Trauma in pregnancy

The trauma in pregnancy is the management of two patients simultaneously — the mother and the foetus — and the Fellowship candidate must know the physiological changes of the pregnancy that alter the response to the injury, the modifications to the primary survey, the perimortem caesarean, the foetal complications (the abruption and the uterine rupture), and the foeto-maternal haemorrhage with the Anti-D prophylaxis. The principles of the trauma resuscitation are unchanged; the modifications are the adaptations that protect the foetus and address the altered physiology.[1]

The physiological changes of pregnancy

The pregnancy alters the physiology in ways that directly affect the trauma management.[1] The blood volume increases by 40 to 50 per cent (so the pregnant patient loses more blood before showing the signs of the shock — the normal maternal blood pressure does not exclude the 1500 millilitres of the blood loss). The heart rate rises by 15 to 20 beats per minute. The blood pressure falls by 5 to 15 mmHg in the second trimester (the progesterone-mediated vasodilation). The clotting factors increase (the pregnancy is a hypercoagulable state — the factor VII, the factor VIII, the fibrinogen, the von Willebrand factor — the VTE risk is 4 to 5 times the non-pregnant). The functional residual capacity falls and the oxygen consumption rises (so the pregnant patient desaturates rapidly on the apnoea). The enlarged uterus (above 20 weeks) compresses the inferior vena cava and the aorta in the supine position (the aortocaval compression), reducing the venous return and the cardiac output by up to 30 per cent.

The cardiovascular system — the expanded but diluted volume

The cardiovascular adaptation of the pregnancy is the expanded blood volume with the relatively reduced red-cell mass — the dilutional anaemia of the pregnancy (the haemoglobin falls by around 20 grams per litre, to a physiologically normal of 105 to 110 by the third trimester). The plasma volume rises more than the red-cell mass (the plasma rises by 50 per cent, the red cells by 20 to 30 per cent), so the pregnant patient is both better protected against the acute haemorrhage (the larger volume to lose) and worse at carrying oxygen (the lower haemoglobin, the lower reserve before the tissue hypoxia). The cardiac output rises by 30 to 50 per cent by the late second trimester (the stroke volume and the heart rate both rise), and the systemic vascular resistance falls (the progesterone-mediated vasodilation, the low-resistance uteroplacental circulation).[1]

The net effect on the trauma management is the deceptively well-looking patient: the pregnant woman compensates through the tachycardia, the vasoconstriction and the expanded volume until 30 to 35 per cent of the circulating volume is lost, and the hypotension is the late, pre-terminal sign. The shock index (the heart rate divided by the systolic blood pressure) is more sensitive than either value alone, and a shock index above 0.9 to 1.0 in the pregnant trauma patient (where the baseline is 0.7 to 0.8) is the early warning of the occult blood loss. [1]

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The respiratory system — the reduced reserve and the rapid desaturation

The functional residual capacity falls by 20 per cent by the third trimester (the gravid uterus elevates the diaphragm), the oxygen consumption rises by 20 to 30 per cent (the metabolic demand of the fetus and the maternal organs), and the closing volume encroaches on the functional residual capacity (the small airways close during the tidal breathing). The net effect is the rapid, precipitous desaturation on the apnoea — the pregnant trauma patient desaturates within 60 to 90 seconds of the apnoea (versus 5 to 8 minutes in the non-pregnant), and the pre-oxygenation (the three minutes of the high-flow oxygen, or the eight vital-capacity breaths of the 100 per cent oxygen) is the non-negotiable before the rapid sequence induction. The minute ventilation rises (the progesterone-driven hyperventilation), the PaCO2 falls to 30 to 32 mmHg (the respiratory alkalosis of the pregnancy — the renal compensation brings the bicarbonate to 18 to 21), and the PaCO2 of 35 in the pregnant patient is the rising CO2, the fatigue, and the impending respiratory failure.[1]

The difficult airway of the pregnancy adds to the risk: the laryngeal and the pharyngeal oedema, the enlarged and friable mucosa (the easy bleeding on the laryngoscopy), the enlarged breasts (the difficult laryngoscopy and the difficult bag-mask), the reduced FRC (the reduced apnoeic tolerance), and the increased aspiration risk (the relaxed lower oesophageal sphincter from the progesterone, the delayed gastric emptying, the raised intra-abdominal pressure). The pregnant airway is the difficult airway, the aspiration prophylaxis (the ranitidine and the sodium citrate before the anaesthesia) and the rapid sequence induction are the standard, and the senior airway operator is summoned early. [1]

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The gastrointestinal system and the aspiration risk

The progesterone relaxes the lower oesophageal sphincter (the reflux is the near-universal complaint of the pregnancy), the gravid uterus displaces and compresses the stomach (the raised intra-gastric pressure), and the gastric emptying is delayed (the opioid analgesia and the pain of the trauma worsen it). The combination makes the pregnant trauma patient the high aspiration risk — the "full stomach" applies even in the absence of the recent food intake. The rapid sequence induction with the pre-oxygenation, the cricoid pressure (the debated but the standard in many units), and the cuffed endotracheal tube are the airway protection, and the aspiration prophylaxis (the sodium citrate 30 mL orally, the ranitidine 50 mg IV, the metoclopramide 10 mg IV) is given before the anaesthesia where the time allows. [1]

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The haematological system — the hypercoagulable state

The pregnancy is the hypercoagulable state: the factor VII, the factor VIII, the factor X, the fibrinogen and the von Willebrand factor all rise, the protein S falls, and the acquired activated protein C resistance develops. The fibrinogen at the term is 4 to 6 grams per litre (versus 2 to 4 in the non-pregnant), and the normal fibrinogen in the bleeding pregnant patient is the abnormal finding — a fibrinogen below 4 g/L in the bleeding third-trimester patient is the marker of the consumptive coagulopathy (the abruption, the amniotic fluid embolism, the massive haemorrhage). The VTE risk is 4 to 5 times the non-pregnant and rises further in the immobility, the surgery and the trauma — the early mechanical and the pharmacological thromboprophylaxis (once the bleeding is controlled) is the non-negotiable.[3]

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The primary survey modifications

The primary survey follows the C-A-B-C-D-E sequence with the pregnancy-specific modifications. The catastrophic haemorrhage step is unchanged. The airway is managed normally, with the awareness that the pregnant patient desaturates rapidly and the intubation is more difficult (the laryngeal oedema, the enlarged breasts, the reduced FRC). The breathing is managed with the higher oxygen flow and the earlier ventilatory support. The circulation is the key modification: the patient is placed in the left lateral tilt of 15 to 30 degrees or the manual left uterine displacement (pushing the uterus to the left) from the first minute, to relieve the aortocaval compression and restore the venous return. The fluids and the blood products are given with the awareness that the expanded blood volume masks the loss. The disability is assessed normally. The exposure includes the vaginal examination (the bleeding, the rupture of the membranes, the cervical dilation) and the abdominal examination (the uterine tenderness, the contractions, the foetal heart rate after 20 weeks).[1][1]

The aortocaval compression and the left lateral tilt

The gravid uterus, from 20 weeks gestation, compresses the inferior vena cava and the aorta against the lumbar spine when the patient is supine — the supine hypotensive syndrome of the pregnancy. The venous return to the heart falls, the cardiac output falls by 10 to 30 per cent, the uteroplacental perfusion falls (the fetal distress), and the lower-body venous pressure rises (the engorgement of the epidural veins, the leg veins). The aortic compression, less discussed but equally important, reduces the perfusion of the lower limbs and worsens the distal ischaemia. The compression is relieved by the left lateral tilt of 15 to 30 degrees (the wedge or the tilted spine board) or the manual left uterine displacement (the operator pushes the uterus to the left with both hands), which shifts the gravid uterus off the great vessels and restores the venous return.[1]

The manual left uterine displacement is the preferred technique in the trauma and the cardiac arrest: it is the hands-only manoeuvre that does not interfere with the CPR (the chest compressions are delivered on the flat, firm surface), it does not move the spine (the cervical-spine protection is maintained), and it is applied from the first minute of the resuscitation. The lateral tilt is the alternative for the supine patient on the trolley (the wedge under the right buttock), but the tilt impairs the CPR effectiveness (the patient rolls during the compressions) and the manual displacement is the better technique in the arrest. [1]

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The perimortem caesarean

The perimortem caesarean (the resuscitative hysterotomy) is performed at 4 minutes of the cardiac arrest in the pregnant patient with the gestation over 20 weeks (the uterus at the level of the umbilicus). The procedure is performed in the resus bay, through a midline vertical incision from the umbilicus to the symphysis pubis, without the anaesthesia (the patient is in the arrest), and the baby is delivered, the cord is clamped, and the placenta is removed. The rationale is the maternal, not just the foetal, survival: the emptying of the uterus relieves the aortocaval compression, restores the venous return and the cardiac output, and improves the effectiveness of the CPR — the maternal survival improves significantly after the perimortem caesarean. The baby survival is best when the delivery occurs within 5 minutes of the arrest.[1]

The timing — the four-minute rule

The American Heart Association's 2015 scientific statement on the cardiac arrest in pregnancy set the operational framework: the chest compressions begin immediately, the resuscitative hysterotomy is begun at 4 minutes of the arrest (the start of the incision, not the delivery), and the delivery is completed by 5 minutes, in the patient with the gestation over 20 weeks (the uterus at or above the umbilicus).[6] The rationale for the 4-minute start is the realistic observation that the preparation (the scalpel, the incision, the delivery, the cord clamp) consumes 1 minute, so the start at 4 minutes achieves the delivery at 5 minutes. The 5-minute delivery is the threshold of the improved neurological outcome for the fetus, and the early emptying of the uterus is the maternal benefit — the cardiac output after the relief of the aortocaval compression rises by 10 to 30 per cent, and the maternal ROSC is more likely after the perimortem caesarean.[6][7]

The historical 5-minute rule (the Katz framework from 1986, refined by the modern guidance) is the operational target, and the reality of the maternal cardiac arrest in the literature (the Get with the Guidelines cohort of over 500 arrests) is that the perimortem caesarean is performed in fewer than a third of the eligible cases, and the median time to the delivery is well beyond 5 minutes.[7] The team that prepares early — the call for the PMCS at the start of the arrest, the obstetric and the neonatal teams summoned, the equipment prepared — is the team that meets the 4-minute target. The delay is the most common failure.

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The foetal assessment and the CTG monitoring

The foetal assessment is the parallel to the maternal resuscitation — the continuous cardiotocography (the CTG) is applied from the arrival in every pregnant trauma patient over 20 weeks, and the monitoring is maintained for a minimum of 4 hours after the injury (the longer for the significant mechanism or the concerning features).[1] The CTG is the most sensitive indicator of the foetal distress, and the foetal heart-rate abnormalities often precede the maternal haemodynamic decompensation — the foetus is the canary in the maternal haemodynamic coal mine. The abnormal CTG triggers the obstetric review, the ultrasound for the foetal viability and the biophysical profile, and the consideration of the emergency delivery.

The indications for the minimum 4 to 6 hours of the continuous CTG monitoring after the trauma are: any abdominal pain or the uterine tenderness, the vaginal bleeding, the uterine contractions, the significant mechanism (the high-speed collision, the fall from the height, the pedestrian struck), the ejection from the vehicle, the maternal tachycardia or hypotension, and the maternal Rh-negative status with the suspected foeto-maternal haemorrhage. The patient with the concerning CTG (the recurrent decelerations, the reduced variability, the foetal tachycardia or bradycardia) is monitored longer and referred for the obstetric assessment. [1]

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The placental abruption

The placental abruption is the most common significant complication of the trauma in pregnancy (the shearing of the placenta from the uterine wall by the deceleration or the direct blow).[1][2] It presents with the abdominal pain, the uterine tenderness, the uterine contractions, the vaginal bleeding (though the bleeding may be concealed behind the placenta), and the foetal distress (the abnormal foetal heart rate pattern, the foetal death). The abruption can present up to 24 hours after the minor trauma, so the patient with the significant mechanism is observed with the continuous foetal monitoring for 4 to 24 hours. The management is the obstetric referral, the foetal monitoring, the resuscitation, and the delivery if the abruption is significant.

The Couvelaire uterus and the consumptive coagulopathy

The concealed abruption is the dangerous variant: the blood is trapped behind the placenta, the vaginal bleeding is minimal or absent despite the massive retroplacental clot, and the diagnosis is missed if the team waits for the external bleeding. The concealed abruption drives the consumptive coagulopathy (the disseminated intravascular coagulation from the release of the thromboplastin and the consumption of the fibrinogen and the platelets), and the Couvelaire uterus — the blood extravasates into the myometrium and the broad ligament, producing the purple, tense, non-contractile uterus that fails to respond to the oxytocin after the delivery. The fibrinogen below 4 g/L in the bleeding third-trimester patient is the marker of the abruption-driven coagulopathy, and the cryoprecipitate and the fresh-frozen plasma are the targeted replacement. [1]

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The uterine rupture

The uterine rupture is the catastrophic complication of the major trauma (the high-speed collision, the direct blow to the abdomen), more common in the previously-scarred uterus (the previous caesarean). It presents with the severe abdominal pain, the loss of the foetal station (the foetal parts felt through the abdominal wall), the shock, and the foetal death. The management is the emergency laparotomy.[1][1]

The foeto-maternal haemorrhage and the Anti-D

The trauma can cause the foetal blood to enter the maternal circulation (the foeto-maternal haemorrhage), which sensitises the Rh-negative mother and produces the haemolytic disease of the newborn in the future pregnancies. The Kleihauer-Betke test (or the flow cytometry) quantifies the foetal cells in the maternal blood. The Anti-D immunoglobulin is given to the Rh-negative mother within 72 hours of the trauma to prevent the sensitisation, at the standard dose (500 IU for the first trimester, 1250 IU for the second or third), with an additional dose if the Kleihauer-Betke shows a large bleed.[1]

The Kleihauer-Betke test and the dose calculation

The Kleihauer-Betke acid-elution test relies on the resistance of the foetal haemoglobin (the HbF) to the acid elution — the maternal adult haemoglobin (the HbA) is eluted from the red cells by the acid, leaving only the foetal cells to stain, and the ratio of the foetal to the adult cells on the blood film estimates the volume of the foeto-maternal haemorrhage. The flow cytometry (the anti-HbF or the anti-D antibody) is the more accurate modern alternative and is increasingly preferred, especially in the larger bleeds. The test is sent in every Rh-negative pregnant trauma patient, and the result guides the additional Anti-D beyond the standard dose. [1]

The additional Anti-D is calculated at 25 IU (or 125 IU in some guidelines) per millilitre of the foetal whole blood identified on the Kleihauer-Betke. The standard prophylactic dose (500 IU in the first trimester, 1500 IU in the second and third) covers up to 4 mL of the foetal cells, and the additional dose is given for the larger bleeds. The test is repeated at 48 hours if the initial Kleihauer-Betke shows a large bleed, because the foeto-maternal haemorrhage can continue. The Anti-D is given within 72 hours of the trauma, and it is given even after a stillbirth or a miscarriage, because the sensitisation risk persists. [1]

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The mechanisms of injury in pregnancy

The trauma in pregnancy reflects the activities and the physiology of the pregnant woman: the motor-vehicle collision (the commonest), the fall (the second commonest, the altered balance and the shifted centre of gravity), the penetrating injury (the stab, the gunshot), the assault and the domestic violence (the under-recognised and the universally screened), and the rare but the distinctive mechanisms (the thermal injury, the electrical injury, the near-drowning). The mechanism-specific injury patterns and the modifications of the management follow from the mechanism. [1]

The motor-vehicle collision and the seatbelt pattern

The motor-vehicle collision is the leading mechanism of the trauma in pregnancy (the deceleration, the direct impact, the ejection). The proper seatbelt use — the three-point restraint with the lap belt below the uterus, across the upper thighs and the pubic symphysis, and the shoulder belt between the breasts and over the mid-clavicle — is the most important modifiable factor in the foetal survival.[8][9] The seatbelt sign (the bruise across the abdomen where the lap belt was incorrectly placed over the uterus) is the marker of the high-energy transfer to the uterus and the foetus, and it is the indication for the prolonged foetal monitoring and the search for the abruption, the uterine rupture and the direct foetal injury. The airbag deployment adds to the chest and the abdominal impact but does not significantly worsen the foetal outcome when the seatbelt is worn correctly.[8]

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The fall — the altered balance and the shifted centre of gravity

The pregnant woman is at the increased risk of the fall: the shifting of the centre of the gravity (the gravid uterus), the joint laxity (the relaxin, the progesterone), the postural instability, the syncope (the supine hypotensive syndrome, the orthostatic hypotension), and the altered gait. The fall from the standing height is the common mechanism, and the injury is usually minor (the soft-tissue, the sprain), but the significant mechanism (the fall down the stairs, the fall from the height, the syncopal fall onto the abdomen) is the indication for the full trauma assessment and the foetal monitoring. The syncopal fall is investigated for the cause (the arrhythmia, the seizure, the ectopic, the pulmonary embolism) — the pregnancy is the pro-thrombotic, the pro-syncopal, and the pro-seizure state. [1]

The penetrating injury and the protecting uterus

The penetrating injury to the pregnant abdomen has a distinctive pattern after the 12 weeks gestation: the gravid uterus, filling the pelvis and rising into the abdomen, becomes the large, vascular, muscular organ that interposes between the penetrating object and the maternal viscera (the bowel, the bladder, the great vessels). The uterus absorbs the energy of the penetrating object, and the maternal visceral injury is less common and less severe than in the non-pregnant patient — but the uterine injury (the foetal injury, the amniotic fluid leak, the abruption, the uterine vascular injury) is the consequence. The lower trajectory of the penetrating object (the pelvic entry, the buttock, the thigh) bypasses the uterus and injures the viscera directly, and the upper trajectory (the chest, the upper abdomen) is managed as in the non-pregnant patient. The management is the surgical exploration for the significant visceral injury, the foetal monitoring, and the delivery if the uterus or the foetus is compromised. [1]

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The domestic violence — the universal screening

The intimate partner violence affects roughly one in six pregnant women (the higher in the younger, the unsupported, the substance-using), and the pregnancy is the time of the increased risk (the controlling partner, the financial dependence, the stress of the new child, the disputed paternity). The trauma from the domestic violence is the under-reported, the under-recognised and the recurring mechanism — the repeated presentations, the inconsistent history, the delay in the presentation, the injury inconsistent with the stated mechanism. The universal screening of every pregnant woman for the intimate partner violence (the structured questions, the private setting, the compassionate and the non-judgmental approach) is the standard of the antenatal and the emergency care, and the positive screen triggers the safety assessment, the social-work referral, the documentation, and the safeguarding plan.[8]

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The imaging and the radiation

The computed tomography is the definitive imaging for the major trauma, and the radiation exposure to the foetus is minimised by the shielding (the lead apron over the uterus where possible), the limited scans (the head, the chest, the abdomen), and the clinical justification (the maternal life comes first — a single CT of the abdomen and the pelvis exposes the foetus to about 25 millisieverts, well below the teratogenic threshold of 100 millisieverts). The FAST scan is the preferred initial bedside modality (no radiation, quick). The MRI is safe in pregnancy but impractical in the acute trauma.[1]

The radiation exposure — the thresholds and the principles

The foetal radiation exposure follows the principle of the ALARA (as low as reasonably achievable) and the clinical justification (the maternal life and the limb come first). The teratogenic threshold is widely cited at 100 millisieverts (the deterministic effects — the growth retardation, the microcephaly, the intellectual disability — peak at 8 to 15 weeks gestation), and the carcinogenic risk (the stochastic effect — the small increase in the childhood-cancer risk) is the small, linear, non-threshold effect. The common exposures: the chest radiograph 0.001 mSv, the abdominal radiograph 1.4 mSv, the pelvic radiograph 0.4 mSv, the CT head 0 mSv (shielded), the CT chest 0.3 mSv, the CT abdomen and pelvis 25 mSv, the CT pulmonary angiogram 0.1 to 0.5 mSv, the ventilation-perfusion scan 0.1 to 0.5 mSv. A single trauma series that includes the CT of the head, the chest, the abdomen and the pelvis keeps the foetal exposure well below the teratogenic threshold, and the maternal clinical indication is never deferred for the foetal radiation concern.[1]

The contrast safety: the iodinated contrast (the CT) crosses the placenta but the modern non-ionic low-osmolar agents are safe in the pregnancy; the gadolinium (the MRI) crosses the placenta, is excreted in the amniotic fluid, and is avoided in the pregnancy unless the essential. The iodinated contrast is given for the indicated CT (the trauma, the pulmonary embolism workup) without the deferral, and the post-contrast hydration is the only precaution. [1]

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The FAST scan — the bedside assessment

The focused assessment with sonography in trauma (the FAST) is the preferred initial bedside imaging modality in the pregnant trauma patient — it is the radiation-free, the rapid, the repeatable and the bedside assessment of the free fluid in the peritoneum (the Morrison's pouch, the splenorenal recess, the pelvis) and the pericardium. The extended FAST (the E-FAST) adds the lung and the pleural views for the pneumothorax and the haemothorax. The pregnant uterus does not significantly interfere with the FAST, and the scan is performed at the arrival as the part of the primary survey. The FAST is the negative in the retroperitoneal bleed and the hollow-viscus injury, so the negative FAST in the haemodynamically unstable patient is the indication for the CT or the laparotomy, and the negative FAST in the stable patient is the reassurance but not the exclusion of the significant intra-abdominal injury. [1]

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The resuscitation, the massive transfusion and the tranexamic acid

The massive transfusion in the pregnant trauma follows the principles of the damage-control resuscitation — the balanced ratio of the packed red cells to the plasma to the platelets (the 1-to-1-to-1 or the 2-to-1-to-1, scaled to the weight), the early tranexamic acid, the warming, the calcium replacement, and the minimisation of the crystalloid.[3] The fibrinogen is the particular concern in the obstetric haemorrhage (the high baseline, the rapid consumption in the abruption and the amniotic fluid embolism), and the cryoprecipitate (two pools, ten units) or the fibrinogen concentrate is the targeted replacement for the fibrinogen below 4 g/L. The O-negative blood is the universal donor for the pregnant patient (the Rh-D negative to protect the current and the future pregnancies), used until the crossmatched blood is ready.[3]

The tranexamic acid is given early (within three hours of the injury) at the dose of 1 gram intravenously over ten minutes, followed by 1 gram over eight hours, in the pregnant trauma patient with the significant bleeding or the risk of the bleeding.[4] The CRASH-2 trial established the mortality benefit of the tranexamic acid in the trauma (the non-pregnant), and the WOMAN trial extended the evidence to the obstetric haemorrhage — the early tranexamic acid reduced the death from the bleeding in the post-partum haemorrhage without the increase in the thromboembolic events.[5] The tranexamic acid crosses the placenta but the safety in the pregnancy (the absence of the teratogenicity) is established, and the benefit outweighs the theoretical risk in the significant haemorrhage.

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The venous thromboembolism — the early prophylaxis

The pregnancy is the hypercoagulable state and the trauma adds the immobility, the surgery, the endothelial injury and the indwelling lines — the VTE risk in the pregnant trauma patient is among the highest in the medicine (50 to 100 times the age-matched non-pregnant). The mechanical prophylaxis (the intermittent pneumatic compression) is applied from the arrival, the pharmacological prophylaxis (the low-molecular-weight heparin, the enoxaparin 40 mg subcutaneously daily) is started as soon as the bleeding is controlled (typically 12 to 24 hours after the injury or the surgery), and the early mobilisation is the adjunct. The pregnant trauma patient is among the highest-risk patients in the hospital for the VTE, and the prophylaxis is the non-negotiable — the omission is the recurring and the litigious error. [1]

Common pitfalls

The recurring errors in the pregnant trauma patient are: not applying the left lateral tilt or the manual uterine displacement (the aortocaval compression worsens every parameter); accepting the normal blood pressure as excluding the shock (the expanded volume masks the loss, the hypotension is late and pre-terminal); failing to pre-oxygenate before the rapid sequence induction (the reduced FRC and the increased oxygen consumption cause the precipitous desaturation); not applying the continuous CTG monitoring from the arrival (the foetal distress is the early warning of the maternal hypovolaemia); discharging the patient before the four-hour CTG (the abruption presents up to 24 hours later); delaying the perimortem caesarean beyond the 4-minute mark (the preparation must precede the start, the delivery is by 5 minutes); forgetting the Anti-D in the Rh-negative patient (the sensitisation harms the future pregnancies); omitting the Kleihauer-Betke (the standard dose may not cover the large bleed); under-appreciating the domestic violence (the universal screening, the repeated presentations, the inconsistent history); deferring the life-saving maternal imaging for the foetal radiation concern (the maternal death is the greater foetal threat); omitting the VTE prophylaxis (the highest-risk patient in the hospital); and the team that focuses on the foetus before the mother (the maternal resuscitation is the foetal resuscitation). [1]

Exam practice

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Red flags

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References

1. [1]El-Kady D, Gilbert WM, Anderson J, et al. Trauma during pregnancy: an analysis of maternal and fetal outcomes in a large population Am J Obstet Gynecol, 2004.PMID 15284764
2. [2]El Kady D. Perinatal outcomes of traumatic injuries during pregnancy Clin Obstet Gynecol, 2007.PMID 17762411
3. [3]Rossaint R, Bouillon B, Cerny V, et al. The European guideline on management of major bleeding and coagulopathy following trauma: sixth edition Crit Care, 2023.PMID 36859355
4. [4]CRASH-2 trial collaborators, Shakur H, Roberts I, et al. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomised, placebo-controlled trial Lancet, 2010.PMID 20554319
5. [5]WOMAN Trial Collaborators. Effect of early tranexamic acid administration on mortality, hysterectomy, and other morbidities in women with post-partum haemorrhage (WOMAN): an international, randomised, double-blind, placebo-controlled trial Lancet, 2017.PMID 28456509
6. [6]Jeejeebhoy FM, Zelop CM, Lipman S, et al. Cardiac Arrest in Pregnancy: A Scientific Statement From the American Heart Association Circulation, 2015.PMID 26443610
7. [7]Zelop CM, Einav S, Mhyre JM, et al. Characteristics and outcomes of maternal cardiac arrest: A descriptive analysis of Get with the guidelines data Resuscitation, 2018.PMID 30170022
8. [8]Owattanapanich N, Moungmaithong K, Khunamornpong S, et al. Motor vehicle crashes in pregnancy: Maternal and fetal outcomes J Trauma Acute Care Surg, 2021.PMID 33496550
9. [9]Klinich KD, Flannagan CA, Rupp JD, et al. Fetal outcome in motor-vehicle crashes: effects of crash characteristics and maternal restraint Am J Obstet Gynecol, 2008.PMID 18395036