Abstract
Background:
Hemodynamic instability and respiratory distress are leading causes of intensive care unit (ICU) admissions following cesarean section (CS). Focused transthoracic echocardiography (FTTE) may help diagnose or rule out a cardiac cause of the clinical dilemma. We studied the diagnostic and therapeutic impact of FTTE in post-CS patients in the ICU.
Patients and Methods:
In this prospective observational study, 60 post-CS patients in the ICU requiring FTTE were studied for indications for FTTE. Following FTTE, the hemodynamic cause of hypotension was differentiated as hypovolemia, cardiac failure due to underlying cardiac conditions such as cardiomyopathy or valvular heart disease, sepsis, pulmonary embolism, and myocardial infarction. In respiratory distress, FTTE differentiated pulmonary edema secondary to cardiac causes from non-cardiac causes. FTTE was considered to have a diagnostic impact whenever, in a clinically unsuspected case, it diagnosed a new cardiac disorder, thus helping to narrow down to a single cause out of multiple differential diagnoses or ruled out a cardiac cause in a clinically suspected case. FTTE was considered to have a therapeutic impact whenever it led to an alteration in management.
Results:
FTTE diagnosed a new cardiac pathology in 18 (30%) patients and ruled out a worsening of existing cardiac function in 18 (30%) patients with known cardiac disease. An underlying cardiac condition was ruled out in 22 (36.66%) patients, supporting an alternate diagnosis. FTTE led to a change in the management of 45 (75%) patients.
Conclusion:
FTTE had a high diagnostic impact of 96.66% and a management impact of 75% in post-CS ICU admissions.
Keywords: Cardiomyopathy, cardiovascular pregnancy, complications, intensive care unit, transthoracic echocardiography
INTRODUCTION
Focused transthoracic echocardiography (FTTE), a point-of-care echocardiographic tool, helps clinicians detect and exclude cardiac abnormalities.[1] Post-cesarean section (CS) intensive care unit (ICU) admissions often result from hemodynamic instability and respiratory distress.[2] Maternal morbidity and mortality due to cardiovascular disease are increasing.[3] This is due to advanced maternal age, obesity, and a lack of universal antenatal care. Early symptoms, resembling normal pregnancy changes, often go unnoticed until late pregnancy or postpartum, when cardiovascular stress peaks.[4] Heart failure (HF), the most common peripartum cardiovascular complication, presents as pulmonary edema with dyspnea, cough, basal crackles, desaturation, arrhythmias, tachycardia, hypertension, or hypotension. Investigations often reveal congenital or acquired heart disease (HD), pulmonary hypertension, cardiomyopathy, or ischemic HD.[5] Peripartum acute breathlessness results from cardiogenic or non-cardiogenic causes. Peripartum shock can occur due to uncontrolled bleeding and cardiac failure secondary to congenital or acquired heart conditions, including valvular HD, cardiomyopathy, or myocardial infarction, sepsis, amniotic fluid, or pulmonary embolism.[6]
FTTE, a non-invasive, accurate, real-time diagnostic tool, assesses volume status, pumping function, and heart defects, aiding in managing fluids and medications, guiding early interventions, and enhancing survival rates by transforming management.[6,7] Limited evidence exists on how FTTE influences the diagnosis and management of patients admitted to the ICU post-CS. Our study evaluates FTTE’s impact on diagnosis and management in this context.
MATERIALS AND METHODS
This prospective observational cohort study was conducted in the post-anesthesia ICU of a tertiary hospital. With ethics committee approval, a consecutive convenient sample of 60 patients over 18 years of age who had undergone CS, admitted to the ICU within 42 days postpartum, and underwent FTTE in 1 year was selected. The trial was registered with the Clinical Trial Registry of India (CTRI/2022/12/047919). Readmissions within 42 days were only counted once. All participants or their next of kin provided written consent, as applicable. The patient’s characteristics, including age, body mass index, American Society of Anesthesiologists grade, gestational age, and gravidity, were noted. History of previous CS, associated medical and obstetric comorbidities, indication and anesthetic technique for present CS, indication for admission to the ICU and for ordering FTTE, and additional tests such as electrocardiogram, chest X-ray, and blood investigations were noted. Ongoing treatments, including oxygen supplementation, mechanical ventilation, fluid therapy, blood transfusions, and the use of vasopressors, inotropes, diuretics, vasodilators, antibiotics, and miscellaneous medications before TTE, were noted.
FTTE was ordered by the treating intensivist when there was a suspicion of an underlying cardiac disorder based on the patient’s clinical findings or when there were multiple differential diagnoses. All patients underwent FTTE after initial resuscitation, within 24 h of admission to the ICU. FTTE was done by cardiology residents trained in echocardiographic diagnosis using the Samsung Medison (Sono Ace R7)/Sonosite M-turbo ultrasound machines. The person performing the FTTE was not directly involved in treating the patient, minimizing observer bias. Two-dimensional parasternal long- and short-axis, apical 4- and 2-chamber, and subcostal 4-chamber views were obtained. Additional modalities included M-mode, Doppler color flow mapping, and pulsed- and continuous-wave Doppler. The following parameters were noted: 1. Left ventricle (LV) cavity size/area, and contractility, 2. Right ventricle (RV) volume and contractility, 3. LV systolic function or ejection fraction (EF), 4. LV primary diastolic dysfunction, 5. Inferior vena cava (IVC) collapsibility, and 6. Valve assessment. The diagnosis after FTTE in conjunction with clinical findings was noted under the following heads.
-
Obstetric hemorrhage: Reduced left ventricular end-diastolic diameter (LVEDD), normal or increased LV and RV contractility, IVC collapsing on inspiration, kissing heart.
Hemodynamic cause of hypotension: Reduced preload.
-
Cardiac failure: Increased LVEDD, reduced LV and RV contractility.
Hemodynamic cause of hypotension: Reduced contractility.
-
Sepsis: Normal LVEDD, increased LV and RV contractility.
Hemodynamic cause of hypotension: Vasodilatation.
-
Sepsis-induced cardiomyopathy: Increased LVEDD, reduced RV and LV contractility.
Hemodynamic cause of hypotension: Reduced contractility.
-
Pulmonary embolism: Increased RV end-diastolic diameter, increased RV size compared with LV, IVC fixed and dilated, presence of a thrombus in pulmonary arteries.
Hemodynamic cause of hypotension: Right HF.
-
Myocardial infarction: Normal LV and RV volumes, reduced LV contractility, regional wall motion abnormality.
Hemodynamic cause of hypotension: Reduced contractility, arrhythmia.
The following definitions were used to calculate the diagnostic and therapeutic impact.
Diagnostic impact: A change in the diagnosis after FTTE, defined as
FTTE was normal, though cardiac pathology was suspected clinically.
FTTE diagnosed new cardiac pathology, though not initially suspected clinically.
FTTE confirmed or ruled out cardiac pathology from multiple clinical differential diagnoses.
No diagnostic impact when FTTE findings matched the clinical diagnosis.
Therapeutic impact: change in management post FTTE, defined as
Step-up therapy: Escalation in treatment including fluid therapy, blood transfusion, escalation of basic O2 therapy to positive pressure ventilation, escalation from non-invasive to an invasive mode of ventilation, vasoactive drugs, diuretics, subspecialty consultation, surgery or invasive procedures, further diagnostic testing, or transfer to a different level of care.
Step-down therapy: Reduction or cessation of treatment, including withdrawing ventilator support, restricting fluid therapy, stopping vasoactive drugs, or medication change.
No therapeutic impact: No change in management.
The patients were followed up till discharge or 42 days postoperatively for survival or mortality. The patients were categorized as having a primary cardiac or non-cardiac pathology based on history, examination, and FTTE findings.
The sample size was calculated using ClinCalc.com with the following assumptions. One-third of obstetric ICU admissions require FTTE (enrolment ratio of 1:2). In 5% of patients, clinical assessment alone is diagnostic (based on our clinical experience). We considered FTTE to have a significant diagnostic impact if it detects the problems in four times more patients compared to clinical assessment. With an alpha error of 0.05 and a power of 80%, the sample size was calculated to be 52. To compensate for dropouts, 60 patients undergoing FTTE were included.
Descriptive data were analyzed using SPSS V23 (IBM SPSS Inc., Chicago, IL, USA). Data were represented as mean ± standard deviation (SD) and median [interquartile range (IQR)] as applicable. Continuous variables were compared by t-tests or Wilcoxon rank sum tests, as appropriate. Categorical outcomes were expressed as numbers (n) and percentages (%) and compared using Chi-square or Fisher’s exact tests, as applicable. P value < 0.05 was considered statistically significant.
RESULTS
Between December 2022 and November 2023, 11,879 deliveries were conducted at the hospital. Of these, 4264 patients underwent a CS. Admission to the ICU was required in 180 patients after CS. Sixty-one patients out of these underwent FTTE. One patient was excluded due to poor window, and data from 60 patients were analyzed (33.33%). Table 1 mentions the patient characteristics. Table 2 enumerates the associated comorbidities, indications for CS, and the anesthesia technique. Among the preoperatively diagnosed HD, three (5%) and 12 (20%) belonged to the modified World Health Organization (mWHO) risk classes III and IV, respectively. Table 3 states the indications for performing FTTE. FTTE was performed in 21 patients with hypotension requiring ionotropic support. Of these, four patients who also had tachycardia and pulmonary edema were diagnosed with cardiomyopathy (three patients had Peripartum cardiomyopathy (PPCM) with EF <35% and one had sepsis-induced cardiomyopathy with EF = 30%). One patient with hypotension and tachycardia disproportionately greater than that attributable to hemorrhage was diagnosed with PPCM with EF = 25%. Hemorrhage was suspected as a cause of hypotension in 12 patients. Of these, one was detected to have rheumatic mitral regurgitation and one had PPCM, ruling out an underlying cardiac cause in the remaining 10 patients. Sepsis was suspected as a cause of hypotension in six patients. One of these had a decreased LV function with EF = 30%, supporting a diagnosis of sepsis-induced cardiomyopathy. One patient was an operated case of double valve replacement, and FTTE ruled out perivalvular leak, clot, and vegetation and hence an underlying cardiac cause of symptoms. FTTE was normal in the rest. None of the patients had an FTTE diagnosis of pulmonary embolism or myocardial infarction.
Table 1.
Patient characteristics
| Parameter (n=60) | Value | |
|---|---|---|
| Age in years (Mean±SD) | 28.06±5.3 | |
| Patients aged >40 years, number (%) | 3 (5%) | |
| Body mass index (BMI) in kg/m2 (Mean±SD) | 27.31±5.08 (20–48) | |
| Patients with BMI >40 kg/m2, n (%) | 2 (3.33%) | |
| Preoperative ASA physical status, number (%) | 2 | 22 (36.7%) |
| 3 | 33 (55%) | |
| 4 | 5 (8.3%) | |
| Gestational age (weeks) | ≥34 | 43 (71.66%) |
| <34 | 17 (28.33%) | |
| Gravida | Primigravida | 24 (40%) |
| Multigravida | 36 (60%) | |
| Previous cesarean section | Yes | 23 (38.33%) |
| No | 37 (61.66%) | |
BMI=Body mass index; ASA=American Society of Anesthesiologists
Table 2.
Associated comorbidities, indication for cesarean section, and anesthesia technique
| Associated comorbidities (overlapping data) | Number of patients (%) | |
|---|---|---|
| Hypertensive disorders of pregnancy | PIH | 14 (23.33%) |
| PIH + HELLP | 7 (11.66%) | |
| Eclampsia | 6 (10%) | |
| Chronic hypertension + PIH | 5 (8.33%) | |
| Total | 32 (53.33%) | |
| Heart disease (Preoperatively diagnosed) |
Rheumatic heart disease | 8 (13.33%) |
| Peripartum cardiomyopathy | 6 (10%) | |
| Congenital heart disease | 2 (3.33%) | |
| Total | 16 (26.66%) | |
| Renal insufficiency: (Serum Creatinine >1.1 mg/dL) |
17 (28.33%) | |
| Anemia (Hemoglobin <7 g/dL) | 8 (13.33%) | |
| Hypothyroidism | 7 (11.66%) | |
| Diabetes mellitus | 5 (8.33%) | |
| Respiratory tract infection | 3 (5%) | |
| Indication for cesarean section (Overlapping data) | Fetal distress | 11 (18.3%) |
| Previous cesarean section | 16 (26.7%) | |
| Severe PIH | 15 (25%) | |
| Rheumatic heart disease | 8 (13.35%) | |
| Eclampsia | 6 (10%) | |
| Peripartum cardiomyopathy | 6 (10%) | |
| Abruptio placenta | 5 (8.33%) | |
| Failure of induction of labor | 4 (6.7%) | |
| Placenta previa | 3 (5%) | |
| Placenta percreta | 3 (5%) | |
| Anesthesia used for cesarean section | Spinal anesthesia | 13 (21%) |
| Combined spinal-epidural | 3 (5%) | |
| Epidural anesthesia | 1 (1.6%) | |
| Total (regional anesthesia) | 17 (28.33%) | |
| General anesthesia | 43 (71.66%) | |
PIH=Pregnancy-induced hypertension; HELLP=Hemolysis, elevated liver enzymes, low platelets
Table 3.
Indications for performing focused transthoracic echocardiography and significance of findings
| Parameter (n=60) | Total no. of patients (n=60) | FTTE: New/Significant finding (n=18) | FTTE: No change/WNL (n=42) |
|---|---|---|---|
| Desaturation | 54 (90%) | 17 (94.44%) | 37 (90.47%) |
| Tachycardia | 31 (51.66%) | 7 (38.88%) | 24 (57.14%) |
| Hypotension | 21 (35%) | 5 (27.77%) | 16 (38.09%) |
| Hypotension+Tachycardia | 3 (5%) | 1 (5.55%) | 2 (4.76%) |
| Hypotension+Desaturation | 3 (5%) | 1 (5.55%) | 2 (4.76%) |
| Tachycardia+Desaturation | 10 (16.66%) | 4 (22.22%) | 6 (14.28%) |
| Hypotension+Tachycardia+Desaturation | 15 (25%) | 3 (16.66%) | 12 (28.57%) |
| Uncontrolled Hypertension (systolic blood pressure >160 mmHg) | 18 (30%) | 8 (44.44%) | 10 (23.80%) |
| Post-cardiac arrest | 1 (1.66%) | 0 (0%) | 1 (2.38%) |
| Hypotension requiring vasopressor | 21 (35%) | 5 (27.77%) | 16 (38.09%) |
| Acute pulmonary edema | 45 (75%) | 14 (77.77%) | 31 (73.80%) |
| Unexplained tachycardia | 29 (48.33%) | 8 (44.44%) | 21 (50%) |
| Suspected valvular heart disease | 3 (5%) | 0 (0%) | 3 (7.14%) |
| Suspected cardiac cause | 36 (60%) | 14 (77.77%) | 22 (52.38%) |
| Suspected pulmonary embolism | 18 (30%) | 8 (44.44%) | 10 (23.80%) |
| Sepsis | 4 (6.66%) | 1 (5.55%) | 3 (7.14%) |
| Systemic emboli | 3 (5%) | 0 (0%) | 3 (7.14%) |
| Oliguria | 12 (20%) | 4 (22.22%) | 8 (19.04%) |
| Electrocardiographic changes/arrhythmia | 9 (15%) | 3 (16.66%) | 6 (14.28%) |
FTTE=Focused transthoracic echocardiography, WNL=Within normal limits
New cardiac conditions were diagnosed in 18 cases (30%). Of these patients, 17 had desaturation. Among the newly diagnosed HD, five (27.77%) patients belonged to the mWHO risk class of IV. Four were diagnosed as PPCM, with two cases having EF <30%. Three of these patients had presented with desaturation requiring oxygen, hypotension requiring vasopressor support, and persistent tachycardia, and the fourth patient presented with desaturation alone. Symptoms had developed gradually after the baby’s delivery in all patients. None had any prior history indicating underlying HD or hypertensive disease of pregnancy. All these patients survived. One patient who had sepsis-induced cardiomyopathy had persistent hypotension, tachycardia, and desaturation. The patient with cardiomyopathy secondary to pregnancy-induced hypertension (PIH) had desaturation and uncontrolled hypertension. One patient with rheumatic valvular HD, having severe pulmonary hypertension, presented with respiratory distress and desaturation postoperatively. Eleven patients with severe PIH had LV diastolic dysfunction with hypertensive HD, including three cases with pulmonary hypertension. All presented with desaturation, and eight also had uncontrolled hypertension. FTTE findings ruled out HF in preoperatively diagnosed cardiac pathology in 18 (30%) patients [Table 4]. It ruled out an underlying cardiac disease in 22 (36.66%) patients.
Table 4.
Diagnostic impact of focused transthoracic echocardiography
| Parameters | n (%) (overlapping data) | |||||
|---|---|---|---|---|---|---|
| I | FTTE detected new cardiac pathology in previously undiagnosed patients | 18 (30) | ||||
| 1 | Newly diagnosed cardiomyopathy with EF <45% | 6 (10) | ||||
| Subclassification as per EF | ||||||
| EF >30% | 4 (6.67) | |||||
| EF <30% | 2 (3.33) | |||||
| Subclassification as per cause | ||||||
| A | Total peripartum cardiomyopathy (PPCM) | 4 (6.67) | ||||
| PPCM <30% | 2 (3.33) | |||||
| PPCM> 30% | 2 (3.33) | |||||
| B | Sepsis-induced cardiomyopathy | 1 (1.67) | ||||
| C | PIH-induced cardiomyopathy | 1 (1.67) | ||||
| 2 | Newly diagnosed valvular heart disease | 2 (3.33) | ||||
| RHD + Valvular HD + severe PAH | 1 (1.67) | |||||
| RHD + Valvular HD + PIH | 1 (1.67) | |||||
| 3 | PIH induced changes | 11 (18.33) | ||||
| Left ventricular diastolic dysfunction | 11 (18.33) | |||||
| Hypertensive heart disease | 8 (13.33) | |||||
| Pulmonary artery hypertension | 3 (5) | |||||
| II | FTTE ruled out cardiac failure in preoperatively diagnosed cardiac pathology | 18 (30%) | ||||
| 1 | Total preoperatively diagnosed PPCM | 6 (10) | ||||
| PPCM EF <30% | 1 (1.67) | |||||
| PPCM EF >30% | 5 (8.33) | |||||
| PPCM + PIH | 5 (8.33) | |||||
| 2 | Preoperatively diagnosed RHD + valvular HD | 8 (13.33) | ||||
| RHD + Valvular HD + PAH | 5 (8.33) | |||||
| RHD + Valvular HD without PAH | 3 (5) | |||||
| RHD + PIH | 1 (1.67) | |||||
| 3 | Preoperatively diagnosed congenital HD | 2 (3.33) | ||||
| Eisenmenger with atrial septal defect with pulmonary artery hypertension | 1 (1.67) | |||||
| 4 | Arrhythmia | 2 (3.33) | ||||
| III | FTTE ruled out new cardiac pathology/cardiac failure with normal findings | 22 (36.67) | ||||
| 1. | Anemia | 21 (35) | ||||
| PIH+Anemia | 10 (16.67) | |||||
| 2. | Hemorrhagic Shock | 10 (16.67) | ||||
| 3. | Sepsis | 7 (11.67) | ||||
| 4. | Associated renal dysfunction | 21 (35) | ||||
| PPCM + Renal insufficiency | 5 (8.33) | |||||
| PIH + Renal insufficiency | 10 (16.67) | |||||
| 5. | Associated respiratory infection | 8 (13.33) | ||||
| 6. | Associated metabolic acidosis | 10 (16.67) | ||||
| Overall Diagnostic Impact | 58 (60) | |||||
FTTE=Focused transthoracic echocardiography; EF=Ejection fraction; PPCM=Peripartum cardiomyopathy; PIH=Pregnancy-induced hypertension; RHD=Rheumatic heart disease; HD=Heart disease; PAH=Pulmonary artery hypertension
The clinical picture was suggestive of multiple differential diagnoses in 58 of 60 patients. Of these, 18 patients were diagnosed with a new cardiac condition, and 18 had pre-existing cardiac conditions without worsening existing cardiac function. In the remaining 22 patients, FTTE was normal. The clinical picture suggested “one particular diagnosis” in two patients. One had a supraventricular tachycardia diagnosed preoperatively, and the postoperative FTTE was normal. The other patient had a convulsion and altered sensorium. FTTE ruled out cardiac vegetation or thrombus as a cause of the symptoms.
The diagnostic impact was 96.66%, with FTTE ruling out cardiac disease or worsening pre-existing cardiac function in 66.66% (40) of cases, confirming alternative diagnoses. FTTE effected changes in treatment in 45 patients (75%) [Table 5], two of whom succumbed. The overall survival rate was 88.33% (53 patients), and the mortality rate was 11.67% (7 patients). Of the 119 patients who did not undergo FTTE, eight died. The mortality rate in patients who did not undergo FTTE was 6.72% (8 of 119 patients) (P = 0.230).
Table 5.
Changes in management after focused transthoracic echocardiography
| Change in management | Number of patients (%) |
|---|---|
| Starting or modifying the furosemide dose | 45 (75%) |
| Guiding fluid/blood therapy | 45 (75%) |
| Weaning from mechanical ventilator | 30 (50%) |
| Weaning from Oxygen | 25 (41.66%) |
| Weaning off inotropic support | 14 (23.33%) |
| Adding anticoagulant | 13 (21.66%) |
| Starting beta-blocker | 10 (16.66%) |
| Starting inotropic support | 4 (6.66%) |
| Ordering computed tomography pulmonary angiography | 4 (6.66%) |
| Modifying the dose of beta-blocker | 2 (3.33%) |
| Adding digoxin | 2 (3.33%) |
| Adding enalapril | 2 (3.33%) |
| Transferring patients to the cardiac intensive care unit | 2 (3.33%) |
DISCUSSION
Maternal cardiovascular disease is a leading cause of maternal death, with HF being the most common major cardiovascular complication arising during and after pregnancy.[5,8] Considering cardiovascular disease in the differential diagnosis could prevent a fourth of maternal deaths.[8,9] Our study found that 30% of patients were newly diagnosed with HD. Indian data indicates that almost 69% of pregnant patients with HD are diagnosed during pregnancy and 31% during labor.[10]
In our study, three patients were over 40 years old, and two had class III obesity. The risk of HD-related death increases 30 times with advancing maternal age.[8] Among our patients, 53 (88.33%) were at risk of developing cardiac complications due to hypertension, diabetes, or pre-existing HD. FTTE confirmed cardiovascular disease in about 36% of suspected patients. Morbid obesity and chronic health conditions such as hypertension, diabetes, and chronic cardiovascular disease significantly raise the risk of myocardial infarction and HF. Obstetric risk factors for HF include multiple gestations, gestational or chronic hypertension, pre-eclampsia/eclampsia, postpartum hemorrhage, and gestational diabetes mellitus.[9]
In our study, 12 patients, including preoperatively and newly diagnosed cases, had PPCM, with half additionally having PIH. There is an increase in the prevalence of high-risk cardiac conditions contributing to 26.7% of pregnancy-related deaths.[11] Cardiomyopathies account for a rise of 18%, the other cause being pulmonary hypertension (PH).[12] Both conditions are mWHO class III or IV pregnancy risk, i.e., pregnancy either significantly elevates the risk of maternal morbidity and mortality or is contraindicated. Cardiomyopathy, the leading cause of HF, carries a 46% risk of cardiovascular adverse events.[13] PIH and eclampsia are substantial risk factors for PPCM, with a prevalence of 22% in patients with PPCM, compared to 5% in the general population.[14] The European Society of Cardiology EUR Observational Research Program PPCM Registry reported a 39% prevalence of hypertensive disorders and a 25% prevalence of pre-eclampsia in patients with PPCM.[15] Women who die from cardiovascular disease have either undiagnosed or new-onset cardiovascular disease of pregnancy, specifically peripartum cardiomyopathy.[3,9,10]
As a tertiary care center, we admit a higher number of at-risk patients. The rate of performing FTTE is higher in our study than in a previous report, likely due to the severity of the illness, with one-third of patients classified as mWHO class III or IV.[16] The American College of Obstetricians and Gynecologists recommends serial monitoring using TTE during pregnancy and postpartum, even in diagnosed cases of HD, due to a 13% risk of acute HF. The risk increases to 33% in pre-existing cardiomyopathy.[8] Acute HF with preserved EF (≥50%) can occur in pregnancy and postpartum, often associated with hypertensive syndromes of pregnancy and acute diastolic HF related to excessive afterload.[5]
Respiratory distress or acute pulmonary edema can have cardiogenic or non-cardiogenic origins and cannot be differentiated clinically.[5,17,18] We found no difference in the clinical features between patients with a new cardiac finding and those without on FTTE [Table 3], proving that clinical evaluation alone is insufficient. FTTE is valuable for identifying or ruling out underlying cardiac conditions, thus impacting diagnosis. Hall and others have concluded likewise.[19] The common differential diagnoses in our study prompting FTTE included acute pulmonary edema and suspected cardiac disorder. In another study, primary indications were myocardial dysfunction, dyspnea, hypoxemia, or undifferentiated respiratory failure.[16]
We diagnosed new cardiac conditions in 30% of patients. Echocardiography is commonly used to assess LV function in shock, volume status, and valvular dysfunction.[1,20] Diastolic dysfunction is an important hemodynamic abnormality in severe pre-eclampsia. Pulmonary edema in the patient with pre-eclampsia may be cardiogenic due to left ventricular hypertrophy with diastolic dysfunction or non-cardiogenic in origin after excessive intravenous fluid administration or a combination of both. Echocardiography helps differentiate between the two.[21,22,23] Smith identified pathological findings in 66% of patients who underwent CS and required ICU admission, including LV and RV dysfunction, valvular regurgitation, pulmonary hypertension, diastolic dysfunction, and valvular stenosis.[16] A systematic review by Heiberg et al.[1] noted a change in diagnosis in 33%–37% of patients due to focused echocardiography in the ICU. LV dysfunction was the most common new diagnosis, followed by valve disease, RV dysfunction, or hypervolemia. Other authors found similar findings.[20,24]
The impact of FTTE on diagnosis and management matches previous research, where it was performed for recognized indications or unanswered clinical questions rather than used as a screening tool.[1,16,20,24] FTTE improved diagnosis and management, probably improving survival and reducing mortality. Common management changes in our study included adjusting diuretics, fluids, blood transfusions, and weaning from ventilators and inotropes. Once the diagnosis is established, the initiation of condition-specific treatment expedites weaning from oxygen, ventilator, and inotropes. Other studies reported similar changes, including adjustments in fluid, inotropes, and medication administration.[1,20] Pharmacological therapy for HF is expedited once the diagnosis is established. Management of patients in cardiogenic shock or newly diagnosed PPCM with severely reduced EF involves optimizing oxygenation with mechanical ventilation and restoration of hemodynamics with vasopressors (norepinephrine being the first line), inotropic support with dobutamine, and preload optimization. FTTE-guided diuretics or fluid therapy avoids fluid overload and intravascular fluid depletion secondary to peripartum blood loss or aggressive diuretic therapy. Diuretics must be used carefully in patients with pulmonary edema, especially in PIH, to avoid further depletion of intravascular volume and subsequent acute kidney injury. Once hemodynamic stabilization is achieved, HF treatment with beta-blockers, angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, angiotensin receptor neprilysin inhibitors, or aldosterone antagonists is started. Hydralazine and nitrates are indicated to reduce blood pressure or afterload in the presence of hypertension, severe LV dysfunction, and/or evidence of congestion in decompensated HF. Low molecular weight or unfractionated heparin is started in patients suspected or at high risk for thromboembolic complications such as those with EF < 35% or pulmonary embolism. Intravenous diuretic therapy and guided fluid therapy benefit patients with severe valvular stenosis, those with failing ventricles, or severe pre-eclamptic patients in whom diastolic dysfunction is a contributor to pulmonary edema. LV diastolic dysfunction hampers weaning from mechanical ventilation, with TTE indices guiding therapeutic interventions.[25,26] Treating PPCM is challenging due to its varied presentation, ranging from subtle signs to cardiogenic shock, requiring careful differentiation from other causes of HF.[5,21,22,23,27,28,29,30,31]
Four newly diagnosed cases of PPCM, including two preoperatively asymptomatic patients with EF < 30%, highlight the crucial role of FTTE in early diagnosis and goal-directed management, impacting patient outcomes and survival. Echocardiography-based recommendations for intravenous fluids and inotropes improved 28-day survival compared to standard treatment in critically ill patients.[32] We performed FTTE only in patients who were sicker or when there was a diagnostic dilemma due to multiple differential diagnoses, explaining the higher mortality in patients in whom FTTE was performed. Despite timely FTTE, two patients could not be saved due to multiple factors such as pre-eclampsia, HELLP syndrome, sepsis, and disseminated intravascular coagulation.
One limitation of our study is its observational nature, as conducting a randomized study would be unethical given FTTE’s life-saving role in critical patients. Including lung ultrasound in the study could have enhanced its diagnostic and therapeutic efficacy.
CONCLUSION
FTTE significantly impacts diagnosis and management in patients admitted to the ICU post-CS. Obstetric anesthesiologists and intensivists managing complex cases should utilize this technology routinely for real-time hemodynamic assessment and immediate diagnostic capability. FTTE should be routinely used in obstetric patients admitted to the ICU, especially in clinical dilemmas with multiple differential diagnoses having similar clinical presentations.
Ethical clearance
The study was performed after approval from the institutional ethics committee (IEC/348/21).
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Conflicts of interest
There are no conflicts of interest.
Funding Statement
Nil.
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