INTRAPARTUM COMPLICATIONS AND OBSTETRIC EMERGENCIES

Most labours are ordinary, and then a small number of them are not. The transition is often measured in seconds: membranes rupture and the fetal heart drops and stays down; the head delivers and retracts against the perineum; the placenta separates and the fundus never firms. In these moments the nurse is the person in the room, and the correct first action is frequently not the intuitive one. You do not push a prolapsed cord back in — you lift the presenting part off it. You do not press on the fundus in shoulder dystocia — you flex the hips and press above the pubic bone. You do not reach for the antidote before you stop the magnesium infusion. This chapter builds each emergency the way it is practised: mechanism first, then what you assess, then what you do and in what order, then what goes wrong afterwards. Numbers are given as they are actually written on the order and drawn into the syringe.

Section 1Reading the Fetal Heart

Baseline and variability: the two numbers that matter most

Electronic fetal monitoring does not measure fetal oxygenation. It measures the fetal autonomic nervous system’s response to oxygenation, which is why the tracing is read as a physiological story rather than a number. Every interpretation starts with the baseline: the mean fetal heart rate rounded to the nearest 5 beats per minute over a 10-minute window, excluding accelerations, decelerations and stretches of marked variability, and requiring at least 2 minutes of identifiable baseline in that window. Normal is 110–160 bpm. Above 160 bpm for 10 minutes or longer is tachycardia — think maternal fever and chorioamnionitis first, then dehydration, thyrotoxicosis, beta-agonists such as terbutaline, and early fetal compensation for hypoxia. Below 110 bpm for 10 minutes or longer is bradycardia — think cord compression or occlusion, maternal hypotension after an epidural, rapid descent, uterine rupture, or maternal hypoxia.

Variability is the irregular fluctuation in the baseline, and it is the single most useful feature on the strip. It reflects an intact, well-oxygenated pathway running from cerebral cortex through midbrain to vagus nerve to the fetal heart, so it tells you about the fetal brain, not just the fetal heart. It is graded by the amplitude of the fluctuation from peak to trough: absent (undetectable), minimal (detectable but 5 bpm or less), moderate (6–25 bpm) and marked (more than 25 bpm). Moderate variability is the reassuring finding of the whole tracing — when it is present, the fetus is very unlikely to be acidaemic at that moment, even in the presence of decelerations.

Minimal or absent variability has benign causes as well as ominous ones, and you sort them by asking what changed. A fetal sleep cycle lasts about 20–40 minutes and rarely longer than 80. Opioids, magnesium sulfate and central nervous system depressants flatten variability. Prematurity produces less variability. Fetal tachycardia mechanically reduces it. But absent variability that arrives with recurrent late decelerations, or that persists after a sleep cycle should have ended, is the tracing telling you the fetal central nervous system is being deprived of oxygen, and it is escalated, not observed.

Accelerations and the mechanism of each deceleration

An acceleration is an abrupt increase in the fetal heart rate — at 32 weeks or more, at least 15 bpm above baseline lasting at least 15 seconds from onset to return; before 32 weeks, at least 10 bpm for at least 10 seconds. Accelerations mean an intact somatic nervous system and a non-acidaemic fetus. They can be provoked deliberately: fetal scalp stimulation during a vaginal examination that produces an acceleration predicts a fetal scalp pH of 7.20 or above, and is a legitimate bedside test when the tracing is ambiguous. An acceleration lasting 2 minutes or more but less than 10 minutes is a prolonged acceleration; 10 minutes or more is a change in baseline.

Decelerations are classified by shape and by timing against the contraction, and every classification exists because the shape reveals the mechanism. Two words do the work. Gradual means the onset to the nadir takes 30 seconds or longer, and gradual implies a reflex or chemoreceptor pathway. Abrupt means onset to nadir takes less than 30 seconds, and abrupt implies mechanical interruption of cord blood flow.

Early decelerations are gradual, mirror the contraction, and the nadir sits under the peak. The mechanism is fetal head compression during descent, which raises intracranial pressure, triggers a vagal response and slows the heart. They are benign, need no intervention, and typically appear in active labour at 4–7 cm and again in the second stage. Variable decelerations are abrupt, drop at least 15 bpm below baseline, last at least 15 seconds but less than 2 minutes, and vary in shape and in their relationship to contractions. The mechanism is umbilical cord compression: the thin-walled umbilical vein is squeezed first, venous return falls, the fetus accelerates briefly, then the arteries are compressed, systemic resistance rises, baroreceptors fire and the rate plunges. Occasional variables are common and tolerated; recurrent deep variables with slow return, loss of variability or a rising baseline are not. Late decelerations are gradual and shifted — the onset, the nadir and the recovery each come after the corresponding point of the contraction. The mechanism is uteroplacental insufficiency: the contraction transiently reduces intervillous perfusion, fetal oxygen tension falls, chemoreceptors respond, and in a fetus with poor reserve the response repeats with every contraction. Late decelerations are never normal. A prolonged deceleration falls at least 15 bpm below baseline for 2 minutes or more but less than 10 minutes; beyond 10 minutes it is a new baseline. A sinusoidal pattern — a smooth, undulating sine wave of 3–5 cycles per minute persisting 20 minutes or more — suggests severe fetal anaemia and is an emergency.

Three categories and the intrauterine resuscitation sequence

The three-tier system converts the description into a decision. Category I requires all of the following: baseline 110–160 bpm, moderate variability, no late or variable decelerations; early decelerations and accelerations may be present or absent. Category I is normal and predicts normal fetal acid–base status. Category III is either absent variability accompanied by recurrent late decelerations, recurrent variable decelerations or bradycardia, or a sinusoidal pattern. Category III predicts abnormal acid–base status and demands prompt evaluation and, if it does not resolve, expedited birth. Category II is everything in between — the great majority of tracings in labour. Category II is not a diagnosis; it is an instruction to look harder, intervene, and re-evaluate.

Intrauterine resuscitation aims at three physiological targets: relieve cord compression, restore uteroplacental perfusion, and reduce uterine activity. The sequence, in the order a nurse actually performs it, is: (1) stop the oxytocin if it is infusing — you remove the cause before you treat the effect; (2) reposition the birthing parent to a lateral position (either side) or knee-chest, which lifts the uterus off the inferior vena cava and often shifts the cord; (3) perform a vaginal examination to exclude cord prolapse and to assess rapid descent; (4) give an intravenous fluid bolus of 500–1000 mL of an isotonic crystalloid such as lactated Ringer’s if the person is not fluid-restricted, which is the specific treatment for post-epidural hypotension; (5) treat hypotension with the ordered vasopressor if fluids are insufficient; (6) consider a tocolytic — terbutaline 0.25 mg subcutaneously — for tachysystole; (7) notify the provider and prepare for expedited birth. Supplemental oxygen at 10 L/min by non-rebreather mask remains in many unit protocols, but current evidence has not demonstrated improved neonatal outcomes from routine maternal oxygen for a category II tracing; follow your facility protocol and know that it is not the intervention that fixes the problem. Amnioinfusion — warmed isotonic fluid instilled through an intrauterine pressure catheter — is the targeted treatment for recurrent variable decelerations caused by oligohydramnios.

Document what you saw, what you did and what happened next, using the standard terminology rather than words such as “good strip” or “fetal distress”. Interpretation of the fetal heart rate tracing is an assessment: it is a registered nurse function and it is not delegated to assistive personnel. Unlicensed personnel may apply the monitor belts and reposition a stable patient; they may not tell you what the strip means.

Section 2When the Labour Pattern Deviates

Describing the pattern, not blaming the patient

The older phrase “failure to progress” is retired for good reason. It assigns the problem to the labouring person, it is imprecise, and it has been associated with caesarean births performed before labour was given a fair chance. Describe what you observe: a protracted pattern (progress slower than expected) or an arrest pattern (no progress over a defined interval despite adequate uterine activity). Contemporary labour curves place the onset of the active phase at about 6 cm, not 4 cm, and the latent phase is now understood to be far longer and far more variable than Friedman’s original curve implied. Arrest of dilatation is defined at 6 cm or more with ruptured membranes and no cervical change for 4 hours or more with adequate contractions, or 6 hours or more with inadequate contractions. In the second stage, arrest is considered after 3 hours of pushing in a nulliparous person and 2 hours in a multiparous person, with an additional hour allowed for regional anaesthesia.

Adequacy of contractions is quantified, not guessed. With an intrauterine pressure catheter, Montevideo units are calculated by summing the peak-minus-baseline pressures of every contraction in a 10-minute window; 200 MVUs or more is adequate. Without a catheter, palpate: a contraction you can indent easily is mild, one that indents with difficulty is moderate, and one that feels like a forehead is strong. A hypotonic pattern gives infrequent, weak, poorly coordinated contractions with a soft resting uterus and slow progress, and it responds to augmentation, amniotomy, position change and emptying the bladder. A hypertonic pattern gives frequent, painful, ineffective contractions with elevated resting tone, most often in the latent phase; it responds to therapeutic rest, hydration and analgesia, and augmenting it makes it worse.

Non-pharmacological measures are genuine interventions. Upright and mobile positions, a birthing ball, hands and knees, side-lying with a peanut ball between the knees for a person with an epidural, hydration, an empty bladder every 2 hours, and continuous labour support all shorten labour and reduce operative birth. Say “your labour is taking a slower path” rather than anything that implies the person is failing at it.

Malposition, malpresentation and the diameters they present

Occiput posterior position is the commonest malposition. The fetal occiput lies against the sacrum, the poorly flexed head presents a larger diameter, and the labour is characterised by severe continuous low back pain, early urge to push, a prolonged second stage and a higher rate of operative birth. Nursing management is positional and effective: hands and knees, lunges, open-knee-chest, side-lying on the side opposite the fetal spine, and counter-pressure to the sacrum. Most rotate spontaneously.

Breech presentation occurs in about 3–4 per cent of term births. Frank breech has hips flexed and knees extended; complete breech has both flexed; footling has one or both feet presenting and carries the greatest risk of cord prolapse because the presenting part does not fill the pelvic inlet. External cephalic version may be offered at 36–37 weeks. Face presentation may deliver vaginally if the chin is anterior (mentum anterior) but cannot if the chin is posterior. Brow presentation presents the largest diameter of all and usually requires caesarean unless it converts. A transverse lie cannot deliver vaginally. Compound presentation, most often a hand alongside the head, raises the risk of cord prolapse and of laceration.

Two nursing observations matter across all of these. First, in any malpresentation, the moment membranes rupture is the moment of highest risk for cord prolapse — auscultate or observe the fetal heart rate immediately after every rupture, spontaneous or artificial, for a full minute. Second, an unengaged presenting part in the presence of ruptured membranes means the patient is not ambulated without a provider order.

Induction, augmentation and tachysystole

Cervical readiness is scored with the Bishop score across dilatation, effacement, station, consistency and position; a score of 8 or more predicts a vaginal birth as likely as spontaneous labour, and 6 or less indicates that cervical ripening should precede oxytocin. Ripening agents include vaginal misoprostol 25 mcg every 3–6 hours, dinoprostone gel or insert, and mechanical methods such as a transcervical balloon catheter. Misoprostol is contraindicated in anyone with a previous caesarean or other uterine scar because it markedly increases the risk of uterine rupture.

Oxytocin is a high-alert medication. It is mixed as a dilute solution (commonly 30 units in 500 mL of isotonic fluid), delivered by infusion pump as a secondary line piggybacked into the primary line at the port closest to the patient so it can be stopped instantly, and titrated against uterine response rather than to a target rate. Typical protocols start at 0.5–2 milliunits per minute and increase by 1–2 milliunits per minute no more often than every 30–60 minutes. The goal is contractions every 2–3 minutes lasting 40–90 seconds, of moderate to strong intensity (40–70 mmHg by catheter), with a resting tone below 20 mmHg and a resting interval of at least 60 seconds. Because oxytocin is structurally similar to antidiuretic hormone, prolonged high-dose infusion in large fluid volumes can cause water intoxication — watch for headache, nausea, confusion and a falling serum sodium.

Tachysystole is more than 5 contractions in 10 minutes averaged over a 30-minute window. It matters because the placenta is perfused between contractions, not during them; take away the resting interval and you take away fetal oxygenation. Management depends on the tracing. With a category I tracing, reposition, give a fluid bolus and reduce the oxytocin rate. With a category II or III tracing, stop the oxytocin outright, reposition, give a bolus, and if the pattern persists give terbutaline 0.25 mg subcutaneously. Never treat tachysystole by increasing the oxytocin because “the contractions are not doing anything”.

Preterm birth, group B streptococcus and trial of labour after caesarean

When preterm labour cannot be stopped, the intrapartum priorities are fetal lung maturity, neuroprotection and infection prophylaxis. Antenatal corticosteroids — betamethasone 12 mg intramuscularly, two doses 24 hours apart, or dexamethasone 6 mg intramuscularly every 12 hours for four doses — reduce respiratory distress syndrome, intraventricular haemorrhage and necrotising enterocolitis. Magnesium sulfate given before 32 weeks reduces the risk of cerebral palsy. Tocolytics such as nifedipine or indomethacin are used to buy the 48 hours that steroids need, not to prolong the pregnancy indefinitely.

Group B streptococcus prophylaxis is given intrapartum, not antenatally, because the aim is to reduce the bacterial load in the birth canal at the time the newborn passes through it. Penicillin G is first line: 5 million units intravenously as a loading dose, then 2.5–3 million units every 4 hours until birth. Prophylaxis is considered adequate only if the first dose was given at least 4 hours before birth — a fact that shapes the newborn’s observation plan. Ampicillin 2 g then 1 g every 4 hours is an alternative; cefazolin is used for low-risk penicillin allergy, clindamycin for high-risk allergy with a susceptible isolate, and vancomycin when susceptibility is unknown.

A trial of labour after caesarean is reasonable after one or two previous low transverse incisions and requires a facility able to perform an immediate caesarean. It is contraindicated after a classical (vertical) uterine incision, previous uterine rupture, or extensive transfundal surgery. Continuous electronic monitoring is standard, prostaglandin ripening with misoprostol is not used, and oxytocin is titrated with particular caution. The nurse’s single most important surveillance task is described in the next section.

Section 3Sudden Intrapartum Emergencies

Umbilical cord prolapse

The cord slips below the presenting part and is compressed between it and the bony pelvis. Blood flow to the fetus stops, and the fetal heart rate shows a sudden prolonged deceleration or severe recurrent variable decelerations, classically within moments of membranes rupturing. Risk factors are anything that prevents the presenting part from filling the pelvic inlet: footling breech, transverse lie, unengaged presenting part, polyhydramnios, prematurity, multiple gestation, a long cord, and artificial rupture of membranes performed at a high station. The cord may be visible at the introitus, palpable in the vagina, or entirely occult with the diagnosis made only from the tracing.

The first action is to call for help and, with a gloved hand in the vagina, elevate the presenting part off the cord — and then to keep that hand exactly where it is, through transfer, through skin preparation, through spinal placement, until the baby is delivered. Simultaneously position the patient in knee-chest or steep Trendelenburg or exaggerated Sims to let gravity assist, stop the oxytocin, give oxygen at 10 L/min by non-rebreather, open the intravenous fluids, and prepare for immediate caesarean birth. A tocolytic such as terbutaline 0.25 mg subcutaneously may be ordered to reduce uterine activity, and filling the bladder with 500–700 mL of sterile saline through an indwelling catheter is an alternative method of elevating the presenting part when a delay is anticipated.

Two actions are wrong and both are intuitive. Do not attempt to push the cord back into the uterus — it does not stay, and manipulation causes vasospasm that worsens the very ischaemia you are trying to relieve. Do not repeatedly handle or palpate the cord to check for pulsation for the same reason. If a loop lies outside the introitus, cover it lightly with a warm saline-moistened gauze and leave it alone.

Shoulder dystocia

The head delivers and the anterior shoulder impacts behind the pubic symphysis. The sign is the turtle sign — the head emerges and retracts tightly against the perineum — along with failure of restitution and failure of the shoulders to deliver with normal gentle traction. Risk factors include fetal macrosomia, diabetes in pregnancy, a previous shoulder dystocia, post-term pregnancy, obesity, prolonged second stage and operative vaginal birth — but roughly half of cases occur with no risk factor at all, which is why every nurse rehearses the sequence.

Call for help and note the time; the clock is the documentation. Then work through HELPERR: Help; Evaluate for episiotomy (which makes room for the operator’s hand, not for the shoulder); Legs — McRoberts manoeuvre, hyperflexing the hips sharply onto the abdomen, which straightens the sacrum and rotates the symphysis cephalad; Pressure — suprapubic pressure, applied by a second person with the heel of the hand just above the pubic bone and directed downward and laterally toward the fetal chest to adduct the shoulder; Enter for internal rotational manoeuvres (Rubin II, Woods corkscrew); Remove the posterior arm; Roll the patient onto all fours (Gaskin manoeuvre). McRoberts plus suprapubic pressure alone resolves more than half of cases, and delivery is aimed for within about 5 minutes.

Fundal pressure is absolutely contraindicated. Pushing on the fundus drives the impacted shoulder harder against the symphysis, and it has caused uterine rupture. Excessive lateral traction on the fetal head causes brachial plexus injury. Complications for the newborn include brachial plexus injury with Erb palsy, clavicular or humeral fracture and hypoxic injury; for the birthing parent, postpartum haemorrhage and third- or fourth-degree perineal laceration. Document who was present, the sequence and duration of each manoeuvre, the time of head and body delivery, and cord gases if obtained.

Uterine rupture, abruption and the bleeding you cannot see

Uterine rupture is a complete separation of the uterine wall. The most common early sign is not pain — it is an abnormal fetal heart rate, usually a prolonged deceleration or sudden bradycardia. Other findings are a sudden tearing or sharp abdominal pain, cessation or loss of the contraction pattern, loss of station as the presenting part retracts upward on examination, palpable fetal parts through the abdominal wall, signs of hypovolaemic shock, and vaginal bleeding that may be minimal because most of the haemorrhage is intra-abdominal. Management is immediate laparotomy: stop the oxytocin, give oxygen, open two large-bore intravenous lines, activate the massive transfusion protocol, notify the operating theatre and the neonatal team, and prepare the patient. Fetal survival falls sharply beyond roughly 10–18 minutes of sustained bradycardia, and hysterectomy may be required.

Placental abruption is premature separation of a normally implanted placenta. The picture is painful dark red bleeding with a firm, board-like, exquisitely tender uterus, elevated resting tone, frequent low-amplitude contractions and a non-reassuring tracing. A concealed abruption bleeds behind the placenta, so the visible loss badly understates the true loss — trust the maternal heart rate, the fundal height rising over time and the fetal tracing more than the pad. Disseminated intravascular coagulation is a real risk. By contrast, placenta praevia presents with painless bright red bleeding and a soft, non-tender uterus, and the absolute rule is that no vaginal examination is performed in a patient with undiagnosed third-trimester bleeding until praevia has been excluded by ultrasound. Vasa praevia produces painless bright red bleeding at the moment of membrane rupture followed within minutes by fetal bradycardia or a sinusoidal pattern; the blood is fetal, the fetal blood volume is only about 80–85 mL per kilogram, and the response is immediate caesarean birth.

Amniotic fluid embolism is rare, unpredictable and catastrophic. Amniotic debris entering the maternal circulation triggers an anaphylactoid response: abrupt hypoxia and respiratory distress, sudden hypotension and cardiovascular collapse, often a seizure, and then disseminated intravascular coagulation with torrential bleeding. Management is supportive and immediate — high-quality cardiopulmonary resuscitation with continuous manual left uterine displacement rather than a tilted board, 100 per cent oxygen and early intubation, aggressive volume and vasopressor support, and massive transfusion. If there is no return of spontaneous circulation, perimortem caesarean birth is begun at 4 minutes with the aim of delivering by 5 minutes, because emptying the uterus restores venous return and improves the chance of resuscitating both patients.

Section 4Hypertensive Crisis and Magnesium Sulfate

Severe features, acute severe hypertension and eclampsia

Pre-eclampsia becomes pre-eclampsia with severe features when any one of the following appears: systolic blood pressure 160 mmHg or above or diastolic 110 mmHg or above on two occasions at least 4 hours apart (or once, if severe hypertension is confirmed on repeat within minutes and treatment is being started); platelet count below 100 000 per microlitre; serum creatinine above 1.1 mg/dL or doubled; transaminases at least twice the upper limit of normal; pulmonary oedema; or new cerebral or visual symptoms. Persistent headache unrelieved by paracetamol, visual scotomata or blurring, and epigastric or right upper quadrant pain are the three symptoms that change the plan, and the epigastric pain is stretching of the hepatic capsule, not indigestion.

Acute-onset severe hypertension — a sustained systolic of 160 mmHg or more or a diastolic of 110 mmHg or more — is a hypertensive emergency because of the risk of haemorrhagic stroke, and it should be treated within 30 to 60 minutes, ideally within 30. Three first-line regimens exist. Intravenous labetalol 20 mg over 2 minutes, then 40 mg after 10 minutes, then 80 mg after another 10 minutes, to a cumulative maximum around 300 mg — avoided in asthma, bradycardia below 60, and decompensated heart failure. Intravenous hydralazine 5–10 mg over 2 minutes, repeated at 10 mg after 20 minutes if the threshold is still exceeded, to a cumulative maximum of about 20–30 mg before moving to labetalol — expect reflex tachycardia, headache and occasional maternal hypotension. Oral immediate-release nifedipine 10 mg, repeated at 20 mg after 20 minutes, which is the option when intravenous access is not yet established. Recheck the blood pressure at 10-minute intervals during treatment and do not aim for normotension — a target of roughly 140–150 over 90–100 mmHg preserves uteroplacental perfusion.

Eclampsia is a generalised tonic-clonic seizure in a person with a hypertensive disorder of pregnancy. The first action during the seizure is protect the airway and prevent injury: stay with the patient, call for help, turn the patient to the side, lower the bed, pad the rails, remove hazards, and note the time. Do not restrain the limbs and do not insert anything into the mouth. After the seizure ends, work airway first and in this order: suction the airway, give oxygen at 10 L/min by non-rebreather, secure or confirm intravenous access, give the ordered magnesium sulfate bolus through it, draw laboratory studies, and only then evaluate the fetus. Transient fetal bradycardia with reduced variability after an eclamptic seizure is expected and usually recovers as the parent is stabilised — rushing to caesarean during or immediately after a seizure endangers an unstable patient. Birth follows stabilisation; it does not replace it. Magnesium sulfate is continued for at least 24 hours after birth or after the last seizure.

Magnesium sulfate: the drug, the monitoring and the toxicity ladder

Magnesium sulfate prevents and treats eclamptic seizures by antagonising calcium at the neuromuscular junction and raising the cerebral seizure threshold. It is not an antihypertensive — a common and dangerous misunderstanding. The standard regimen is a loading dose of 4–6 g intravenously over 15–30 minutes, followed by a maintenance infusion of 1–2 g per hour. It is a high-alert medication: it goes on a volumetric pump, on its own clearly labelled secondary line, with an independent double-check by a second nurse of the concentration, the pump settings and the dose.

The therapeutic serum range is roughly 4–7 mEq/L (about 5–8 mg/dL). Toxicity then declares itself in a predictable order, and knowing the order is what makes the monitoring meaningful: deep tendon reflexes disappear before respiratory depression appears. The patellar reflex is therefore the early-warning system, and it is checked hourly. If the epidural blocks the patellar reflex, use the biceps or brachioradialis reflex instead.

Monitoring parameters are checked hourly and the infusion is held if any one of them fails: respiratory rate below 12 per minute, absent deep tendon reflexes, urine output below 30 mL per hour (or below 100 mL in 4 hours), a serum level above the therapeutic range, or a sudden fall in level of consciousness. Urine output matters because magnesium is cleared entirely by the kidney — a patient with oliguria accumulates the drug even on an unchanged infusion rate. Also monitor continuous pulse oximetry, cardiac and fetal heart rate, lung sounds for pulmonary oedema, and strict intake and output.

The antidote is calcium gluconate 1 g, which is 10 mL of a 10 per cent solution, given intravenously over about 3 minutes. The sequence when toxicity is recognised is: (1) stop the magnesium infusion; (2) call for help and notify the provider; (3) give calcium gluconate as ordered; (4) support ventilation with oxygen, bag-mask or intubation as needed; (5) draw a magnesium level; (6) continuous monitoring. Stopping the infusion comes before the antidote — giving calcium while magnesium continues to run is treating a tap that is still open. Keep the calcium gluconate, a bag-valve-mask and suction at the bedside of every patient on magnesium.

The newborn is also a magnesium patient. Babies born to a parent on infusion may show hypotonia, lethargy, poor suck and respiratory depression at birth. Anticipate the need for respiratory support and have the neonatal team present; naloxone is not the answer here and is no longer part of neonatal resuscitation at all.

HELLP syndrome and the coagulation problem

HELLP is Haemolysis, Elevated Liver enzymes and Low Platelets, and it can occur with only modest hypertension, which is exactly why it is missed. The laboratory definition uses lactate dehydrogenase of 600 units/L or more or bilirubin of 1.2 mg/dL or more with schistocytes on the smear, transaminases at least twice the upper limit of normal, and a platelet count below 100 000 per microlitre. The classic presenting complaint is right upper quadrant or epigastric pain, often with nausea, vomiting and general malaise that the patient may describe as feeling like influenza.

The nursing implications are bleeding implications. Platelets below 100 000 mean minimising venipunctures, using the smallest needle, applying pressure for longer, avoiding intramuscular injections where possible, using a soft toothbrush, and watching for petechiae, gum bleeding, bruising and haematuria. Regional anaesthesia is generally withheld below a platelet count in the 70 000–80 000 range because of the risk of epidural haematoma — the exact threshold is set by anaesthesia and by institutional policy. Subcapsular hepatic haematoma is a rare but lethal complication; sudden severe right upper quadrant pain with shoulder pain and shock suggests rupture and no one palpates that abdomen deeply. Definitive treatment of HELLP, like that of pre-eclampsia with severe features, is birth.

Section 5The Fourth Stage and Two Patients at Once

Postpartum haemorrhage: massage the fundus first

Postpartum haemorrhage is a cumulative blood loss of 1000 mL or more, or blood loss accompanied by signs or symptoms of hypovolaemia, within 24 hours of birth regardless of route. Loss is quantified, not estimated: blood is measured in graduated under-buttock drapes and soaked materials are weighed, with 1 gram of weight above dry weight counted as 1 mL of blood. Visual estimation understates loss by 30–50 per cent, and the healthy young obstetric patient compensates so well that the blood pressure may not fall until 25–30 per cent of blood volume is gone. Tachycardia, narrowing pulse pressure, restlessness, air hunger and a rising shock index (heart rate divided by systolic blood pressure; 0.9 or above is concerning) all appear first.

Causes are organised as the four Ts. Tone — uterine atony — causes 70–80 per cent of cases and is more likely after an over-distended uterus, prolonged or very rapid labour, prolonged oxytocin exposure, grand multiparity, chorioamnionitis or magnesium sulfate. Trauma covers lacerations, haematoma and uterine inversion. Tissue covers retained placental fragments and abnormally adherent placenta. Thrombin covers coagulopathy, including disseminated intravascular coagulation after abruption or amniotic fluid embolism.

The first action for heavy postpartum bleeding is to palpate and massage the fundus, because tone is the most likely cause and fundal massage is both the assessment and the treatment. Only after the uterus is being massaged do you call for help, empty the bladder (a full bladder displaces the uterus — a fundus that is boggy and deviated to the right is a bladder problem until proven otherwise), establish or check large-bore intravenous access, begin or increase oxytocin, quantify the loss, and send a full blood count, coagulation screen, fibrinogen and crossmatch. If the fundus is firm and midline and the patient is still bleeding steadily bright red, tone is not the cause — look for a laceration and call the provider to inspect the birth canal. If the patient reports severe unrelenting perineal, vaginal or rectal pressure and pain with a firm fundus and rising pulse, suspect a concealed haematoma.

If bleeding continues, escalation is stepwise and rapid: bimanual uterine compression, intrauterine balloon tamponade, a vacuum-induced haemorrhage-control device, uterine artery embolisation, compression sutures, arterial ligation, and hysterectomy as the definitive last step. Activate the massive transfusion protocol early, transfusing red cells, plasma and platelets in roughly a 1:1:1 ratio, keep the patient warm, and remember that hypothermia and acidosis worsen coagulopathy. One special case: never pull on a cord against an unseparated placenta, because uterine inversion — sudden severe pain, profound shock out of proportion to visible loss, and a fundus that cannot be found — is managed by stopping uterotonics, replacing the uterus, and only then restarting them.

The newborn who does not transition, and weight-based dosing

At every birth, three questions are asked in the first seconds: is the baby term, does the baby have good tone, and is the baby breathing or crying? Three yeses mean skin-to-skin contact with the parent, delayed cord clamping for 30–60 seconds, drying and routine care. Any no means the baby goes to the radiant warmer for the initial steps — warm, dry, stimulate, position the airway in the sniffing position, clear secretions only if they are obstructing — with heart rate and respirations assessed within the first 60 seconds, the “Golden Minute”.

If the heart rate is below 100 beats per minute or the baby is apnoeic or gasping, begin positive-pressure ventilation at 40–60 breaths per minute, starting with 21 per cent oxygen for babies of 35 weeks or more and 21–30 per cent for those below 35 weeks, with the pulse oximeter on the right hand or wrist to read preductal saturation. Ventilation is the single most important step in neonatal resuscitation; almost every newborn who needs help needs air moved into the lungs and nothing more. If the chest does not rise, run MR SOPA: Mask adjust, Reposition the head, Suction mouth then nose, Open the mouth, Pressure increase, Alternative airway. If the heart rate remains below 60 after 30 seconds of ventilation that visibly moves the chest, start chest compressions with the two-thumb encircling technique at a ratio of 3 compressions to 1 breath, giving 90 compressions and 30 breaths — 120 events — each minute, with oxygen increased to 100 per cent. Targeted preductal saturations climb slowly and deliberately: 60–65 per cent at 1 minute, 65–70 at 2, 70–75 at 3, 75–80 at 4, 80–85 at 5 and 85–95 at 10 minutes. The Apgar score is assigned at 1 and 5 minutes, and every 5 minutes to 20 minutes if it remains below 7, but it is a description of the transition, not the trigger for it — you never wait for an Apgar score to start resuscitating.

If the heart rate is still below 60 after 60 seconds of coordinated compressions and ventilation through a secure airway, epinephrine is given, preferably through an umbilical venous catheter. The intravenous dose is 0.02 mg/kg (acceptable range 0.01–0.03 mg/kg) of the 0.1 mg/mL concentration, repeated every 3–5 minutes; the endotracheal dose, used only while access is being obtained, is higher at 0.05–0.1 mg/kg. For suspected hypovolaemia — pallor, weak pulses, poor response, a history of abruption, vasa praevia or cord accident — give a volume expander of 10 mL/kg of normal saline or O-negative blood over 5–10 minutes. Work the arithmetic every time, out loud, with a second nurse:

The Apgar score has five components, each scored 0, 1 or 2 for a total out of 10, and the mnemonic APGAR names them: Appearance (colour), Pulse (heart rate), Grimace (reflex irritability), Activity (muscle tone) and Respiration (respiratory effort). Heart rate scores 0 if absent, 1 if below 100 and 2 if 100 or above. Respiratory effort scores 0 if absent, 1 for slow, irregular or a weak cry, and 2 for a good lusty cry. Tone scores 0 for flaccid, 1 for some flexion, 2 for active motion. Reflex irritability scores 0 for no response, 1 for a grimace, 2 for a cry, cough or sneeze. Colour scores 0 for blue or pale, 1 for a pink body with blue hands and feet — acrocyanosis, which is normal in the first hours — and 2 for completely pink. A total of 7 to 10 is reassuring, 4 to 6 is moderately depressed, and 0 to 3 is severely depressed. Note again what the score is not: it is scored after the Golden Minute has already been spent resuscitating, and it never determines whether resuscitation starts.

Escalation, delegation and the debrief

Escalate in a structure the receiving clinician can act on. SBAR for an intrapartum haemorrhage sounds like this: Situation — “This is Priya, registered nurse in room 4. Ms Okafor is 20 minutes postpartum from a vaginal birth and I have quantified 900 mL of blood loss and it is continuing.” Background — “Gravida 4, 41 weeks, oxytocin augmentation for 14 hours, birth weight 4.3 kg, shoulder dystocia resolved with McRoberts and suprapubic pressure.” Assessment — “The fundus is boggy two fingerbreadths above the umbilicus and deviated right. Heart rate 122, blood pressure 96 over 54, she is pale and anxious. I have massaged the fundus, emptied 400 mL from the bladder and increased the oxytocin.” Recommendation — “I need you at the bedside now, I am activating the haemorrhage protocol, and I would like an order for a second uterotonic. Her blood pressure history is normal, so methylergonovine is appropriate.”

Red flags that trigger that call without waiting: any category III tracing; a prolonged deceleration lasting more than 2 minutes; sudden fetal bradycardia after rupture of membranes; loss of station with abdominal pain in a person labouring after caesarean; a saturated pad in less than 15 minutes or a clot larger than a lemon; systolic 160 or diastolic 110 mmHg confirmed on repeat; a new headache, visual change or epigastric pain in a hypertensive patient; absent deep tendon reflexes or a respiratory rate below 12 on magnesium; and a newborn heart rate below 100 after 30 seconds of effective ventilation.

Delegation limits do not soften in an emergency. Assessment, teaching, evaluation, fetal heart rate interpretation, titration of oxytocin or magnesium, intravenous push medication, blood product administration and the care of an unstable patient stay with the registered nurse. Assistive personnel may take vital signs on stable patients, provide comfort measures and positioning, assist with ambulation of a stable patient, weigh pads for quantification (with the nurse interpreting the result), obtain supplies and the emergency trolley, and call for extra hands. Delegating a task never delegates the accountability for the outcome. Afterwards, hold a team debrief, because obstetric emergencies are traumatic for staff as well as families, and explain to the family in plain, non-blaming language what happened and why — a parent who believes their body failed carries that belief into the next pregnancy.

Words worth knowing