far sooner.
• Over-correcting hyponatraemia. Rapid sodium correction causes irreversible osmotic demyelination (central pontine myelinolysis). Correct enough to stop seizures/cerebral oedema, then slowly.
• Treating an energy-on uterine perforation as minor. A live-energy or lateral perforation can have injured bowel/bladder/vessels beyond the uterine wall — the threshold for diagnostic laparoscopy is low. A cold fundal perforation in a stable woman can be observed.
• Missing gas embolism. A sudden fall in end-tidal CO2 with cardiovascular collapse at insufflation is gas embolism — stop and desufflate, 100% O2, left-lateral head-down (Durant), aspirate via central line. Treating it as ordinary hypotension wastes the survivable window.
• Not closing a ≥10 mm non-midline port sheath. Incisional hernia through an unclosed 10 mm-plus port is preventable.
• Claiming an entry technique is "proven safest." The Cochrane evidence shows no technique prevents major injury — only that some reduce failed entry. Over-claiming reads as uncritical.

Evidence anchors

• Cochrane — Laparoscopic entry techniques, Ahmad et al., Cochrane Database Syst Rev 2019;1:CD006583
• BSGE/ESGE guideline on management of fluid distension media in operative hysteroscopy, Umranikar et al., Gynecol Surg 2016;13:289–303
• AAGL Practice Report — Management of Hysteroscopic Distending Media, Munro et al., J Minim Invasive Gynecol 2013;20:137–148
• RCOG Green-top Guideline No. 49 — Laparoscopic (entry-related) Injuries (2008; 2nd edition with BSGE in development — current full text hosted on the BSGE website)
• RCOG Green-top Guideline No. 59 — Outpatient Hysteroscopy (2nd edition, 2024)
• CO2 gas embolism recognition and management (sudden end-tidal CO2 fall, mill-wheel murmur; stop/desufflate, 100% O2, Durant left-lateral head-down position, central-line aspiration) — established anaesthetic physiology.
• South Africa: NDoH district→regional→tertiary referral structure and SAMF drug availability shape where laparoscopic and hysteroscopic surgery is offered and what monitoring equipment is to hand; HIV terminology per the SA 2026 Consolidated Guidelines is PVT.