Home About us Editorial board Search Ahead of print Current issue Archives Submit article Instructions Subscribe Contacts Login 
Journal of Obstrectic Anaesthesia and Critical Care
Search articles
Home Print this page Email this page Small font size Default font size Increase font size Users Online: 416

 Table of Contents  
REVIEW ARTICLE
Year : 2017  |  Volume : 7  |  Issue : 1  |  Page : 3-12

Management of critically ill obstetric patients: A review


Department of Anaesthesiology Pain Medicine and Critical Care, All India Institute of Medical Sciences, New Delhi, India

Date of Web Publication1-Jun-2017

Correspondence Address:
Anjan Trikha
Department of Anaesthesiology Pain Medicine and Critical Care, All India Institute of Medical Sciences, New Delhi - 110 029
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/joacc.JOACC_21_17

Rights and Permissions
  Abstract 

Critically ill obstetric patients present a unique challenge as outcome of indwelling life is dependent upon the maternal well-being. Optimal patient management involves early detection and the multidisciplinary treatment by obstetricians, pediatricians, and anesthesiologists based on knowledge of physiological and pathophysiological alterations. This article aims to provide a comprehensive review of the available literature for the management of critically ill obstetric patient and recent update on commonly encountered situations.

Keywords: Critical illness, obstetric, pregnancy


How to cite this article:
Kaur M, Singh PM, Trikha A. Management of critically ill obstetric patients: A review. J Obstet Anaesth Crit Care 2017;7:3-12

How to cite this URL:
Kaur M, Singh PM, Trikha A. Management of critically ill obstetric patients: A review. J Obstet Anaesth Crit Care [serial online] 2017 [cited 2017 Oct 23];7:3-12. Available from: http://www.joacc.com/text.asp?2017/7/1/3/207390


  Introduction Top


Management of a critically ill obstetric patient is very challenging due to the unique maternal physiological adaptations and care of another indwelling life whose outcome is dependent upon the maternal well-being. Although obstetric patients are young and healthy, maternal mortality for those admitted to an intensive care unit (ICU) ranges 5–20% in developed nations [1] and 15–30% in developing nations.[1] There is a paucity of well-defined guidelines for the management of critically ill obstetric patients; most of the ICU physicians apply general critical care principles for the care of these parturients. Maternal well-being is the priority when faced with the clinical situation of a deteriorating parturient.

Successful maternal and foetal outcomes are largely dependent upon a multidisciplinary involvement of anaesthesiologists, obstetricians and neonatologists. This article aims to provide a comprehensive review of the available literature for the management of critically ill obstetric patient.


  Indications for Admission of Critically Ill Obstetric Patients Top


There are no well-defined criteria that determine admission of an obstetric patient to an ICU. Most of them seek ICU admission based on local criteria and local practices. Majority are admitted to the ICU due to either of the following reasons:

  • Pregnancy specific conditions – Haemorrhage, sepsis, hypertensive disorders of pregnancy, amniotic fluid embolism, complex cardiac diseases, acute fatty liver, aspiration syndromes, infections, ovarian hyperstimulation syndrome, tocolytic-induced pulmonary edema, etc.[2]
  • Surgical/medical condition not related to pregnancy – Trauma, asthma, diabetes, autoimmune diseases, etc.
  • Medical diseases that may worsen during pregnancy – Anemia, congenital heart diseases, rheumatic and non-rheumatic valvular diseases, pulmonary hypertension, renal failure, autoimmune diseases (e.g., SLE, myasthenia gravis) etc.


General care

Management of a critically ill obstetric patient involves a multidisciplinary approach with active involvement of intensivists, obstetricians, nurses, paediatricians, physiotherapists, pharmacists, etc. Maternal haemodynamic optimisation requires application of basic intensive care principles with modifications based on physiological changes during pregnancy. Simultaneous stabilisation of maternal condition and foetal well-being should be the goal.

For any pregnant patient admitted in the ICU after 24 weeks, preparation for unanticipated emergency caesarean section should be done.

Initial assessment and management

Initial evaluation and resuscitation of the obstetric patient is similar to a non-pregnant patient and follows the same protocol wherein airway (A), breathing (B) and circulation (C) are focused upon. Uterine displacement should be considered a part of the initial ABC evaluation in any haemodynamically unstable obstetric patient. In addition, foetal monitoring should be performed simultaneously every 4–8 hours and even more frequently if the clinical condition of the parturient deteriorates.

Monitoring of critically ill obstetric patients

There are no clear ICU admission criteria for obstetric patients, however, in general, if two organ systems are failing with a need of ventilator support, parturients should be admitted in the ICU. Foetal monitoring must be performed after 24 weeks of gestation because it can help in determining the adequacy of maternal cardiorespiratory and metabolic parameters.[3] Different scoring systems are validated for critically ill non-obstetric patients which are either based on physiological variables [Acute Physiology and Chronic Health Evaluation (APACHE) II, Simplified Acute Physiology Score (SAPS) II] or organ failure based [Sequential Organ Failure Assessment (SOFA), and Multiple Organ Dysfunction Score (MODS)]. Physiology based scores are not very reliable as normal physiological changes of pregnancy make the parameters fall into an abnormal range altering these scores. A new scoring system for septic obstetric patients, the Sepsis in Obstetrics Score (SOS), has recently been developed which determines predictability of admission from emergency department (ED).[4] However, organ failure based scores such as MODS have been found to be superior to SOS in mortality prediction.[5] Further studies are needed to make these part of routine protocols.

Ventilator strategies for managing critically ill parturients

Positive pressure ventilation can be delivered as non-invasive positive pressure ventilation (NIPPV) or invasively using an endotracheal tube (ETT) or tracheostomy.

For a NIPPV trial, basic pre-requisites include presence of a good respiratory drive, stable haemodynamics and absence of excessive secretions.[2] NIPPV has been shown to benefit a subset of patients with obstructive airway diseases, as well as sleep disordered breathing in pregnancy.[6] However, NIPPV needs further evaluation in parturients because of higher risk for aspiration though the published case reports and series have reported good outcomes.

A low threshold for ETT intubation should be kept in view of high aspiration risk. Standard protocols for initiation of ventilation in parturients should be in accordance to the physiological changes in the respiratory parameters during pregnancy. Airway oedema warrants the use of smaller size ETT which otherwise increases airway resistance and interferes with successful weaning during prolonged ventilation.

When conventional methods of ventilation fail, newer modes such as Airway Pressure Release Ventilation (APRV) and high-frequency oscillatory ventilation (HFOV) have been tried. There are isolated reports of its successful use in a parturient,[7] however, these small trials and observational studies do not show any mortality benefit.[8],[9]

Though pregnancy was considered to be a contraindication to prone position ventilation, there are individual reports of its successful use in parturients.[10],[11] However, it would seem reasonable to perform foetal monitoring during prone positioning.

Extracorporeal membrane oxygenation (ECMO) was used in 12 parturients during the 2009 H1N1 pandemic. It should be used early in acute respiratory failure with refractory hypoxemia. Major disadvantage of ECMO is that it exposes the indwelling foetus to extracorporeal circulation and systemic heparinisation. Moreover, ECMO is subject to availability only in tertiary centers and there is a potential risk of death due to bleeding in mothers.[12]

Sedation

Use of sedatives and analgesics might be required in parturient being mechanically ventilated. Most of the commonly used ICU sedatives cross the placenta to varying degrees based upon the agent, its dose, duration of use and any organ dysfunction altering its metabolism and excretion. Risks and benefits must be assessed prior to their use [Table 1].[13] The paediatric team must be made aware of all the sedatives used in parturient at the time of delivery so that timely preparation of potential foetal complications can be taken care of.
Table 1: Obstetric ICU Sedatives

Click here to view


Antibiotics/Antivirals/Antifungals

US Food and Drug administration (FDA) categorises drugs from A to D (in order of increasing foetal risks) and X (contraindicated) according to the risk to foetus. Commonly used antimicrobials such as penicillin, cephalosporin, macrolides and acyclovir fall into category A whereas aminoglycosides, quinolones, vancomycin and amphotericin fall in category C. The ICU team must know this information on drugs. Dictum “Avoid use of any medication in pregnancy that is not absolutely necessary” holds true.

Parturient have high incidence of vaginal candidiasis because of increased secretion of sex hormones. Topical azoles should be the first line in the first trimester. There is a raised concern regarding oral fluconazole (category D) being associated with an increased risk of spontaneous abortions and stillbirths in addition to its teratogenicity in high dosage.

Nutrition

Maternal nutrition during pregnancy affects placental growth and development. Enteral nutrition is considered the optimal method for providing nutrition compared to parenteral nutrition even in obstetric patients. However, a parturient is more likely to reject enteral nutrition and develop constipation due to relaxation of the bowel smooth muscles by progesterone. Hence, prokinetic agents should be routinely used.

Aspiration risk can be minimised with anti-aspiration prophylaxis (H2 blockers or proton pump inhibitors), using semi-recumbent position for administering enteral feeds and routine radiological confirmation of the nasogastric tube position.

There is a paucity of literature on parenteral nutrition in obstetric patients. Nutritional goal in such patients is to nurture the critically ill parturient and her indwelling foetus. The caloric requirement can be met with conventionally available preparations but with a few modifications. The basal caloric requirement of a critically ill patient is 25 kcal/day/kg (ideal body weight) that turns out to be 2200 to 2800 kcal/day for an average sized female.[14] The specific needs for the foetus are different in each trimester. The first trimester usually does not warrant need of extra calories. However, a parturient needs additional 340 kcal/day and 452 kcal/day in the second and third trimesters, respectively. The protein requirement is twice that of a non-obstetric patient, and this supplementation must be carried on till lactation.

There is paucity of data regarding any alteration in percentage of carbohydrates and fats in pregnant patients. Hence, carbohydrates meet up to 70% caloric requirements while fats meet 30% carbohydrate requirements. Proteins in diet compensate for negative nitrogen balance and hence are not included in the caloric needs of the critically ill patient.

The nutritional goals must be adjusted according to the associated ailments. Each degree rise in temperature increases the caloric needs by 10% and sepsis steps up the need by 19%. Inotropes use may increase caloric requirement by 2.5 times. Neither weight gain nor albumin values have a role in the nutritional assessment in parturient because of the effects of pregnancy. Indicators such as prealbumin and serum transferrin are used for assessing the response to nutritional support.[2]

An optimal nutritional solution needs to have additional amounts of zinc, folate and vitamin B12 in the first trimester. Nutrient requirements of Vitamin D, E, K and fluoride do not change with pregnancy. Multivitamins are recommended in parturient with higher than average needs (pregnancy with multiples, HIV patients, smokers, alcoholics, etc.).[14] The iron content needs to be almost double that of non-obstetric population, corresponding to 4–6 mg/day. Long-chain polyunsaturated fatty acids (LC-PUFA), especially docosahexaenoic acid (DHA) and arachidonic acid, (n-3 and n-6 family members, respectively) have a promising role in foetal and maternal outcomes.[15] However, more trials are needed to establish their usefulness in regular clinical practice.

Thromboprophylaxis

Obstetric critically ill patients have four times higher risk of developing deep vein thrombosis compared to other critically ill patients. This is because all three components of Virchow's triad are potentiated during pregnancy:

  • Stasis: Gravid uterus compresses IVC blood flow
  • Hypercoagulability: Increased secretion of clotting factors due to high oestrogen levels
  • Endothelial injury: Utero-placental vascular injury at the time of delivery. There is a diversity of recommendations with American Congress of Obstetricians (ACOG) recommending pharmacological prophylaxis for a small minority of patients and the Royal College of Obstetricians and Gynecologists (RCOG) recommending treatment for a large majority of patients [Table 2].[16],[17] Further research is warranted to compare the risks and benefits of recommendations. However, patients admitted in ICU must be started on thromboprophylaxis (if there are no other contraindications) as soon as possible.
Table 2: Summary of thromboprophylaxis guideline recommendations for obstetric patients

Click here to view


Pharmacological thromboprophylaxis (LMWH) can be achieved with both unfractionated and low molecular weight heparins such as enoxaparin, dalteparin and tinzaparin. However, in case of heparin-induced-thrombocytopenia (HIT) or severe allergic reactions, a feasible alternative could be provided by argatroban, danaparoid, fondaparinux or lepirudin.[18] However, safety of these agents is not well established and is still investigational (poor evidence by retrospective studies only).[18],[19]


  Specific Conditions Pertaining to Pregnancy Top


Haemorrhage

Obstetric haemorrhage is responsible for more than 30% of all maternal deaths in low income countries [20] and over 10% of maternal deaths in high-income countries.[21] Obstetric haemorrhage can be due to uterine atony, placentation abnormalities (placenta previa, accreta, increta, percreta), uterine rupture, surgical and genital tract trauma. The use of uterotonic agents, uterine massage, controlled cord traction, intrauterine balloon tamponade, uterine artery embolisation or ligation and even hysterectomy might be ineffective in controlling postpartum haemorrhage (PPH) in all.

Conventional vital signs are not as quick detector as proposed Shock index (SI) i.e. the ratio of pulse to systolic blood pressure (using vital sign alert device) for detection of hypovolemic shock secondary to obstetric haemorrhage.[22] Normal SI (no Shock) ranges 0.7–0.9 for obstetric populations. A value of 0.9 is considered to be the threshold for referral to a tertiary hospital, 1.4 as the threshold for intensive care treatment, and 1.7 as an indicator of high risk for adverse events.[22],[23] However, it needs stronger clinical evidence to be incorporated into the routine practice.

Viscoelastic haemostatic assays provide a real-time assessment of coagulation and fibrinolysis, especially when standard laboratory tests are too slow to be of clinical utility.[24]Hypofibrinogenemia is an important predictor for the progression from moderate to severe PPH.[25] A plasma level below 2 g/L in the early phase of PPH is associated with increased risk of severe haemorrhage.[26] For each 1 g/L decrease in fibrinogen, there was a 2.6 fold increased odds of severe PPH.[25] Hence, if hypofibrinaemia is detected by thromboelastography, administering fibrinogen concentrates is an important early intervention.[27] The FIBTEM values [A5 assay (available within 10 min) indicating fibrin polymerisation process] can serve as an earlier point for guiding intervention as it declines more rapidly than fibrinogen.[28]

There is no ideal ratio of red blood cells (RBC): fresh frozen plasma (FFP) or RBC: platelets for the management of PPH, although a commonly followed massive transfusion protocol is (RBC: FFP: platelets as 4:4:1 ratio)[21] and 1:1:1 ratio.[29] Compared to formula-driven strategies (such as fixed ratios of blood products), the use of goal-directed resuscitation using point-of-care coagulation tests (thromboelastography, rotational thromboelastometry) has been proposed [29] but is still investigational.

Early use of fibrinogen concentrates and tranexamic acid have a promising role in managing PPH, however, current evidence supporting it is limited.[30],[31] and different societies have different recommendations [29],[32],[33] [Table 3]. Activated factor VII has gained popularity but is not US FDA approved and is very expensive. It has been used for treating life-threatening PPH and to prevent hysterectomy,[34] but its routine use needs it to be cost effective and a stronger evidence to be a part of routine protocols.
Table 3: Strategies for postpartum haemorrhage management by different evidence groups

Click here to view


Sepsis

Maternal sepsis causes 15% of maternal deaths worldwide.[35],[36] There is an urgent need to address the issue of paucity of any valid sepsis guidelines for parturients. Hence, Royal College of Obstetricians and Gynecologists (RCOG) has devised guidelines for the prediction of clinical deterioration, specific scoring systems and treatment of maternal sepsis.[37]

Diagnosing sepsis in a parturient is a challenge because of complex pathophysiological changes that can mask its initial presentation [Table 4]. To add to it, clinical features of sepsis in a pregnant patient might be absent or be even less distinctive. Hence, till date there is no validated definition of sepsis in pregnant.
Table 4: Pathophysiological changes during pregnancy

Click here to view


Puerperal sepsis and urinary tract infections [38],[39] are the most important causes of sepsis in developed nations whereas HIV, malaria and community-acquired pneumonia are important causes in developing countries.[40] However, septic shock are most commonly seen in patients with pyelonephritis, chorioamnionitis and endometritis.[41] Hepatitis E virus, herpes simplex virus and malaria are much more severe in pregnancy.[42] In addition to the systemic symptoms, a few local symptoms such as lower abdominal pain or perineal pain, frequent micturition and diarrhea can also be present. The outcome of a parturients is better than non-pregnant critically sick patients due to younger age, fewer comorbidities and usually localised source of infection.[43]

Management of sepsis in a pregnant patient involves taking care of the well being of both the mother and child. Because uteroplacental circulation does not have auto-regulation, infection can easily spread to foetus [36] and maternal well-being governs the well-being of foetus. RCOG has suggested the management of sepsis in obstetrics in accordance with the Surviving Sepsis (SS) Campaign guidelines.

Initial resuscitation: 'resuscitation bundle' goals within the first 6 h are the same as described in the SS guidelines.

Antibiotics and source control: besides blood culture, vaginal or uterine culture should also be sent for culture and sensitivity. Ultrasound and CT of the pelvis is an additional investigation to rule out pyometra and abscess. Quest for an ideal regimen of antibiotics include the one with the greatest effectiveness and least foetal harm, which is not always possible.[40] The most commonly used combination in obstetric sepsis is ampicillin, gentamicin, clindamycin or metronidazole.[44] Antibiotic treatment should continue for at least 7–10 day [36] and should be reassessed for de-escalation. Majority of obstetrical infections are polymicrobial, and hence, de-escalation is difficult.

Fluid management and haemodynamic support: Critically ill obstetric patients need judicious fluid administration due to vulnerability to fluid overloading. Fluid resuscitation should be crystalloid based, and if vasopressor is needed, norepinephrine is the first-choice vasopressor. If patient has low cardiac output in the presence of adequate volume resuscitation, dobutamine is the treatment of choice.[37]

Adjunctive measures: Nutritional support and thromboprophylaxis should be given to all septic obstetric patients. Tocodynamic monitoring after foetal viability should be a routine practice. The use of corticosteroids during pregnancy, human-activated protein C and intravenous immunoglobulin (IVIG) for sepsis is not recommended.

Early warning systems: A few physiological criteria can serve as early indicators for the need to escalate monitoring. These have been incorporated into scores such as modified early obstetric warning system (MEOWS). However, there is insufficient literature for its usefulness in improvement in obstetric morbidity.[45] A recent scoring system, SOS uses parameters such as temperature, heart rate, respiratory rate, oxygen saturation, leukocyte count and lactic acid to predict the need of ICU admission, but it also lacks sufficient evidence for its routine use.[4]

Complex cardiac diseases

Cardiac disorders affect 1–3% pregnant women and account to 10–15% of maternal mortality.[46] Peripartum cardiac diseases in pregnancy range from congenital anomalies to valvular heart diseases, myocardial infarction, dilated cardiomyopathy, pulmonary hypertension, etc., which are further worsened by high cardiac output physiology of pregnancy.

Uterine oxygen delivery is dependent upon blood flow (UBF), haemoglobin concentration and oxygen saturation. Any reduction in either can compromise foetal oxygen delivery and any increase in one variable can compensate for the fall in other.

Decreased UBF in maternal shock can lead to impaired foetal oxygenation and ultimately to foetal distress. Hence, optimizing maternal condition can only support foetal well-being. Different causes of shock require different interventions. Hypovolemic shock needs volume replenishment and correction of the underlying cause. Septic shock needs early fluid resuscitation, source control with appropriate antibiotics, and vasopressors. Cardiogenic shock can be managed with timely correction of pump failure that includes early revascularisation, inotropic support for impaired myocardial contractibility and even mechanical circulatory support for refractory cases. Patients in whom medical management fails in cardiogenic shock and valvular repair is not feasible, use of intra-aortic balloon pump (IABP), ECMO and continuous flow left ventricular assist device (LVAD) have been tried, but data on their use is limited.[46]

Different vasopressors such as norepinephrine (Category C) and phenylephrine (Category C) and inotropes such as dobutamine (Category B) and milrinone (Category C) and the inotrope/vasopressor epinephrine (Category C) have been used in pregnancy. The potential risk of placental vasoconstriction by vasopressors must be weighed against the risk of hypoperfusion caused by systemic hypotension. It is difficult to conduct randomised control trials in pregnant patients, hence, most of the experimental data on vasopressors has been obtained from healthy animals.[46]

Another factor determining uterine oxygen delivery is haemoglobin concentration. Raising haemoglobin concentration can compensate any reduction in UBF, uterine oxygen delivery, and hence, the transfusion trigger which is unlike other critically ill ICU patients. Colloids such as hydroxyethyl starch (HES) has resulted in renal failure in a general ICU population and should be avoided in pregnancy also.

Obstructive valvular lesions such as mitral stenosis (MS) and aortic stenosis (AS) have worsened functional status with pregnancy due to increased cardiac output, ventricular volume, transvalvular pressure, decreased diastolic time and associated pulmonary hypertension. Severe MS may present with pulmonary oedema and atrial fibrillation while AS may develop fatal arrhythmias and refractory heart failure. American heart association (AHA) recommend beta-blockers, nondihydropyridine calcium channel blockers (All class C to D) and digoxin for atrial fibrillation in pregnancy. Patients of MS/AS who are refractory to medical management or have severe refractory heart failure can undergo percutaneous balloon mitral valvuloplasty after 20 weeks. If percutaneous technique cannot be done, open mitral commisurotomy might be a reasonable option [47] in MS while in AS there is limited literature comparing percutaneous technique with open valve repair.[48] In AS with refractory HF, early cesarean section followed by valve replacement must be advocated.[49]

Another unique subset of population is parturient with pulmonary hypertension (PAH), and WHO considers the risk of pregnancy in PAH as class IV (i.e. extremely high risk of maternal mortality). PAH offers enormous physiological burden for women and hence pregnancy is contraindicated. If pregnancy occurs, termination should be discussed, and if pregnancy still continues, elective LSCS should be done at 34–36 weeks of gestation preferentially under epidural or low-dose combined spinal-epidural anaesthesia in tertiary referral centers by a multidisciplinary team. Pulmonary hypertension therapies (PHT) calcium channel blockers, prostacyclin's (epoprostenol, iloprost), and phosphodiesterase-5-inhibitors (sildenafil) must be continued throughout pregnancy, whereas endothelin-receptor-antagonists and soluble guanylate cyclase stimulators must be discontinued. Immediate postpartum period has the greatest risk of acute right heart failure due to sudden increase in pulmonary vascular resistance. Uterotonics should be used cautiously at the lowest effective dose and never as a bolus. It is advocated to use echocardiography as a point of care in these patients.[50]

In cardiopulmonary bypass (CPB), challenge of increased uteroplacental vascular resistance by decreased maternal mean arterial pressure (MAP) and temperature dependent alterations affecting UBF has to be met. Strategies used to minimise foetal risks are uterine displacement, minimal blood loss, reduce CPB duration, high flow rates (>2.4 L/min/m 2) and maintenance of MAP 70–75 mmHg.[51]

Critically ill cardiac obstetric patients must be monitored in an ICU for several days for early detection of impending failure. A negative fluid balance with aggressive diuretics, specific PHT with inhaled nitric oxide, epoprostenol-infusion, or inhaled iloprost and anticoagulation with heparin can be initiated after delivery.

Amniotic fluid embolism

Amniotic fluid embolism (AFE) is a clinical diagnosis of exclusion which carries very high mortality (approximately 40%).[52] The most widely accepted mechanism of its occurrence is 'anaphylactoid reaction of pregnancy' associated with AFE.

At present, there is no laboratory parameter available for diagnosing AFE. However, recent research focus is to find novel biomarkers and immune-histochemical staining techniques that can aid in predicting and diagnosing AFE. These include Zinc coproporphyrin-1, sialyl Tn antigen (STN), complement C3, C4, interleukin-8, insulin-like growth factor-binding protein-1 (IGFBP-1), etc., Though these are of limited clinical value because of the rapid disease progression, none of them provide 'early warning'.[53]

Detection of high plasma levels of Insulin-like growth factor-binding protein-1 (IGFBP-1) is a useful biomarker indicating amniotic fluid passage into the maternal circulation. A combination of maternal serum IGFBP-1, alpha-fetoprotein and foetal fibronectin has been proposed to be a confirmatory test for AFE.[54] Level of biomarkers depend upon the type of AFE, e.g. zinc coproporphyrin-1 and STN are increased in cardiopulmonary collapse type AFE, whereas a fall of C3 and C4 is observed in disseminated intravascular coagulation (DIC) type AFE.[55]

Sialyl Tn structure (NeuAc alpha 2-6 GalNAc 1-0-Ser/Thr), which is an important component in meconium- and/or amniotic fluid-derived mucin, is detected by immunohistochemical staining using monoclonal antibody TKH-2.[54]

Management of AFE is mainly supportive and should be managed in an ICU setting by a multi-disciplinary team. Intra-aortic balloon counter pulsation, cardiopulmonary bypass and extracorporeal membrane oxygenation have been tried.[56] Recombinant factor VII can be used as treatment option in DIC associated with AFE [57] when the haemorrhage cannot be stopped by massive blood component replacement.[58] AFE is a potentially catastrophic condition with high maternal mortality and treatment is still only supportive.

Local anaesthetic systemic toxicity

Systemic toxicity of local anaesthetics (LA) can be very challenging and usually manifested as neurological or cardiovascular manifestations. Pregnancy increases the risk for local anaesthetic systemic toxicity (LAST) due to epidural venous distention entraining LA, increased cardiac output altering uptake of LA and decreased plasma protein binding increasing free fraction of drug. Estradiol and progesterone alter cardiomyocyte electrophysiology increasing susceptibility to arrhythmias. There is decreased threshold to seizures because of increased neuronal susceptibility to LA.[59]

In addition to supportive management, use of lipid emulsion therapy as 'lipid sink' for drawing LA from within cardiac tissue is effective in non-obstetric patients. However, its therapeutic application in pregnant patients is not clear. There is a single documented case report of LAST being successfully treated with 20% intralipid, but additional reports are required to fully validate its usefulness.[60]

Issues such as upper limit for intralipid administration in parturient and timing of infant delivery and intralipid administration are still unresolved.[59]

Cardiopulmonary resuscitation in a pregnant patient

Survival of the indwelling foetus is largely dependent upon successful maternal resuscitation. 2015 International Liaison Committee on Resuscitation (ILCOR) largely bases American Heart Association (AHA) Guidelines Update for Cardiopulmonary Resuscitation (CPR) upon extensive evidence review. Two main problems addressed are patient positioning during CPR and role of perimortem caesarean delivery (PMCD).

Patient positioning during cardiopulmonary resuscitation

After 20 weeks of gestation (fundus at or above umbilicus), aortocaval compression impedes venous return in a singleton pregnancy.[61]

Left lateral tilt during CPR is recommended for its prevention (manikin study based), which is not feasible in live patients in view of decreased chest compression quality. Manual left lateral uterine displacement (LUD) can relieve aortocaval compression, however, this lacks any published cardiac arrest outcome studies.[62] If the fundus height is at or above the level of the umbilicus, manual LUD can be beneficial in relieving aortocaval compression during chest compressions. (Class IIa, LOE C-LD).

Role of perimortem caesarean delivery

If after 20 weeks the initial resuscitative efforts and manual LUD are futile, PMCD should be considered regardless of foetal viability as it would relieve aortocaval compression. No conclusive evidence for the timing of PMCD has come in systematic reviews because of case heterogeneity and reporting bias.[63] During cardiac arrest, if a pregnant woman with a fundal height at or above the umbilicus has not achieved return of spontaneous circulation (ROSC) with usual resuscitation measures and manual LUD, it is advisable to prepare to evacuate the uterus while resuscitation continues (Class I, LOE C-LD).

The acronym BEAU-CHOPS (bleeding/DIC, embolism, anaesthetic complications, uterine atony, cardiac disease, hypertension/pre-eclampsia/eclampsia, other, placenta abruption/previa and sepsis) are specific for obstetrics and may help in treating possible causes in obstetric patients.

Foetal well-being in intensive care unit in pregnancy

Optimal foetal health can be assured only with maternal well-being. It must be stressed that maternal haemoglobin, oxygen saturation and cardiac output have an impact on foetal perfusion. It is prudent to record daily FHR tracing, weekly umbilical artery Doppler and every fortnight ultrasound scan for foetal growth and monitoring.[64]

Routinely used foetal monitoring techniques such as changes in foetal heart rate, foetal pulse oximetry and measurement of foetal scalp pH can sample only foetal peripheral oxygenation and has poor correlation with cord blood gas measurements. This is because of compensatory mechanisms that can compensate until late hypoxemia by preferentially shunting blood to the heart and brain.[46]

A recently proposed monitor for central oxygenation is foetal electrocardiogram monitoring with ST waveform analysis (ST Analyzer – STAN), which reflects myocardial hypoxemia. Failure of compensatory centralisation of perfusion/oxygenation occurs when foetal myocardium is deprived of oxygen and is reflected by ST segment changes.[46] However, clinical trials have shown varied results for its utility.[65]


  Conclusion Top


Critical illness may complicate any pregnancy. Optimal patient management involves early detection and the multidisciplinary treatment by obstetricians, paediatricians and anaesthesiologists based on knowledge of physiological and pathophysiological alterations. Timely management of obstetric complications can improve both maternal and foetal outcome.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Boerma JT. Maternal mortality in sub-Saharan Africa: Levels, causes and interventions. Ann IFORD 1988;12:49–68.  Back to cited text no. 1
    
2.
Trikha A, Singh P. The critically ill obstetric patient-Recent concepts. Indian J Anaesth 2010;54:421–7.  Back to cited text no. 2
[PUBMED]  [Full text]  
3.
Gaffney A. Critical care in pregnancy--is it different? Semin Perinatol 2014;38:329–40.  Back to cited text no. 3
    
4.
Albright CM, Ali TN, Lopes V, Rouse DJ, Anderson BL. The Sepsis in Obstetrics Score: A model to identify risk of morbidity from sepsis in pregnancy. Am J Obstet Gynecol 2014;211:39.e1–8.  Back to cited text no. 4
    
5.
Aarvold ABR, Ryan HM, Magee LA, von Dadelszen P, Fjell C, Walley KR. Multiple Organ Dysfunction Score Is Superior to the Obstetric-Specific Sepsis in Obstetrics Score in Predicting Mortality in Septic Obstetric Patients. Crit Care Med 2017;45:e49–57.  Back to cited text no. 5
    
6.
Izci B, Vennelle M, Liston WA, Dundas KC, Calder AA, Douglas NJ. Sleep-disordered breathing and upper airway size in pregnancy and post-partum. Eur Respir J 2006;27:321–7.  Back to cited text no. 6
    
7.
Hirani A, Marik PE, Plante LA. Airway pressure-release ventilation in pregnant patients with acute respiratory distress syndrome: A novel strategy. Respir Care 2009;54:1405–8.  Back to cited text no. 7
    
8.
Putensen C, Zech S, Wrigge H, Zinserling J, Stüber F, Von Spiegel T, et al. Long-term effects of spontaneous breathing during ventilatory support in patients with acute lung injury. Am J Respir Crit Care Med 2001;164:43–9.  Back to cited text no. 8
    
9.
Hering R, Peters D, Zinserling J, Wrigge H, von Spiegel T, Putensen C. Effects of spontaneous breathing during airway pressure release ventilation on renal perfusion and function in patients with acute lung injury. Intensive Care Med 2002;28:1426–33.  Back to cited text no. 9
    
10.
Samanta S, Samanta S, Wig J, Baronia AK. How safe is the prone position in acute respiratory distress syndrome at late pregnancy? Am J Emerg Med 2014;32:687.e1-3.  Back to cited text no. 10
    
11.
Kenn S, Weber-Carstens S, Weizsaecker K, Bercker S. Prone positioning for ARDS following blunt chest trauma in late pregnancy. Int J Obstet Anesth 2009;18:268–71.  Back to cited text no. 11
    
12.
Nair P, Davies AR, Beca J, Bellomo R, Ellwood D, Forrest P, et al. Extracorporeal membrane oxygenation for severe ARDS in pregnant and postpartum women during the 2009 H1N1 pandemic. Intensive Care Med 2011;37:648–54.  Back to cited text no. 12
    
13.
Karaman S, Evren V, Firat V, Cankayali I. The effects of dexmedetomidine on spontaneous contractions of isolated gravid rat myometrium. Adv Ther 2006;23:238–43.  Back to cited text no. 13
    
14.
Cox JT, Phelan ST. Nutrition during pregnancy. Obstet Gynecol Clin North Am 2008;35:369–383, viii.  Back to cited text no. 14
    
15.
De Giuseppe R, Roggi C, Cena H. n-3 LC-PUFA supplementation: Effects on infant and maternal outcomes. Eur J Nutr 2014;53:1147–54.  Back to cited text no. 15
    
16.
Palmerola K, D'Alton M, Brock C, Friedman A. A comparison of recommendations for pharmacologic thromboembolism prophylaxis after caesarean delivery from three major guidelines. BJOG Int J Obstet Gynaecol 2016;123:2157–62.  Back to cited text no. 16
    
17.
Lindqvist PG, Hellgren M. Obstetric Thromboprophylaxis: The Swedish Guidelines. Adv Hematol [Internet]. 2011. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3226316/ [Last cited on 2017 Jan 08].  Back to cited text no. 17
    
18.
Chaudhary RK, Nepal C, Khanal N, Pathak R, Giri S, Bhatt VR. Management and Outcome of Heparin-Induced Thrombocytopenia in Pregnancy: A Systematic Review. Cardiovasc Hematol Agents Med Chem 2015;13:92–7.  Back to cited text no. 18
    
19.
De Carolis S, di Pasquo E, Rossi E, Del Sordo G, Buonomo A, Schiavino D, et al. Fondaparinux in pregnancy: Could it be a safe option? A review of the literature. Thromb Res 2015;135:1049–51.  Back to cited text no. 19
    
20.
Khan KS, Wojdyla D, Say L, Gülmezoglu AM, Van Look PFA. WHO analysis of causes of maternal death: A systematic review. Lancet Lond Engl 2006;367:1066–74.  Back to cited text no. 20
    
21.
Le Gouez A, Mercier FJ. Major obstetric hemorrhage. Transfus Clin Biol J Soc Francaise Transfus Sang 2016;23:229–32.  Back to cited text no. 21
    
22.
El Ayadi AM, Nathan HL, Seed PT, Butrick EA, Hezelgrave NL, Shennan AH, et al. Vital Sign Prediction of Adverse Maternal Outcomes in Women with Hypovolemic Shock: The Role of Shock Index. PloS One 2016;11:e0148729.  Back to cited text no. 22
    
23.
McNab A, Burns B, Bhullar I, Chesire D, Kerwin A. A prehospital shock index for trauma correlates with measures of hospital resource use and mortality. Surgery 2012;152:473–6.  Back to cited text no. 23
    
24.
Ekelund K, Hanke G, Stensballe J, Wikkelsøe A, Albrechtsen CK, Afshari A. Hemostatic resuscitation in postpartum hemorrhage - A supplement to surgery. Acta Obstet Gynecol Scand 2015;94:680–92.  Back to cited text no. 24
    
25.
Butwick AJ, Goodnough LT. Transfusion and coagulation management in major obstetric hemorrhage. Curr Opin Anaesthesiol 2015;28:275–84.  Back to cited text no. 25
    
26.
Wikkelsoe AJ, Afshari A, Stensballe J, Langhoff-Roos J, Albrechtsen C, Ekelund K, et al. The FIB-PPH trial: Fibrinogen concentrate as initial treatment for postpartum haemorrhage: Study protocol for a randomised controlled trial. Trials 2012;13:110.  Back to cited text no. 26
    
27.
Charbit B, Mandelbrot L, Samain E, Baron G, Haddaoui B, Keita H, et al. The decrease of fibrinogen is an early predictor of the severity of postpartum hemorrhage. J Thromb Haemost 2007;5:266–73.  Back to cited text no. 27
    
28.
de Lange NM, Lancé MD, de Groot R, Beckers EAM, Henskens YM, Scheepers HCJ. Obstetric hemorrhage and coagulation: An update. Thromboelastography, thromboelastometry, and conventional coagulation tests in the diagnosis and prediction of postpartum hemorrhage. Obstet Gynecol Surv 2012;67:426–35.  Back to cited text no. 28
    
29.
Collis RE, Collins PW. Haemostatic management of obstetric haemorrhage. Anaesthesia 2015;70(Suppl 1):78–86.  Back to cited text no. 29
    
30.
Sentilhes L, Lasocki S, Ducloy-Bouthors AS, Deruelle P, Dreyfus M, Perrotin F, et al. Tranexamic acid for the prevention and treatment of postpartum haemorrhage. Br J Anaesth 2015;114:576–87.  Back to cited text no. 30
    
31.
Kaufner L, Henkelmann A, von Heymann C, Feldheiser A, Mickley L, Niepraschk-von Dollen K, et al. Can prepartum thromboelastometry-derived parameters and fibrinogen levels really predict postpartum hemorrhage? J Perinat Med 2016 [Epub ahead of print].  Back to cited text no. 31
    
32.
WHO Guidelines for the Management of Postpartum Haemorrhage and Retained Placenta [Internet]. Geneva: World Health Organization; 2009. (WHO Guidelines Approved by the Guidelines Review Committee). Available from: http://www.ncbi.nlm.nih.gov/books/NBK148662/ [Last cited 2017 Jan 08].  Back to cited text no. 32
    
33.
Kenyon S, Ullman R, Mori R, Whittle M. Care of healthy women and their babies during childbirth: Summary of NICE guidance. BMJ 2007;335:667–8.  Back to cited text no. 33
    
34.
James AH, McLintock C, Lockhart E. Postpartum hemorrhage: When uterotonics and sutures fail. Am J Hematol 2012;87(Suppl 1):S16–22.  Back to cited text no. 34
    
35.
Bamfo JEAK. Managing the risks of sepsis in pregnancy. Best Pract Res Clin Obstet Gynaecol 2013;27:583–95.  Back to cited text no. 35
    
36.
Lucas DN, Robinson PN, Nel MR. Sepsis in obstetrics and the role of the anaesthetist. Int J Obstet Anesth 2012;21:56–67.  Back to cited text no. 36
    
37.
Galvão A, Braga AC, Gonçalves DR, Guimarães JM, Braga J. Sepsis during pregnancy or the postpartum period. J Obstet Gynaecol J Inst Obstet Gynaecol 2016;1–9.  Back to cited text no. 37
    
38.
Morgan J, Roberts S. Maternal sepsis. Obstet Gynecol Clin North Am 2013;40:69–87.  Back to cited text no. 38
    
39.
Maupin RT. Obstetric infectious disease emergencies. Clin Obstet Gynecol 2002;45:393–404.  Back to cited text no. 39
    
40.
Guinn DA, Abel DE, Tomlinson MW. Early goal directed therapy for sepsis during pregnancy. Obstet Gynecol Clin North Am 2007;34:459–479, xi.  Back to cited text no. 40
    
41.
van Dillen J, Zwart J, Schutte J, van Roosmalen J. Maternal sepsis: Epidemiology, etiology and outcome. Curr Opin Infect Dis 2010;23:249–54.  Back to cited text no. 41
    
42.
Kourtis AP, Read JS, Jamieson DJ. Pregnancy and infection. N Engl J Med 2014;370:2211–8.  Back to cited text no. 42
    
43.
Paruk F. Infection in obstetric critical care. Best Pract Res Clin Obstet Gynaecol 2008;22:865–83.  Back to cited text no. 43
    
44.
Hopkins L, Smaill F. Antibiotic regimens for management of intraamniotic infection. Cochrane Database Syst Rev 2002;3:CD003254.  Back to cited text no. 44
    
45.
Mackintosh N, Watson K, Rance S, Sandall J. Value of a modified early obstetric warning system (MEOWS) in managing maternal complications in the peripartum period: An ethnographic study. BMJ Qual Saf 2014;23:26–34.  Back to cited text no. 45
    
46.
Hu H, Pasca I. Management of Complex Cardiac Issues in the Pregnant Patient. Crit Care Clin 2016;32:97–107.  Back to cited text no. 46
    
47.
Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP, Guyton RA, et al. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: Executive summary: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2014;63:2438–88.  Back to cited text no. 47
    
48.
Banning AP, Pearson JF, Hall RJ. Role of balloon dilatation of the aortic valve in pregnant patients with severe aortic stenosis. Br Heart J 1993;70:544–5.  Back to cited text no. 48
    
49.
Guntupalli KK, Hall N, Karnad DR, Bandi V, Belfort M. Critical illness in pregnancy: Part I: An approach to a pregnant patient in the ICU and common obstetric disorders. Chest 2015;148:1093–104.  Back to cited text no. 49
    
50.
Rex S, Devroe S. Anesthesia for pregnant women with pulmonary hypertension. Curr Opin Anaesthesiol 2016;29:273–81.  Back to cited text no. 50
    
51.
John AS, Gurley F, Schaff HV, Warnes CA, Phillips SD, Arendt KW, et al. Cardiopulmonary bypass during pregnancy. Ann Thorac Surg 2011;91:1191–6.  Back to cited text no. 51
    
52.
Legrand M, Rossignol M, Muller F, Payen D. [Amniotic fluid embolism: An update]. Ann Fr Anesth Reanim 2013;32:189–97.  Back to cited text no. 52
    
53.
Balinger KJ, Chu Lam MT, Hon HH, Stawicki SP, Anasti JN. Amniotic fluid embolism: Despite progress, challenges remain. Curr Opin Obstet Gynecol 2015;27:398–405.  Back to cited text no. 53
    
54.
Thongrong C, Kasemsiri P, Hofmann JP, Bergese SD, Papadimos TJ, Gracias VH, et al. Amniotic fluid embolism. Int J Crit Illn Inj Sci 2013;3:51–7.  Back to cited text no. 54
[PUBMED]  [Full text]  
55.
Kanayama N, Tamura N. Amniotic fluid embolism: Pathophysiology and new strategies for management. J Obstet Gynaecol Res 2014;40:1507–17.  Back to cited text no. 55
    
56.
Kaur K, Bhardwaj M, Kumar P, Singhal S, Singh T, Hooda S. Amniotic fluid embolism. J Anaesthesiol Clin Pharmacol 2016;32:153–9.  Back to cited text no. 56
[PUBMED]  [Full text]  
57.
Kahyaoglu I, Kahyaoglu S, Mollamahmutoglu L. Factor VIIa treatment of DIC as a clinical manifestation of amniotic fluid embolism in a patient with fetal demise. Arch Gynecol Obstet 2009;280:127–9.  Back to cited text no. 57
    
58.
Leighton BL, Wall MH, Lockhart EM, Phillips LE, Zatta AJ. Use of recombinant factor VIIa in patients with amniotic fluid embolism: A systematic review of case reports. Anesthesiology 2011;115:1201–8.  Back to cited text no. 58
    
59.
Bern S, Weinberg G. Local anesthetic toxicity and lipid resuscitation in pregnancy. Curr Opin Anaesthesiol 2011;24:262–7.  Back to cited text no. 59
    
60.
Dun-Chi Lin J, Sivanesan E, Horlocker TT, Missair A. Two for One: A Case Report of Intravenous Lipid Emulsion to Treat Local Anesthetic Systemic Toxicity in Term Pregnancy. Case Rep 2017 [Epub ahead of print].  Back to cited text no. 60
    
61.
Ueland K, Novy MJ, Peterson EN, Metcalfe J. Maternal cardiovascular dynamics. IV. The influence of gestational age on the maternal cardiovascular response to posture and exercise. Am J Obstet Gynecol 1969;104:856–64.  Back to cited text no. 61
    
62.
Lavonas EJ, Drennan IR, Gabrielli A, Heffner AC, Hoyte CO, Orkin AM, et al. Part 10: Special Circumstances of Resuscitation: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2015;132(18 Suppl 2):S501–18.  Back to cited text no. 62
    
63.
Einav S, Kaufman N, Sela HY. Maternal cardiac arrest and perimortem caesarean delivery: Evidence or expert-based? Resuscitation 2012;83:1191–200.  Back to cited text no. 63
    
64.
Bhatia PK, Biyani G, Mohammed S, Sethi P, Bihani P. Acute respiratory failure and mechanical ventilation in pregnant patient: A narrative review of literature. J Anaesthesiol Clin Pharmacol 2016;32:431–9.  Back to cited text no. 64
[PUBMED]  [Full text]  
65.
Blix E, Brurberg KG, Reierth E, Reinar LM, Øian P. ST waveform analysis versus cardiotocography alone for intrapartum fetal monitoring: A systematic review and meta-analysis of randomized trials. Acta Obstet Gynecol Scand 2016;95:16–27.  Back to cited text no. 65
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]



 

Top
 
 
Search
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)  

 
  In this article
Abstract
Introduction
Indications for ...
Specific Conditi...
Conclusion
References
Article Tables

 Article Access Statistics
    Viewed1329    
    Printed22    
    Emailed0    
    PDF Downloaded455    
    Comments [Add]    

Recommend this journal