SEPT 10 Built from the handwritten pages you uploaded on 10 September 2026.
Obstetric emergencies
Magnesium sulphate levels and toxicity, HELLP, and amniotic fluid embolism.
Magnesium sulphate — the level ladder
mmol/L
mg/dL · mEq/L
Effect
0.7–1.0
1.8–2.4 · 1.2–2
Normal
2–4
4.8–9.6 · 4–8
Therapeutic — seizure prophylaxis in pre-eclampsia
2.5–5
6–12 · 5–10
ECG changes — prolonged PR, widened QRS
5
12 · 10
Loss of deep tendon reflexes — the first clinical warning
7.5
18 · 15
SA/AV node block · respiratory paralysis
10–12
24 · 20
Cardiac arrest
Monitoring and reversal
Deep tendon reflexes go first, at around 5 mmol/L — which is why reflexes are checked hourly rather than levels.
Also monitor respiratory rate and urine output (magnesium is renally excreted, so oliguria causes accumulation).
Antidote: calcium gluconate 1 g IV — calcium directly antagonises magnesium at the neuromuscular junction.
Regimen for eclampsia: 4 g loading dose over 5–10 minutes, then 1 g/h. Magnesium is superior to phenytoin and diazepam for both treating and preventing eclamptic seizures.
Anaesthetic interactions
Magnesium blocks the neuromuscular junction — it reduces prejunctional acetylcholine release and reduces the sensitivity of the postjunctional membrane.
So it markedly potentiates non-depolarising blockers — reduce the dose and use a nerve stimulator.
It reduces the incidence of suxamethonium fasciculations.
Magnesium plus a calcium channel blocker can cause profound hypotension and neuromuscular weakness — use the combination cautiously.
Other useful effects: bronchodilatation, antiarrhythmic in torsades, and analgesic adjunct through NMDA antagonism.
HELLP syndrome
The worst complication of pre-eclampsia — Haemolysis, Elevated Liver enzymes, Low Platelets.
Component
Threshold
Note
Haemolysis
Bilirubin > 1.2 mg/dL (> 20 µmol/L)
With schistocytes on film and a low haptoglobin
Elevated liver enzymes
AST > 70 · LDH > 600
LDH reflects both haemolysis and hepatic injury
Low platelets
< 100 000
The count that decides whether neuraxial blockade is safe
Definitive treatment is delivery of the fetus. Everything else is supportive.
Supportive care: magnesium for seizure prophylaxis, blood pressure control (labetalol, hydralazine, nifedipine), steroids for fetal lung maturity, and correction of coagulopathy.
Feared complications: hepatic subcapsular haematoma and rupture (sudden shoulder-tip or epigastric pain with shock), DIC, placental abruption, acute kidney injury, pulmonary oedema.
Anaesthetic implication: a falling platelet count in HELLP can fall fast. Check a recent count and the trend before neuraxial blockade — a count of 90 falling by 30 000 a day is not the same as a stable 90. Many would proceed above 75–80 with a stable trend; general anaesthesia with a difficult, oedematous airway is the alternative.
Ergometrine is contraindicated in pre-eclampsia — use oxytocin, given slowly.
Amniotic fluid embolism
Recognition
First sign: HYPOTENSION.
The pickup point: OOZING FROM IV LINES, with cyanosis and hypotension. Sudden coagulopathy out of proportion to blood loss is the giveaway.
Full picture: sudden cardiovascular collapse, hypoxia, seizures in about 20%, fetal distress, then DIC in the majority of survivors of the first phase.
Biphasic: an initial phase of pulmonary vasoconstriction with right ventricular failure, followed by left ventricular failure and a massive consumptive coagulopathy.
Now understood as an anaphylactoid immune reaction to fetal antigen rather than a true embolic obstruction.
Diagnosis
Fundamentally a clinical diagnosis of exclusion — exclude haemorrhage, high block, local anaesthetic toxicity, anaphylaxis, eclampsia, air embolism and pulmonary embolism.
Supportive investigations described in your notes: cytological analysis of pulmonary artery or bronchoalveolar lavage fluid for fetal squames and mucin; sialyl Tn antigen; and zinc coproporphyrin concentration.
None of these is available in time to change management, and fetal squames are found in normal pregnancy too — so do not delay treatment to confirm.
Treatment
Supportive, and aggressive. There is no specific therapy.
Airway and 100% oxygen · large-bore access · left uterine displacement · fluid and vasopressors, with noradrenaline and inotropic support for the failing right ventricle.
Early activation of the major haemorrhage protocol — this coagulopathy consumes product fast. Fibrinogen and cryoprecipitate matter particularly.
Perimortem caesarean section within 5 minutes of maternal arrest.
Consider echocardiography to guide the right heart, and ECMO or cardiopulmonary bypass in refractory cases.